%42%69%6f%6c%6f%67%69%63%61%6c%20%53%63%69%65%6e%63%65%73
-
KAIST Identifies a “Hidden Amplification Switch” in Lymphangiogenic Signaling
Lymphatic vessels act as the body’s “drainage system,” collecting excess fluid from tissues. When lymphatic drainage is impaired because lymphatic vessels are underdeveloped, damaged, or dysfunctional, lymphedema can develop, causing swelling, particularly in the arms and legs. Conversely, excessive lymphatic vessel growth around tumors can facilitate cancer metastasis by providing routes for tumor cells to spread. Korean researchers have discovered that VEGF-C brings two VEGFR-3 receptors together, and the resulting VEGF-C–VEGFR-3 complexes further cluster to amplify signaling. Targeting this clustering process may provide a new strategy for either enhancing or suppressing lymphangiogenic signaling, depending on the disease context.
KAIST (President Choongsik Bae) announced on October 2 that a joint research team led by Professor Ho Min Kim from the Department of Biological Sciences at KAIST and Dr. Sangkyu Lee of the Institute for Basic Science (IBS; President Suk Bok Chang) determined the three-dimensional structure of the VEGF-C–VEGFR-3 complex and identified how higher-order clustering of these complexes amplifies signaling.
When VEGF-C binds to VEGFR-3 on the cell surface, the receptor is activated and signals that regulate the formation and function of lymphatic vessels are transmitted into the cell. Until now, VEGF-C-mediated dimerization of two VEGFR-3 receptors has been considered a key step in receptor activation. However, how the signal becomes further amplified after this step has not been fully understood.
The research team examined the structure of VEGF-C bound to VEGFR-3 using cryogenic electron microscopy (cryo-EM), which enables detailed visualization of the three-dimensional structures of proteins. They found that VEGF-C-induced complexes containing two VEGFR-3 receptors further assembled side by side into higher-order clusters. This revealed a new structural mode by which VEGF-C–VEGFR-3 complexes can organize laterally along the cell membrane.Simply put, it is like two people first forming a team to begin a task, and then multiple teams gathering together to increase their collective strength. The researchers also tested whether this clustering actually amplifies signaling. By altering the regions where the complexes contact one another and by using light to control receptor clustering, they confirmed that the gathering of multiple complexes plays an important role in signal amplification.
This study identifies a new point at which lymphangiogenic signaling could potentially be regulated. In the future, researchers may explore ways to enhance signaling when lymphatic vessel formation is insufficient and to suppress signaling when excessive lymphatic vessels form around tumors. However, this study did not demonstrate therapeutic effects for lymphedema or the inhibition of cancer metastasis, and further research will be required before the findings can be applied to actual treatments.
Professor Ho Min Kim said, “This study reveals how two VEGFR-3 receptors first form a ligand-induced pair, after which multiple such complexes cluster together to further amplify the signal for lymphangiogenesis ,” adding, “By identifying this previously unseen ‘hidden amplification switch’ in lymphangiogenic signaling, we expect this work to provide an important foundation for developing new therapeutic strategies for related diseases such as lymphedema and cancer metastasis.”
Dr. Ryeongeun Cho of the KAIST InnoCORE AI-CRED Innovative Drug Research Group and Dr. Jinsook Ahn of the KAIST Department of Biological Sciences participated in the study as co-first authors. Professor Ho Min Kim of KAIST and Dr. Sangkyu Lee of IBS led the research as co-corresponding authors. The findings were published online on September 9 in the international journal Advanced Science.
Paper title: Structural Basis of Lymphangiogenic Receptor VEGFR-3 Activation Mediated by Distinctive Clustering of the Ligand–Receptor Complex, DOI: 10.1002/advs.77728
Related videos:
Video showing cryo-EM sample preparation by rapidly freezing protein samples at cryogenic temperatures: https://drive.google.com/file/d/1OGPpkzmZMaWU3oxfswpbcEtt3NzX3n4q/view?usp=drive_link
Video showing the grid screening process for cryo-EM image collection: https://drive.google.com/file/d/1Bg6zEPeS9NZDO8zFaj59Fe7L_f8tBWwQ/view?usp=drive_link
Video showing the loading of frozen protein samples into the cryo-EM instrument: https://drive.google.com/file/d/19c1INwek38B72KKPPXmPVTggYAoO4aY3/view?usp=drive_link
Titan Krios cryo-EM instrument installed at KAIST KARA: https://drive.google.com/file/d/1c5Wmj44_9taYIW4N_mumg6tT21iOUYNQ/view?usp=drive_link
Video of the molecular structure of the VEGF-C and VEGFR-3 complex identified in this study: https://drive.google.com/file/d/198bcFoTb_pv__Ep-MHwcI47G4gv5yisx/view?usp=drive_link
This work was supported by the National Research Foundation of Korea (RS-2024-00397681, RS-2025-00523615 to H.M.K. and RS-2025-00523575 to J.A.), the InnoCORE program of the Ministry of Science and ICT (N10250153 to H.M.K. and R.C.), the NEXUS & CELINE consortium, the KAIST Convergence Research Institute Operation Program, and the Institute for Basic Science (IBS-R001-Y4 to S.L.), among others.
2026.10.02 View 837 -
KAIST Researchers Uncover How Neurons Deliver RNA to Where It Is Needed
Much like a courier reading an address on a package, neurons must deliver RNA to the precise locations where it is needed. A KAIST research team has discovered how a small chemical modification on RNA acts as a “delivery tag,” helping selected RNAs travel to distant regions of neurons.
The findings provide a basis for investigating RNA “delivery errors” in brain disorders—cases in which RNA is produced normally but fails to reach its intended destination—and may ultimately inform the development of new therapeutic strategies.
KAIST (President Choongsik Bae) announced on September 14 that a research team led by Professor Ki-Jun Yoon of the Department of Biological Sciences has identified a mechanism through which N6-methyladenosine, or m6A, facilitates the transport of specific RNAs to distal axons, the long, cable-like projections of neurons.
Unlike most other cells, neurons have long, highly branched extensions. Axons transmit signals to other neurons, while dendrites receive incoming signals. For the brain to develop and function normally, these structures must grow properly and form appropriate connections.
Because neurons can extend over considerable distances, RNA produced in the cell body may be needed far away, including at the growing tip of an axon. Neurons must therefore identify particular RNAs among thousands of candidates and transport them to the correct subcellular locations.
