Jin Lab News

See what we invented

 

    • New publications at Angewandte Chemie International Edition by Dr. Deng, Z.; Dr. Chen, Li; Dr. Qian, C; Dr. Liu, J; Dr. Wu, Q; Dr. Song, X; Dr. Xiong, Y; Dr. Wang, Z; Dr. Hu, X; Dr. Inuzuka, H; Zhong, Y; Xiang, Y; Lin, Y; Dr. Pham, N. D.; Dr. Shi, Y, Prof. Dr. Wei, W and Prof. Jin, and their Collaborators Published a Research Article Entitled “The First-in-class Deubiquitinase-targeting Chimera Stabilizes and Activates cGAS” in Angewandte Chemie International Edition.

      • The research team led by Dr. Jian Jin and Dr. Wenyi Wei, a Professor at Harvard Medical School, discovered the first-in-class cGAS deubiquitinase-targeting chimeras (DUBTACs), which effectively stabilized cGAS protein and activated the cGAS-STING-IRF3 signaling. (https://doi.org/10.1002/anie.202415168). These DUBTACs were generated by exploiting an improved small-molecule ligand of the deubiquitinase OTUB1. This work advances the targeted protein stabilization field.
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        • New publications at Science Advances by Drs. Lihuai Qin, Kaixiu Luo, Brandon Dale, H Ümit Kaniskan, Jian Jin, and Their Collaborators Published a Research Article Entitled “A potent and selective ENL degrader suppresses oncogenic gene expression and leukemia progression”

          • The research team led by Dr. Hong Wen, a Professor at Van Andel Institute, and Dr. Jian Jin discovered a novel, highly potent and selective ENL degrader, MS41, which effectively inhibits the growth of ENL-dependent leukemia cells both in vitro and in vivo (https://www.science.org/doi/10.1126/sciadv.ado1432). ENL, a histone acylation reader protein, plays a pivotal role in sustaining oncogenesis in acute leukemias. MS41-induced ENL degradation reduces
            the chromatin occupancy of ENL-associated transcription elongation machinery, resulting in the suppression of key oncogenic gene expression programs and the activation of differentiation genes. The key findings in this study emphasize the therapeutic potential of pharmacological ENL degradation for treating ENL-dependent cancers.

            • Drs. Xiaoping Hu, Kaixiu Luo, Yan Xiong, Chao Qian, Xufen Yu and Jian Jin, and Their Collaborators Published a Research Article Entitled “USP7-Based Deubiquitinase-Targeting Chimeras Stabilize AMPK” in Journal of the American Chemical Society

            • The research team led by Dr. Wenyi Wei, a Professor at Harvard Medical School, and Dr. Jian Jin has demonstrated for the first time that USP7, a deubiquitinase (DUB), can be harnessed for development of Deubiquitinase-Targeting Chimeras (DUBTACs) utilizing non-covalent small-molecule inhibitors of USP7 (https://pubs.acs.org/doi/full/10.1021/jacs.4c02373) Using this technology, the team developed proof-of-concept DUBTACs that stabilize and activate the tumor suppressor AMPK. This work advances the targeted protein stabilization field.

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              • Md Kabir, Ning Sun, Xiaoping Hu, Yue Zhong, Yan Xiong, H. Umit Kaniskan and Dr. Jin and Their Collaborators Published a Research Article Entitled “Acetylation Targeting Chimera Enables Acetylation of the Tumor Suppressor p53” in Journal of the American Chemical Society

           The research team led by Dr. Jin developed a novel technology, termed Acetylation Targeting Chimera (AceTAC), for inducing targeted acetylation of proteins of interest (https://pubs.acs.org/doi/full/10.1021/jacs.3c04640). AceTAC, which is a heterobifunctional small molecule with one moiety that binds the protein of interest and the other moiety that recruits a histone acetyltransferase, induces close proximity between the protein of interest and histone acetyltransferase, leading to selective acetylation of the protein of interest. Applying this technology to target the tumor suppressor p53, the team discovered MS78, the first AceTAC of the p53 Y220C mutant, which effectively acetylated p53Y220C and suppressed proliferation and clonogenicity of cancer cells harboring the p53Y220C mutation with little toxicity in cancer cells with wild-type p53 and normal cells. This novel AceTAC technology could provide a generalizable platform for targeting proteins, such as tumor suppressors, via acetylation.