Just as producing a package does not complete its delivery—the package must also reach the correct address—producing RNA is only part of the process. RNA must arrive at the right place at the right time. However, the mechanisms through which neurons select and transport RNAs over long distances have remained incompletely understood.
The research team found that m6A, a small chemical modification added to RNA, plays an important role in this process. m6A is a modification of adenosine, one of the building blocks of RNA, and is known to influence several aspects of RNA metabolism, including stability and translation. The new study shows that m6A can also function as a molecular “delivery tag” that promotes the transport of specific RNAs to distal regions of neurons.
The researchers first examined mice in which Mettl14, a component of the enzyme complex that installs m6A on RNA, was deleted from developing neurons. In the absence of normal m6A modification, the neurons exhibited impaired axon projection and neurite development. These findings confirmed that m6A plays an important role in the early development of neurons.
The team then used a high-resolution technique known as m6A-SAC-seq to map the precise locations of m6A modifications in RNA from the developing mouse brain at single-nucleotide resolution. The resulting map revealed that RNAs associated with axon development and synapse organization were among those marked by m6A.
The researchers also identified how this “delivery tag” is recognized and connected to the cellular transport machinery. They found that YTHDF2, a protein that recognizes m6A-modified RNA, works with the RNA-binding protein FMRP and the motor protein KIF5C to facilitate the transport of RNA along neuronal processes.
In the delivery analogy, m6A serves as the tag attached to the RNA, YTHDF2 reads the tag, and FMRP and KIF5C help connect the RNA to the cellular machinery that carries it toward its destination.
YTHDF2 has previously been studied primarily for its role in promoting the degradation of RNA that is no longer needed. This study reveals an additional function: in developing neurons, YTHDF2 also helps transport specific RNAs to distal locations rather than simply directing them toward degradation.
The findings offer a new perspective on the study of brain disorders. Research has traditionally focused on whether RNA is produced and maintained correctly. The new results suggest that researchers should also consider whether normally produced RNA is delivered to the correct location within a neuron.
In other words, neurological dysfunction may potentially arise not only from defects in RNA itself, but also from problems with the molecular tags or transport machinery that determine where the RNA travels.
Future studies could investigate whether such RNA delivery errors occur in neurodevelopmental or neurodegenerative disorders and whether they contribute to neuronal dysfunction or disease onset. If such links are established, the findings could eventually support the development of therapeutic approaches that regulate RNA transport and restore the delivery of specific RNAs to their intended locations.
The high-resolution m6A map of the developing nervous system generated in this study may also serve as a valuable resource for examining how RNA modification and intracellular transport change during brain aging and neurodegenerative disease.
“Our study shows that a small chemical modification on RNA does more than regulate RNA stability—it also plays an important role in delivering specific RNAs to the locations where they are needed within neurons,” said Professor Yoon. “We hope these findings will provide a foundation for understanding why RNA may fail to reach its intended destination in brain disorders and for exploring new therapeutic possibilities.”
Bonsang Koo, Dr. Ajeet Kumar, and Huiseon Hwang of the KAIST Department of Biological Sciences contributed equally to the study as co-first authors. The paper was published in Nature Communications on July 30.
Paper title: The m⁶A reader YTHDF2 regulates mRNA transport and axon outgrowth in developing neurons
DOI: 10.1038/s41467-026-76161-8
Author information: Co-first authors (Bonsang Koo, Ajeet Kumar, Huiseon Hwang); Contributing authors (Minyeong Park, Sung-Min Lee, Ki-Heon Lee, Ji-Hoon Moon, Jaewon Yang, Chan-Woo Park, Saebom Lee, Hee-Jung Jo, Woo-il Kim, Eunji Cho, Hagyeong Lee, Chang-Won Lee, Jae-Sung Woo, Jong Hyuk Yoon, Yoon Ki Kim); Corresponding author (Ki-Jun Yoon)
This work was supported by National Research Foundation of Korea (NRF) grants (2020M3A9E403967022, RS-2024-00332454, RS-2024-00440778, and RS-2026-25488918 to K.-J.Y.) funded by the Korean Ministry of Science and ICT, and Future Planning (MSIP), the POSCOScience Fellowship from the POSCO TJ Park Foundation (to K.-J.Y.), the Young Investigator Grant from the Suh Kyungbae Foundation (to K.-J.Y.), the Korea Brain Research Institute (KBRI) Basic Research Program through the Korea Brain Research Institute, funded by the Ministry of Science and ICT (MSIT) (24-BR-02-03 to J.H.Y).
2026.09.14 View 3709 -
Vitamin A Derivative Preserves T Cells’ Function as KAIST Points to a New Strategy for Treating Intractable Brain Tumors
Immune cells can become exhausted after prolonged exposure to cancer, gradually losing their ability to attack tumor cells. This phenomenon is particularly pronounced in aggressive brain tumors and can severely limit the effectiveness of immunotherapy. A KAIST research team has now discovered that all-trans retinoic acid (ATRA), a vitamin A derivative, may help prevent such exhaustion and enhance the efficacy of immune checkpoint inhibitors.
KAIST (President Choongsik Bae) announced on September 8 that a research team led by Professor Heung Kyu Lee from the Department of Biological Sciences, in collaboration with researchers from Seoul St. Mary's Hospital, and Konyang University College of Medicine, has found that all-trans retinoic acid (ATRA), a form of active vitamin A metabolite, suppresses the "terminal exhaustion" of CD8⁺ T cells that attack cancer cells within brain tumors, and can enhance the effect of anti-PD-1 immunotherapy. Anti-PD-1 is a leading immuno-oncology drug (immune checkpoint inhibitor).
Glioblastoma is a representative form of intractable brain cancer that frequently recurs even after surgery, radiation, and chemotherapy. Immune checkpoint inhibitors have shown only limited effect against the disease. One key reason is that immune cells that infiltrate the tumor become exhausted after prolonged combat and lose their functional capacity.
Cells that reach a state of terminal exhaustion in particular lose their ability to kill cancer cells, much like soldiers who have exhausted themselves in prolonged combat. In this state, achieving sufficient therapeutic effect is difficult even with anti-PD-1 therapy, which releases the "brake" cancer cells impose on immune cells.
To address this problem, the research team tried to figure out how to prevent immune cells from reaching total burnout, rather than how to revive the cells. Subsequently, the research team focused on the signaling of ATRA, an active vitamin A metabolite known to regulate cell differentiation and function.
Using an in-vitro model that mimicked the hypoxic, exhaustion-promoting tumor microenvironment of brain tumors, the team induced exhaustion in CD8⁺ T cells. Those conditioned with ATRA progressed to terminal exhaustion at a markedly lower rate. These cells also produced higher levels of immune molecules essential for attacking cancer — including interleukin-2 (IL-2), interferon gamma (IFN-γ), and tumor necrosis factor alpha (TNF-α) — and retained their ability to kill brain tumor cells.
The team also confirmed that ATRA activates WNT/β-catenin signaling within CD8⁺ T cells and increases TCF-1βBD, a TCF-1 isoform important for maintaining T-cell function. In simple terms, the vitamin A metabolite turns on a "function-preserving switch" inside immune cells, helping them avoid complete exhaustion even during prolonged combat with cancer cells.
The effect was also confirmed in mouse glioma models. CD8⁺ T cells conditioned with ATRA maintained better immune function within the tumor, and oral administration of ATRA alone also increased both the number and function of tumor-infiltrating CD8⁺ T cells. As tumor burden decreased, survival was also extended. Notably, in a model of recurrent brain tumors, anti-PD-1 immunotherapy alone showed only limited effect, but combining it with ATRA substantially improved tumor suppression and long-term survival outcomes.
In other words, if anti-PD-1 therapy releases the "brake" imposed on immune cells, ATRA keeps their "battery" from running completely dead. By combining the two approaches, the researchers propose a new combination-therapy strategy that could help overcome the limitations of existing immunotherapy.
The team also analyzed publicly available human glioblastoma datasets. In single-cell transcriptomic data from patients treated with anti-PD-1 therapy, CD8⁺ T cells from responders showed higher retinoic-acid-responsive and WNT signaling gene signatures than those from non-responders. Separately, in an immunotherapy-naïve glioblastoma cohort, patients with a higher proportion of retinoic-acid-responsive CD8⁺ T cells showed significantly better overall survival. The team noted that this study does not directly demonstrate ATRA's therapeutic efficacy in patients, and that further clinical research will be needed to confirm appropriate administration methods, dosages, and combination effects with immunotherapy drugs before it can be applied to actual brain tumor treatment.
Professor Heung Kyu Lee said, "Glioblastoma is one of the cancers most resistant to immunotherapy, because immune cells within the tumor readily become exhausted." He added that the study is meaningful for presenting a molecular mechanism by which active vitamin A signaling helps prevent the terminal exhaustion of CD8⁺ T cells while preserving their anti-cancer function. He also noted that future work validating more precise delivery methods or combination strategies could establish this as a new approach for improving the responsiveness of immunotherapy against intractable brain tumors.
The study was conducted with Dr. In Kang, a postdoctoral researcher in KAIST's Department of Biological Sciences, as first author, and Professor Heung Kyu Lee as corresponding author. Professor Jae-Byum Chang from KAIST's Department of Materials Science and Engineering, Professor Sung Ki Lee from Konyang University College of Medicine, and Professor Stephen Ahn from Seoul St. Mary's Hospital also participated in the research. The findings were published on August 26 in the international journal Signal Transduction and Targeted Therapy.
Paper title: All-trans retinoic acid suppresses CD8⁺ T-cell terminal exhaustion and potentiates anti-PD-1 therapy in glioblastoma
DOI: 10.1038/s41392-026-02852-9
This work was supported by National Research Foundation of Korea grants (RS-2023-NR077244, RS-2024-00439735, RS-2026-25509011 to H.K.L. and RS-2024-00352668 to S.A.). This study was also supported by the Samsung Science and Technology Foundation (SSTF-BA1902-05 to H.K.L.), Republic of Korea. This research was also supported by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (RS-2023-00302794 to J.B.C.).
2026.09.08 View 3735 -
KAIST Professor Jaekyung Kim Selected as One of Asia's 12 Next-Generation Scientists
KAIST (President Choongsik Bae) announced on September 4 that Professor Jaekyung Kim from the Department of Biological Sciences has been selected as a Fellow of the “2026 Asian Young Scientist Fellowship (AYSF),” a program that supports promising young scientists across Asia.
The Asian Young Scientist Fellowship (AYSF) is a privately funded research fellowship in Asia, established to support young scientists in carrying out creative and challenging research. Since selecting its first cohort of Fellows in 2023, the AYSF selects 12 early-career researchers each year across the fundamental science disciplines of life sciences, physical sciences, and mathematics and computer science. Each selected Fellow receives a total of $100,000 USD over two years to support their research.
The AYSF does more than support young scientists across individual academic disciplines —it actively encourages interdisciplinary research that transcends traditional disciplinary boundaries to open new research directions. It places particular emphasis on supporting young scientists at the critical stage of launching their careers as independent researchers, helping them develop creative ideas and pioneer new areas of research.
Candidates are nominated from among full-time researchers at universities or research institutions in Asia who are within 10 years of completing their terminal degree (Ph.D./M.D.). Among the nominated candidates, a Selection Committee composed of scientists from Asia and around the world conducts a comprehensive evaluation of each candidate’s research achievements and future research potential.
This year, 12 early-career researchers in Asia were selected as 2026 Fellows Professor Kim was named a Fellow in the life sciences category, alongside Professor Mikyung Shin of Sungkyunkwan University, making them the two Fellows affiliated with Korean universities. Previous AYS Fellows from Korea include Professor Kyeongsu Choi of the Korea Institute for Advanced Study (KIAS) in 2023; Professor Jiheong Kang of Seoul National University in 2024; and Professor Seongjun Park of Seoul National University and Professor In-Jee Jeong of KIAS in 2025.
Professor Kim studies how the brain organizes experiences and information into memories during sleep. Using a systems- and computational-neuroscience approach, he focuses on memory consolidation—the process by which information learned during the day becomes stabilized into long-term memory during sleep—and the neural mechanisms involved. He also analyzes biological signals related to dreaming and investigates how sleep affects higher cognitive functions such as creative thinking.
Professor Kim received his bachelor's degree from Hanyang University and his Ph.D. from KAIST, and completed postdoctoral research at the University of California, San Francisco (UCSF) and the San Francisco VA Medical Center. He joined the KAIST Department of Biological Sciences in 2023 and currently leads the Neural Processing Lab.
The 2026 AYS Fellows will attend the 2026 AYSF Annual Conference on November 9, 2026, at the University of Hong Kong to showcase their research work and innovative ideas.