                • Drs. Fanye Meng, Xiangyang Song, H. Umit Kaniskan and Jian Jin in Collaboration with the Ivan Marazzi Lab Published a Research Article Entitled “Generation of host-directed and virus-specific antivirals using targeted protein degradation promoted by small molecules and viral RNA mimics” in Cell Host & Microbe

          The research team led by Drs. Ivan Marazzi and Jian Jin developed a novel broad-spectrum antiviral therapeutic strategy, which was achieved by degrading GSPT1, a host factor that is critical for many viruses (https://www.sciencedirect.com/science/article/pii/S1931312823002238). The team developed a novel GSPT1 degrader, FM-74-103, which effectively inhibited IAV, SARS-CoV-2, and CMV infections.

                • Dr. Jian Jin has received an GlaxoSmithKline Inventor Award for Daprodustat, an oral medication that has been approved in the U.S. and Japan for the treatment of anemia caused by chronic kidney disease. Dr. Jin is one of several inventors of Daprodustat, which is a small-molecule inhibitor of hypoxia-inducible factor (HIF) prolyl hydroxylase.
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              • Kwang-Su Park, Lihuai Qin, Md Kabir, Kaixiu Luo, Brandon Dale, Yue Zhong, H. Ümit Kaniskan and Dr. Jin and Their Collaborators Published a Research Article Entitled “Targeted Degradation of PRC1 Components, BMI1 and RING1B, via a Novel Protein Complex Degrader Strategy” in Advanced Science

        The research team led by Dr. Jian Jin discovered MS147, the first small-molecule degrader of polycomb repressive complex 1 (PRC1) components, BMI1 and RING1B, using the bridged PROTAC technology developed by the Jin lab, which is a novel protein complex degradation strategy to target undruggable proteins (https://onlinelibrary.wiley.com/doi/full/10.1002/advs.202205573). MS147, which is a EED-binding and VHL E3 ligase-recruiting PROTAC, preferentially degraded PRC1 components BMI1 and RING1B over PRC2 components such as EED, EZH2 and SUZ12, and effectively suppressed the proliferation in cancer cell lines that are not dependent on EZH2/PRC2.

         

              • Dr. Jian Jin has been inducted to the National Academy of Inventors (NAI) as an NAI Fellow.

        Dr. Jin currently is the Mount Sinai Endowed Professor in Therapeutics Discovery, the Director of the Mount Sinai Center for Therapeutics Discovery, and a Co-Leader of the Cancer Clinical Investigation Program at The Tisch Cancer Institute. Dr. Jin is an inventor of >80 issued U.S. patents and published international patent applications. He has also published >258 peer-reviewed papers and delivered >100 invited talks.

         

              • Drs. Kwang-Su Park, Xufen Yu and Jian Jin and Their Collaborators Published a Research Article Entitled “A Cryptic Transactivation Domain of EZH2 Binds AR and AR’s Splice Variant, Promoting Oncogene Activation and Tumorous Transformation” in Nucleic Acids Research

         The research team led by Dr. Ling Cai (Assistant Professor at University of North Carolina at Chapel Hill (UNC – CH), Dr. Greg Wang (Professor at UNC – CH), and Dr. Jian Jin discovered that EZH2, an oncogenic histone methyltransferase, binds both AR and AR spliced variant 7 (AR-V7), a constitutively active AR variant enriched in advanced castration-resistant prostate cancer (CRPC), via a cryptic transactivation domain (EZH2TAD), mediating assembly and/or recruitment of transactivation-related machineries at genomic sites that lack PRC2 binding and promoting CRPC growth in vitro and in vivo (https://academic.oup.com/nar/article/50/19/10929/6775399). Using MS177, the EZH2 PROTAC degrader recently developed by this team, the researchers demonstrated that EZH2 degraders are superior to EZH2 catalytic inhibitors in suppressing both canonical and non-canonical oncogenic activities of EZH2 in CRPC, resulting in much more effective growth inhibition of CRPC cells.

         

              • Yan Xiong, Yue Zhong, Hyerin Yim, Xiaobao Yang, Kwang-Su Park, Jing Liu, and Dr. Jin and Their Collaborators Published a Research Article Entitled “Bridged Proteolysis Targeting Chimera (PROTAC) Enables Degradation of Undruggable Targets” in Journal of the American Chemical Society

         The research team led by Dr. Jian Jin developed a new technology, termed as bridged PROTAC, for targeting undruggable proteins, which lack small-molecule binders (https://pubs.acs.org/doi/10.1021/jacs.2c09255). Bridged PROTAC utilizes a small-molecule binder of the target protein’s binding partner to recruit the protein complex into close proximity with an E3 ubiquitin ligase to target undruggable proteins. Applying this technology, the team discovered MS28, the first degrader of cyclin D1, which is undruggable and a top cancer target. MS28, which is a CDK4/6-binding PROTAC, preferentially degraded cyclin D1 over CDK4/6. Bridged PROTAC as a novel PROTAC strategy provides a generalizable platform for targeting undruggable proteins and expands the targetable human proteome.

              • Drs. Xufen Yu, He Chen, H. Ümit Kaniskan and Jian Jin and Their Collaborators Published a Research Article Entitled “TF-DUBTACs Stabilize Tumor Suppressor Transcription Factors” in Journal of the American Chemical Society

        The research team led by Dr. Wenyi Wei, a Professor at Harvard Medical School, and Dr. Jian Jin, the Mount Sinai Endowed Professor in Therapeutics Discovery and Director of the Mount Sinai Center for Therapeutics Discovery, developed a new technology, termed as TF-DUBTAC, for stabilizing tumor suppressor transcription factors (TFs) by hijacking the cellular deubiquitination system (https://pubs.acs.org/doi/10.1021/jacs.2c04824). TF-DUBTACs, which are novel heterobifunctional molecules, provide a generalizable platform to achieve selective stabilization of tumor suppressor TFs and a new therapeutic strategy for treating cancer.

              • Drs. Jian Jin and Greg Wang (UNC) Have Received a New R01 Grant from NCI Entitled “Discovery of First-in-class WDR5 PROTACs as a Novel Therapeutic Strategy for MLL-rearranged Leukemias”

        Dr. Jian Jin and Dr. Greg Wang, Professor at University of North Carolina at Chapel Hill, have received a new five-year multiple-PI R01 grant from the National Cancer Institute (NCI) to discover first-in-class WDR5 PROTACs as a novel therapeutic strategy for MLL-rearranged Leukemias. The research team led by Drs. Jin and Wang has generated promising preliminary results, some of which were published in Science Translational Medicine (https://pubmed.ncbi.nlm.nih.gov/34586829/) last September. In this newly funded project, the team will validate their previous findings, develop and optimize novel WDR5 PROTAC degraders, and demonstrate that pharmacological degradation of WDR5 is a superior therapeutic strategy to inhibition of protein-protein interactions between WDR5 and its binding partners for treating MLL-rearranged leukemias.