2026.09.04 View 2716 -
KAIST Gives Antibodies “Eyes” to Detect Cancer, Targeting Cancer Mutations Inside Cells
Antibodies are like “guided missiles” that find and attack cancer cells, but cancer-causing mutations inside cells have remained a “blind spot” for treatment because antibodies cannot reach them. KAIST researchers have now succeeded in precisely targeting even intracellular cancer mutations using a newly designed antibody created through computational methods. This achievement is expected to open a new path toward next-generation precision therapies for difficult-to-treat cancers, going beyond the limitations of conventional antibody treatments.
KAIST (President Choongsik Bae) announced on the 24th of July that a research team led by Professor Byung-Ha Oh from the Department of Biological Sciences, together with researchers from Therazyne, a KAIST faculty startup specializing in protein design and headed by Professor Oh, has developed an antibody that selectively recognizes only cancer cells carrying KRAS(G12D), a representative cancer-driving mutation. By combining computational antibody design with experimental validation, the team designed a new antibody that would have been difficult to develop through conventional approaches and is now verifying its efficacy in animal disease models.
KRAS(G12D) is a mutated form of the KRAS protein, which regulates cell growth and proliferation. It is one of the most common cancer-driving mutations found in pancreatic, colorectal, and lung cancers. However, because the KRAS protein exists inside cells, it has long been considered an “undruggable target” that is difficult to directly target with conventional antibody therapeutics.
The research team focused on the natural process by which cells break down aged or damaged proteins into small fragments. The KRAS(G12D) protein inside cells is also processed in this way into small protein fragments, known as neoantigens, which serve as clues that allow immune cells to distinguish cancer cells. Some of these fragments are then transported to the cell surface and presented to immune cells. By combining computational protein design with experimental screening, the team developed a TCR-like antibody that precisely recognizes only this cancer-mutation-derived fragment.
TCR, or T cell receptor, acts as a “sensor” that allows T cells, the body’s immune cells, to read protein fragments displayed on the surface of cells and identify cancer cells or virus-infected cells. The TCR-like antibody developed in this study works on a similar principle, effectively giving an antibody the “eyes” of a T cell. It was designed to selectively recognize traces of intracellular cancer mutations that conventional antibodies cannot easily access.
Experimental results confirmed that the antibody developed by the team selectively recognizes only cancer cells carrying the KRAS(G12D) mutation, while showing little to no reaction with normal cells or other proteins. When applied to immunotherapy, it was also shown to effectively eliminate only cancer cells carrying the mutation. This finding suggests the possibility of expanding antibody therapy to intracellular cancer-driving proteins that conventional antibody treatments have been unable to target. It is also expected to serve as a platform technology for developing next-generation precision antibody therapies targeting not only KRAS but also a wide range of cancer mutations.
Professor Byung-Ha Oh said, “The antibody developed in this study can selectively identify only cancer cells carrying the KRAS(G12D) mutation, demonstrating the potential for precision antibody therapeutics that minimize damage to normal cells.” He added, “The computational antibody design technology developed in this research is expected to be widely applicable to the development of next-generation antibody therapeutics targeting KRAS as well as various other cancer mutations.”
Both the first author and corresponding authors of this study are KAIST-affiliated researchers. SangPhil Ahn, a researcher at Therazyne, participated as the first author, while Professor Byung-Ha Oh and Bo-Seong Jeong, Head of Research at Therazyne, jointly led the study as co-corresponding authors. The research was published online on June 3 in Molecular Therapy, a leading international journal in the field of gene and cell therapy.
Paper title: Discovery of TCR-like antibodies to the KRAS G12D neoantigen via in silico-in vitro workflow DOI: https://doi.org/10.1016/j.ymthe.2026.05.032
This research was conducted in collaboration with Therazyne and the New Drug Development Center of the Osong Biomedical Innovation Foundation, and was supported by the Ministry of Science and ICT’s Industry-Academia-Research Linked New Drug Development Program and the National Research Foundation of Korea’s Bio & Medical Technology Development Program.
2026.07.24 View 4285 -
KAIST Uncovers the “Hidden Key” to Immunotherapy for Intractable Brain Tumors
Researchers have uncovered a clue to why immune checkpoint inhibitors—cancer therapies that release the immune “brakes” exploited by tumors to evade attack—show limited efficacy in some brain tumors. A KAIST research team found that B cell and antibody responses initiated in tumor-draining lymph nodes, rather than T cells alone, are critical to the antitumor effects of anti-CTLA-4 therapy, opening a new avenue for treating intractable brain tumors.
KAIST (President Choongsik Bae) announced on the 19th of July that a research team led by Professor Heung Kyu Lee from the Department of Biological Sciences has identified a previously unrecognized immune mechanism through which anti-CTLA-4, a type of immune checkpoint inhibitor, promotes B-cell responses in tumor-draining lymph nodes, thereby helping the immune system attack brain tumors.
Glioblastoma is one of the most aggressive malignant brain tumors, with frequent recurrence and a poor prognosis even after surgery and radiation therapy. Immune checkpoint inhibitors, which restore the ability of immune cells to attack cancer cells, have produced substantial therapeutic benefits in various cancers. However, their effectiveness in glioblastoma has remained limited because of the highly immunosuppressive environment surrounding the tumor.
Researchers have traditionally regarded T cells—immune cells that can directly attack cancer cells—as the primary target of immune checkpoint inhibitors. B cells, meanwhile, are well known for producing antibodies following infection or vaccination, but their role in brain tumor immunotherapy has remained largely unexplored. The research team therefore investigated whether anti-CTLA-4 could influence B-cell responses as well as T-cell responses.
The findings challenged the prevailing T-cell-centered view. In mouse glioma models, anti-CTLA-4 treatment reduced tumor burden and significantly prolonged survival. However, these therapeutic effects were largely lost in mice lacking B cells, demonstrating that B cells are required for the efficacy of anti-CTLA-4 treatment in these models.
The team also identified where B cells played their key role. Rather than being prominent in the brain, where the tumor cells were located, the response increased markedly in the Deep Cervical Lymph Nodes, which are located deep in the neck and receive lymphatic drainage from the brain. In particular, germinal center B cells and T follicular helper cells, both of which are important for antibody formation, increased together in these lymph nodes. This was accompanied by an increase in immunoglobulin G, or IgG, responses. IgG is a major class of antibody that can recognize cancer cells as targets and help immune cells eliminate them.
The resulting IgG antibodies bound to the surface of glioma cells, helping macrophages—immune cells that engulf foreign substances and cancer cells—remove the tumor cells more effectively.
The research team also examined this process directly in vivo. Using a specialized dual-reporter glioma model expressing the red fluorescent protein mCherry and the green fluorescent protein EGFP, the researchers successfully visualized tumor-infiltrating phagocytes actively engulfing glioma cells following anti-CTLA-4 treatment.