              • Drs. Xufen Yu and Jian Jin and Their Collaborators Published a Research Article Entitled “EZH2 Noncanonically Binds cMyc and p300 through a Cryptic Transactivation Domain to Mediate Gene Activation and Promote Oncogenesis” in Nature Cell Biology

        The research team led by Dr. Greg Wang, Associate Professor at University of North Carolina at Chapel Hill, and Dr. Jian Jin, the Mount Sinai Endowed Professor in Therapeutics Discovery and Director of the Mount Sinai Center for Therapeutics Discovery, discovered that EZH2, an oncogenic histone methyltransferase, has a non-canonical function in activation of oncogenes through its hidden transactivation domain (TAD) in mixed-lineage leukemia (MLL)-rearranged leukemias, which differs from the well-known canonical function of EZH2 related to gene repression via trimethylation of histone H3 lysine 27 (H3K27me3). The team developed a novel EZH2 PROTAC degrader, MS177, which effectively suppressed both canonical and non-canonical oncogenic activities of EZH2, resulting in much superior growth inhibition of MLL-rearranged leukemia cells both in vitro and in vivo to EZH2 catalytic inhibitors (https://www.nature.com/articles/s41556-022-00850-x). This research provides support for pharmacological degradation of EZH2 as a novel and superior therapeutic strategy to pharmacological inhibition of EZH2 for the treatment of MLL-rearranged leukemias and other EZH2-dependent cancers.

              • Drs. Greg Wang (UNC) and Jian Jin Have Received a New R01 Grant from NCI to Dissect and Target Canonical and Non-canonical Oncogenic Functions of EZH2 in Cancer

        Dr. Greg Wang, at University of North Carolina at Chapel Hill, and Dr. Jian Jin, the Mount Sinai Endowed Professor in Therapeutics Discovery and Director of the Mount Sinai Center for Therapeutics Discovery, have received a new five-year multiple-PI R01 grant from the National Cancer Institute (NCI) to dissect and target canonical and non-canonical oncogenic functions of EZH2, a histone methyltransferase, in cancer. The research team has recently uncovered that EZH2 has a non-canonical function in activation of oncogenes in mixed-lineage leukemia (MLL)-rearranged leukemias, which differs from the well-known canonical function of EZH2 related to gene repression. The team will develop and optimize novel EZH2 PROTAC degraders that effectively suppress both canonical and non-canonical oncogenic activities of EZH2, as a novel and superior therapeutic strategy to inhibition of EZH2’s enzymatic activity alone for treating MLL-rearranged leukemias.

                • THE JIN LAB AT THE FOREFRONT OF CANCER DRUG DISCOVERY (Featured in the Department of Pharmacological Sciences Newsletter in Q32021)

        Targeted protein degradation (TPD) with heterobifunctional proteolysis targeting chimera (PROTAC) technology is the new frontier of cancer drug discovery. Prof. Jian Jin is widely recognized as a pioneer and leader in this emerging field (Dale, Nature Reviews Cancer, 2021. https://pubmed.ncbi.nlm.nih.gov/34131295/). The Jin Lab has made seminal contributions to the TPD field through developing new technologies, including: (1) harnessing the E3 ligase KEAP1 for TPD with a selective small-molecule KEAP1 ligand (Wei, JACS, 2021. https://pubmed.ncbi.nlm.nih.gov/34520194/); (2) novel opto-PROTAC (Liu, Science Advances, 2020. https://pubmed.ncbi.nlm.nih.gov/32128407/) and folate-caged PROTAC (Liu, JACS, 2021a. https://pubmed.ncbi.nlm.nih.gov/33970635/) technologies as precision medicine in collaboration with Professor Wenyi Wei; and (3) invention of a novel universal strategy for selective degradation of “undruggable” transcription factors (TFs), termed TF-PROTACs (Liu, JACS, 2021b. https://pubmed.ncbi.nlm.nih.gov/34100597/), also in collaboration with Professor Wenyi Wei. These novel TPD technologies have enabled the Jin Lab to create novel small-molecule degraders as new anti-cancer therapies for some of the most challenging onco-proteins. For example, in collaboration with Professor Ramon Parsons, the Jin Lab discovered first-in-class degraders for histone lysine methyltransferase EZH2, a key oncogenic driver for triple-negative breast cancer (Ma, Nature Chemical Biology, 2020. https://www.nature.com/articles/s41589-019-0421-4). Recently, together with Professors Greg Wang and Aneel Aggarwal, the Jin Lab has developed using rational structure-based design a potent and selective WDR5 PROTAC degrader that shows robust in vivo antitumor activity (Yu, Science Translational Medicine, 2021. https://pubmed.ncbi.nlm.nih.gov/34586829/). Since 2020, Prof. Jin and his colleagues have published 15 papers in the TPD field, and their research has further resulted in 15 patent applications filed through Mount Sinai Innovation Partners.