The study provides the first functional evidence that B-cell immune responses—previously known mainly for their roles in infection and vaccination—can be a key factor determining the effectiveness of immunotherapy for hard-to-treat brain tumors. It also expands the conventional T-cell-centered framework of cancer immunotherapy by showing that treatment efficacy can be strongly shaped by immune responses originating not only within the tumor, but also in tumor-draining lymph nodes outside it.
Yumin Kim, a postdoctoral researcher in the KAIST Department of Biological Sciences, served as the first author of the study, with Professor Heung Kyu Lee serving as the corresponding author. Professor Ji Eun Oh from the KAIST Graduate School of Medical Science and Engineering also contributed to the research. The findings were published on July 10 in Science Immunology.
Paper title: The efficacy of immunotherapy in glioma requires distal B-cell responses in tumor-draining lymph nodes
DOI: 10.1126/sciimmunol.adz2494
Authors: Yumin Kim, In Kang, Byeong Hoon Kang, Won Hyung Park, Chae Won Kim, Hyun-Jin Kim, Jeongwoo La, Myoung Seung Kwon, Sang Hee Park, Seo Hyeon Im, Hyeon Cheol Kim, Keun Bon Ku, Minji Kim, and Ji Eun Oh from KAIST, with Heung Kyu Lee from KAIST as the corresponding author.
This research was supported by National Research Foundation of Korea grants RS-2023-NR077244 (to H.K.L.), RS-2024-00439735 (to H.K.L.), RS-2024-00411928 (to Y.K.), RS-2025-00517107 (to J.E.O.), and RS-2026-25509011 (to H.K.L.). This study was also supported by Samsung Science and Technology Foundation grants SSTF-BA1902-05 (to H.K.L.) and SSTF-BA2201-11 (to J.E.O.).
2026.07.20 View 5268 -
KAIST Identifies New Therapeutic Target by Revealing How Cancer ‘Hijacks’ the Blueprint for Blood Vessel Development
Anti-angiogenic therapies targeting VEGF have been widely used in cancer treatment, yet their long-term efficacy remains limited. Tumor vascular endothelial cells (TECs) exhibit high adaptive plasticity, enabling them to resist treatment and sustain tumor growth, but the molecular mechanism underlying this plasticity has remained poorly understood.
KAIST, led by President Kwang Hyung Lee, announced that a joint research team led by Professor Inkyung Jung (Department of Biological Sciences), Professor Ji Min Lee (Graduate School of Medical Science and Engineering), and Professor Gou Young Koh (Institute for Basic Science) has now uncovered the answer. By integrating cross-cancer single-cell transcriptomic and epigenomic atlases across eight solid tumor types with multiomic profiles, including 3D chromatin contact maps, of human embryonic stem cell (hESC)-derived vascular endothelial cell differentiation, the team demonstrated that TECs reactivate a gene regulatory program normally confined to the late progenitor stage of vascular development. Much like reusing an old blueprint rather than drawing up a new one, tumors co-opt this pre-existing developmental program to fuel blood vessel growth.
The team’s integrative framework combined single-cell RNA-seq and ATAC-seq across multiple tumor types with H3K27ac ChIP-seq, Hi-C-based 3D chromatin mapping across a dense time series of hESC-to-EC differentiation. This approach resolved the EC-progenitor specific regulatory program that defines the shared pro-angiogenic program between late EC progenitors and TECs.
Within this framework, integrin receptor (ITGAV) emerged as a functional mediator specifically upregulated in both late EC progenitors and TECs. Cell-to-cell interaction analysis identified multiple key ligands from tumor micro enviroment (TME) that reactivate the progenitor-associated gene regulatory program. Pharmacologic inhibition attenuated endothelial migration, invasion, and tube formation in vitro, and significantly reduced tumor vascularization and growth in a colorectal cancer xenograft model in vivo.
Professor Inkyung Jung noted that this study reframes how we understand tumor angiogenesis: tumors do not invent new mechanisms, but exploit regulatory programs already embedded in normal vascular development. This insight offers a new conceptual basis for why anti-VEGF therapies face limitations, and points toward targeting the underlying regulatory architecture of endothelial plasticity as a complementary anti-angiogenic strategy.
The study was co-first authored by Dr. Andrew J. Lee, Dr. Sunwoo Min, Ph.D. student Su Chan Park; and Dr. Mei-Yu Qiu. Professors Inkyung Jung, Ji Min Lee, and Gou Young Koh served as corresponding authors. The findings were published on June 8 in Cancer Research [IF = 22.3].
※ Paper title: "A Co-opted Developmental Gene Regulatory Program in Endothelial Progenitors Promotes Tumor Angiogenic Phenotypes"
※ DOI: 10.1158/0008-5472.CAN-25-5094
※ Authors: Andrew J. Lee (KAIST, first author), Sunwoo Min (KAIST, co-first), Su Chan Park (KAIST, co-first), Mei-Yu Qiu (IBS, co-first), Gou Young Koh (IBS, co-corresponding), Ji Min Lee (KAIST, co-corresponding), Inkyung Jung (KAIST, corresponding)
This research was supported by the National Research Foundation of Korea and the Institute for Basic Science.
2026.07.01 View 2675 -
Simultaneous Decoding of Genetic Maps Inside Cells... A Game Changer for Understanding Complex Human Diseases
< (Clockwise from top left) Professor Inkyung Jung (KAIST), Dr. Dongchan Yang (KAIST), Dr. Kyukwang Kim (KAIST), Dr. Yueyuan Xu (Duke University), Dr. Xiaolin Wei (Duke University), Professor Yarui Diao (Duke University) >
The origin of many diseases begins at the cellular level and involves multiple molecular interactions. However, previous methods have struggled to accurately observe changes in individual cells. Analyzing average values across thousands of cells made it challenging to detect the early signals of disease.
Our university's research team has pioneered groundbreaking technology that decodes the genetic blueprint within a cell in 3D, akin to zooming in on Earth using Google Earth. This innovation is poised to transform research into complex diseases such as cancer, dementia, and Parkinson's disease.
KAIST announced on March 4th that Professor Inkyung Jung's research team from the Department of Biological Sciences, in collaboration with Professor Yarui Diao's team at Duke University, has developed scHiCAR (single-cell Hi-C with assay for transposase-accessible chromatin and RNA sequencing). This is the world’s first ultra-high throughput & precise molecular map decoding technology that simultaneously analyzes gene expression (transcriptome), the epigenome, and the 3D genome structure within a single cell.
The key to determining a cell's state lies in how its genes operate. Genes are not simply switches that turn on and off. The destiny of a cell is determined by which genes are actually active (transcriptome), why they are active (epigenome), and within what spatial structure they operate (3D genome structure). Existing technologies required obtaining this information from different cells separately and then matching them afterward, which could lead to the distortion or omission of subtle changes.
The research team introduced ‘Trimodal Multi-omics’ technology, an integrated precision analysis method that concurrently examines these three types of genetic information within a single cell. By incorporating Artificial Intelligence (AI) analysis, they significantly enhanced accuracy and reproducibility, culminating in a unified platform that reads internal cellular genetic information akin to a ‘single 3D map.’
<Ultra-precision Single-cell Molecular Map>
Notably, the team succeeded in lowering the analysis cost to approximately $0.04 (approx. 50 KRW) per cell. Using this, they constructed a high-resolution molecular map of 1.6 million cells in mouse brain tissue. This means it is now possible to precisely identify when, where, and within what structure disease genes are turned on or off at the cellular level.
The research team applied this technology to brain tissue and the muscle regeneration process, revealing distinct gene operation principles across 22 major cell types. Notably, they successfully tracked in real-time how the 3D structure of genes dynamically changes to influence cell fate during muscle stem cell regeneration. This advancement is expected to lay a crucial foundation for developing treatment strategies for aging and incurable diseases.
<Research Result Image (AI-generated)>
Professor Inkyung Jung remarked, ‘This research transcends mere observation of cells; it opens the door to precisely reading and controlling the genomic blueprints within them. It represents a significant turning point in elucidating the developmental mechanisms of complex diseases like Parkinson's and cancer, as well as identifying target points for patient-specific new drugs.’
The study was published on February 19th in the international academic journal Nature Biotechnology (IF=46.9).
Paper Title: Trimodal single-cell profiling of transcriptome, epigenome and 3D genome in complex tissues with scHiCAR
DOI: 10.1038/s41587-026-03013-7
Meanwhile, this research was conducted with support from the Suh Kyungbae Foundation, the Samsung Science and Technology Foundation, and the Basic Research Program and Bio-Medical Technology Development Program of the National Research Foundation of Korea (Ministry of Science and ICT).
2026.03.06 View 3605 -
Unraveling the Secret of Cell Movement
<(From left) Professor Won Do Heo (KAIST), Postdoctoral Researcher Heeyoung Lee (KAIST, First Author), Professor Kwang-Hyun Cho (KAIST), Professor Kapsang Lee (Johns Hopkins University, USA), Dr. Sangkyu Lee (IBS), Dr. Dongsan Kim (LIBD), Dr. Yeaji Seo (Hulux) (Co-First Authors)>
Cell movement is an essential biological process, whether it's cancer cells metastasizing to other parts of the body or immune cells migrating to heal a wound. However, the principle by which cells autonomously determine their direction of movement without external stimuli has remained unknown until now.
Through this research, KAIST and an international joint research team have elucidated the principle by which cells decide their direction and move on their own, offering a crucial clue for identifying the causes of cancer metastasis and immune diseases and establishing new treatment strategies.
KAIST announced on the 10th of November that the research team led by Endowed Chair Professor Won Do Heo of the Department of Biological Sciences, in collaboration with the research team of Endowed Chair Professor Kwang-Hyun Cho of the Department of Bio and Brain Engineering, and Professor Kapsang Lee's research team at Johns Hopkins University in the US, has for the first time in the world identified the 'autonomous driving mechanism' by which cells determine their direction of movement without external signals.
The research team developed a new imaging technique called 'INSPECT (INtracellular Separation of Protein Engineered Condensation Technique)' that allows direct visualization of how proteins interact within living cells. Using this technology, they revealed the principle of the cell's internal program for autonomously deciding its direction of movement.
The team newly analyzed the operation of the key proteins that regulate cell movement, the Rho family proteins (Rac1, Cdc42, RhoA). The results showed that these proteins do not merely divide the front and back of the cell, as previously theorized, but that the cell's decision to move straight or change direction depends on which protein it binds with.
The INSPECT technology artificially implements the phenomenon of 'phase separation,' where proteins, upon binding, naturally form segregated regions that do not mix well. This technique allows for the direct visualization of how proteins actually bind within the cell using a fluorescent signal.
<Figure 1. INSPECT: A technique for visualizing Intracellular Protein-Protein Interactions">
The research team used the proteins ferritin and the fluorescent protein DsRed to make the clusters, or 'condensates,' visible to the eye when proteins bind together like small droplets.
Using this technology, the team analyzed a total of 285 pairs of interactions by combining 15 types of Rho proteins with 19 types of binding proteins, confirming actual binding in 139 pairs. Specifically, they identified that the Cdc42–FMNL protein combination is the core circuit responsible for the cell's 'straight movement,' while the Rac1–ROCK protein combination is responsible for the cell's 'change of direction.'
The research team slightly modified a part of the Rac1 protein (the 37th amino acid), which is crucial for cell direction control, to prevent it from binding well with the 'steering wheel' protein, ROCK. As a result, the cells could not change direction and continued to move in a straight line.
In contrast, in normal cells, Rac1 and ROCK bind well, forming a structure called 'arc stress fiber' at the front of the cell. This fiber enables the cell to make near-perpendicular turns when changing direction.
Furthermore, in an experiment where the environment the cells were attached to was changed, normal cells adjusted their moving speed according to the surrounding environment, but the Rac1F37W cells (cells with a broken 'steering wheel') maintained the same speed regardless of environmental changes. This demonstrates that the Rac–ROCK protein axis subtly controls the cell's ability to recognize and adapt to its surrounding environment.
<Figure 2. Analysis of the Signaling Network through Screening of Protein Interactions that Bind to a Cell Migration-Controlling Protein>
Professor Won Do Heo stated, "This research reveals that cell movement is not a random motion but is precisely controlled by an intrinsic program created by the ensemble of Rho signaling proteins and cell migration-related proteins." He added, "The newly developed INSPECT technology is a powerful tool for visualizing intracellular protein interactions and will be broadly utilized to uncover the molecular mechanisms of various life phenomena and diseases, such as cancer metastasis and neuronal cell migration."
This research, in which Dr. Heeyoung Lee of KAIST, Dr. Sangkyu Lee (currently at IBS), Dr. Yeji Seo (currently at Hulux Co., Ltd.), and Dr. Dongsan Kim (currently at LIBD) participated as co-first authors, was published in Nature Communications on October 31st.
Journal Name: A Rho GTPase-effector ensemble governs cell migration behavior
DOI: https://doi.org/10.1038/s41467-025-64635-0
The research was supported by the Samsung Future Technology Foundation and the National Research Foundation of Korea.
2025.11.10 View 4593 -
KAIST Discovers Role of Huntingtin Protein in Building the Cell Skeleton
<(From Left) Professor Ji-Joon Song, Ph.D candidate Jaesung Kim, Dr. Hyeongju Kim of KAIST’s Department of Biological Sciences>
Huntington’s disease is a rare genetic disorder and a representative neurodegenerative disease, characterized by loss of motor control, cognitive decline, and psychiatric problems. An international research team has discovered that the “huntingtin protein,” the causal protein of Huntington’s disease (whose mutations are the direct cause of the disease), also performs a new function: directly organizing the cytoskeleton, the fine structural framework inside cells. This discovery is expected to contribute not only to understanding the pathogenic mechanism of Huntington’s disease, but also to research on neurodevelopmental disorders such as Alzheimer’s disease and Parkinson’s disease, as well as muscle- or mobility-related diseases such as muscular dystrophy.
KAIST (President Kwang Hyung Lee) announced on September 30 that a research team led by Professor Ji-Joon Song of the Department of Biological Sciences, in collaboration with the Institute of Science and Technology Austria (ISTA), Sorbonne University/Paris Brain Institute, and the Swiss Federal Institute of Technology Lausanne (EPFL), has uncovered—through cryo-electron microscopy (cryo-EM) and cell biology methods—the structural principle by which the huntingtin protein arranges cytoskeletal microfilaments (F-actin) into bundles.
Until now, the huntingtin protein was known only to “use” the cytoskeleton, being involved in vesicle transport or microtubule-based transport. The team, however, demonstrated that huntingtin physically organizes the cytoskeleton itself. This study is considered the first in the world to prove this new role of the huntingtin protein at the molecular level.
The researchers confirmed that huntingtin binds directly to cytoskeletal microfilaments (F-actin), and that pairs of huntingtin proteins bundle the cytoskeleton into arrays at intervals of about 20 nanometers.
Such cytoskeletal bundles play a crucial role in the development of neural connectivity. Indeed, structural development of neurons was found to be impaired in nerve cells deficient in the huntingtin protein.
<Elucidation of the Mechanism of Cytoskeletal Microfilament Bundle Formation by Huntingtin Protein and Its Impact on Neuronal Development>
First author Jaesung Kim, a PhD candidate at KAIST, stated, “This study provides a new perspective for understanding the molecular mechanism of the huntingtin protein, the cause of an incurable disease that has long remained a mystery.”
Professor Ji-Joon Song of KAIST’s Department of Biological Sciences explained, “This achievement not only provides an important clue to understanding the pathogenic mechanism of Huntington’s disease, but is also expected to have a far-reaching impact on research into cytoskeleton-related diseases,” and added that “it opens new avenues for exploring the role of the huntingtin protein in diverse biological phenomena such as cell division, migration, and mechanical signal transduction.”
This research was conducted with Jaesung Kim (PhD candidate, KAIST), Hyeongju Kim (now at Harvard University), Rémi Carpentier (Paris Brain Institute), Mariacristina Capizzi (Paris Brain Institute), and others as co-first authors, and was published on September 19 in Science Advances, a sister journal of Science.
※ Paper title: “Structure of the Huntingtin F-actin complex reveals its role in cytoskeleton organization,” DOI: https://doi.org/10.1126/sciadv.adw4124※ Co-corresponding authors: Ji-Joon Song (KAIST), Florian Schur (ISTA), and Sandrine Humbert (Sorbonne University/Paris Brain Institute).
This research was supported by the Ministry of Health and Welfare’s Global Research Collaboration Program (Korea–Switzerland Biohealth International Joint Research) and the Korea–Austria Cooperation Program.
2025.09.30 View 6885 -
KAIST team links early life epigenetic memory to adult brain inflammation
<(From left) Professor Won-Suk Chung, Ph.D. Ph.D candidate Hyeonji Park Dr. Seongwan Park, Professor Inkyung Jung>
Why do some people remain healthy through childhood yet become more vulnerable to brain disorders such as dementia later in life? A KAIST (President Kwang Hyung Lee) -led team has uncovered a key part of the answer: a developmental ‘switch’ in astrocytes—the brain’s most abundant support cells that shapes how strongly the brain’s immune system reacts in adulthood. The study identifies a gene, NR3C1 (encoding the glucocorticoid receptor), as a master regulator of this switch and shows how early-life epigenetic ‘memory’ can predispose the adult brain to excessive inflammation.
The work was carried out by a joint team led by Professor Inkyung Jung (Department of Biological Sciences, KAIST) and Associate Director Won-Suk Chung (Center for Vascular Research, Institute for Basic Science; Professor, KAIST Biological Sciences). Using mouse models, the researchers mapped gene-regulatory programs across multiple stages of astrocyte development and found that NR3C1 acts during a brief early-postnatal window to enforce long-term immune restraint.
<The schematic illustrates how the NR3C1 gene (glucocorticoid receptor) suppresses the immune response of astrocytes. In normal (control) astrocytes, NR3C1 binds to specific regulatory regions of DNA (nGRE) to inhibit the expression of immune-related genes, thereby maintaining brain homeostasis even under immune stimulation. In contrast, in NR3C1-deficient astrocytes (KO), this suppression is lost, leading to excessive activation of inflammation-related genes such as Gfap, Il6st, Stat2, and Cxcl10. As a result, in an autoimmune encephalomyelitis (EAE) model, pronounced neuroinflammation and clinical symptoms (paralysis and severe debilitation) are observed>
To build this map, the team combined state-of-the-art 3D epigenome profiling with RNA sequencing and chromatin accessibility analyses, capturing how DNA folds and which regulatory elements contact target genes. They identified 55 stage-specific transcription factors that guide astrocyte maturation; among them, NR3C1 emerged as the critical ‘switch’ in early life. Notably, deleting NR3C1 in astrocytes did not disrupt normal development. However, when the adult mice were challenged with an autoimmune model of multiple sclerosis, animals lacking astrocytic NR3C1 mounted exaggerated inflammatory responses and developed more severe disease.
Mechanistically, the study shows that early loss of NR3C1 epigenetically primes immune genes - keeping their regulatory elements open and ready - so that later in life these genes respond too strongly to inflammatory cues. In effect, NR3C1 serves as an early ‘brake’ that prevents over-activation of astrocyte immune programs in adulthood.
“This is the first demonstration that astrocyte immune functions are governed by epigenetic memory,” said Professor Won-Suk Chung. “Our findings offer new clues to the origins of degenerative brain disorders, including Alzheimer’s disease.”
“We reveal a temporal regulatory window in astrocyte development that can set the stage for disease vulnerability in adulthood,” added Professor Inkyung Jung. “Understanding the 3D genome logic behind these programs could open paths to therapies for immune-related brain disorders such as multiple sclerosis.”
<The figure shows the three-dimensional genome structure of astrocytes at specific gene loci, illustrating how NR3C1 regulates their expression. In normal cells, NR3C1 binds to DNA and maintains the chromatin in a closed state, thereby preventing unnecessary activation between distal regulatory elements (enhancers) and gene promoters. In contrast, when NR3C1 is absent, the chromatin becomes open, creating a state in which enhancers and genes can be more easily activated. As a result, genes such as Mxi1 are overexpressed, triggering inflammatory responses. This clearly demonstrates that NR3C1 plays an essential role in maintaining immune homeostasis by stabilizing three-dimensional gene regulatory mechanisms.>
The results of this study were published online on September 22 in the international journal Nature Communications (IF 15.7), with Dr. Seongwan Park and PhD student Hyeonji Park of KAIST’s Department of Biological Sciences as co-first authors.
※ Paper title: “NR3C1-mediated epigenetic regulation suppresses astrocytic immune responses in mice,” DOI: https://www.nature.com/articles/s41467-025-64088-5
In addition, on September 17, the journal published a commentary article introducing this research: https://www.nature.com/articles/s41467-025-64102-w
This research was supported by the Suh Kyungbae Science Foundation, the Ministry of Health and Welfare, the Ministry of Science and ICT, and IBS.
Glossary - Epigenetic priming: preparing genes for rapid future activation by altering chromatin without changing DNA sequence
2025.09.25 View 7273 -
“Why are we depressed?” KAIST is identifying the cause of depression and uncovering clues for treatment
Major depressive disorder (MDD) is one of the most common psychiatric illnesses worldwide, but its molecular causes* have still not been clearly identified. A domestic research team has discovered that depression may not simply be caused by neuronal damage, but can also arise from the dysregulation of specific neural signaling pathways. In particular, they identified the molecular reason why elderly patients with depression do not respond to conventional antidepressants. This study suggests the possibility of therapeutic approaches using optogenetic technology to regulate neural signaling, and it provides clues for the development of new treatment strategies targeting the protein ‘Numb’ protein for elderly patients with depression.
*Molecular causes: explanations for the origin of a disease at the level of molecules, proteins, or genes in the brain.
KAIST (President Kwang Hyung Lee) announced on the 19th of August that a research team led by Distinguished Professor Won Do Heo of the Department of Biological Sciences at KAIST, in collaboration with forensic pathologist Minju Lee of the National Forensic Service (Director Bong Woo Lee) and Professor Seokhwi Kim of the Department of Pathology at Ajou University Medical Center (Director Sangwook Han), identified a new molecular mechanism for depression through RNA sequencing and the immunohistochemical analysis of brain tissue from patients who had committed suicide. Furthermore, they demonstrated in animal models that antidepressant effects can be restored by regulating the signaling pathway that induces neural recovery using optogenetic technology.
The research team focused on the hippocampus, the brain region responsible for memory and emotion, and in particular on the dentate gyrus (DG). The DG is the entry point of information into the hippocampus, playing a role in new memory formation, neurogenesis, and emotional regulation, and is closely linked with depression.
Using two representative mouse models for depression (the corticosterone stress model and the chronic unpredictable stress model), the team found that stress induced a striking increase in the signaling receptor FGFR1 (Fibroblast Growth Factor Receptor 1) in the DG. FGFR1 receives growth factor (FGF) signals and transmits growth and differentiation commands within cells.
Subsequently, using conditional knockout (cKO) mice in which the FGFR1 gene was deleted, the researchers revealed that the absence of FGFR1 made mice more vulnerable to stress and led them to exhibit depressive symptoms more quickly. This indicates that FGFR1 plays a critical role in proper neural regulation and stress resistance.
The team then developed an ‘optoFGFR1 system’ using optogenetics, enabling FGFR1 —essential for stress resistance—to be activated by light. They observed that activating FGFR1 in depression mouse models lacking FGFR1 restored antidepressant effects. In other words, they experimentally demonstrated that the activation of FGFR1 signaling alone could improve depressive behavior.
Surprisingly, however, in aged depression mouse models, the activation of FGFR1 signaling through the optoFGFR1 system did not yield antidepressant effects. Investigating further, the researchers found that in the aged brains, a protein called ‘Numb’ was excessively expressed and interfered with FGFR1 signaling.
Indeed, analysis of postmortem human brain tissue also showed the specific overexpression of Numb protein only in elderly patients with depression. When the researchers suppressed Numb using a gene regulatory tool (shRNA) while simultaneously activating FGFR1 signaling in mouse models, neurogenesis and behavior—previously unrecoverable—returned to normal even in aged depression models. This shows that the Numb protein acts as a “blocker” of FGFR1 signaling and is a key factor preventing the hippocampus from executing antidepressant mechanisms.
Distinguished Professor Won Do Heo of KAIST said, “This study is meaningful in that it revealed that depression may not only result from simple neuronal damage, but can also arise from the dysregulation of specific neural signaling pathways. In particular, we identified the molecular reason why antidepressants are less effective in elderly patients, and we expect this to provide a clue for the development of new therapeutic strategies targeting the Numb protein.”
He added, “Moreover, this interdisciplinary study, which combined KAIST’s expertise in neuroscience with the National Forensic Service’s forensic brain analysis technologies, is expected to serve as a bridge between basic research on psychiatric disorders and clinical applications.”
This study, led by first author Jongpil Shin, a PhD student in the Department of Biological Sciences at KAIST, was published on August 15, 2025, in the international journal Experimental & Molecular Medicine.
Paper title: “Dysregulation of FGFR1 signaling in the hippocampus facilitates depressive disorder”
DOI: https://doi.org/10.1038/s12276-025-01519-9
This research was supported by the Ministry of Science and ICT’s National Research Foundation of Korea through the ASTRA program and the Bio-Medical Technology Development project.
2025.08.19 View 6635