                • Drs. Xufen Yu and Jian Jin and Their Collaborators Published a Research Article Entitled “A Selective WDR5 Degrader Inhibits Acute Myeloid Leukemia in Patient-derived Mouse Models” in Science Translational Medicine

        The research team, led by Drs. Jian Jin, Greg Wang and Aneel Aggarwal, investigated pharmacological degradation of WDR5 as a novel and superior therapeutic strategy to pharmacological inhibition of WDR5 for the treatment of WDR5-dependent cancers (https://www.science.org/doi/10.1126/scitranslmed.abj1578). The researchers solved a high-resolution crystal structure of the WDR5-MS33-VHL ternary complex, which is the first WDR5-PROTAC-E3 ligase ternary complex structure, and developed MS67, a novel, highly potent, selective and in vivo efficacious WDR5 PROTAC degrader, based on the WDR5-MS33-VHL ternary complex structure. MS67 was able to significantly suppress tumor growth, prolong survival, and degrade WDR5 in vivo. These research findings suggest that pharmacological degradation of WDR5 is a promising and superior therapeutic strategy to pharmacological inhibition of WDR5 for treating WDR5-dependent cancers such as MLL-rearranged acute myeloid leukemia.

         

                • Drs. Jian Jin and H. Ümit Kaniskan and Their Collaborators Published a Research Article Entitled “Harnessing the E3 Ligase KEAP1 for Targeted Protein Degradation” in Journal of the American Chemical Society

        Targeted protein degradation induced by proteolysis targeting chimeras (PROTACs) has emerged as a hottest research topic in drug discovery. However, a key challenge in the PROTAC field is that out of approximately 600 ubiquitin E3 ligases, only a very limited number of them have been harnessed to generate effective PROTACs. The research team led by Drs. Jian Jin and H. Ümit Kaniskan has demonstrated for the first time that KEAP1, a Cullin 3 ubiquitin E3 ligase, can be leveraged for PROTAC development using a highly selective, non-covalent small-molecule ligand of KEAP1 (https://pubs.acs.org/doi/10.1021/jacs.1c04841). The team developed MS83, a proof-of-concept KEAP1-recruiting BRD3/4 PROTAC, which degrades BRD4 and BRD3 more durably than the well-known CRBN-recruiting BRD2/3/4 PROTAC dBET1. MS83 also selectively degrades the BRD4 short isoform over the BRD4 long isoform and has a superior selectivity profile to dBET1. This work expands the limited toolbox for targeted protein degradation.

                • Drs. Xufen Yu and Jian Jin and Their Collaborators Published a Research Article Entitled “AKT Degradation Selectively Inhibits the Growth of PI3K/PTEN Pathway Mutant Cancers with Wild-type KRAS and BRAF by Destabilizing Aurora kinase B” in Cancer Discovery

        The research team led by Drs. Ramon Parsons and Jian Jin, reported the discovery and characterization of MS21, a novel, potent, selective and in vivo efficacious PROTAC degrader of AKT, which is overly active in many cancers (https://cancerdiscovery.aacrjournals.org/content/11/12/3064). The team also discovered a new AKT substrate, aurora kinase B (AURKB), which is required for cell viability, and that AKT degradation induced by MS21 led to effective downregulation of AURKB. The study lays a solid foundation for the clinical development of an AKT degrader for the treatment of human cancers with PIK3CA, PTEN, HER2 and AKT1 alterations based on the premise that MS21 can selectively degrade phosphorylated but not unphosphorylated AKT.

                • Brandon Dale, Drs. Kwang-Su Park, H. Ümit Kaniskan and Jian Jin and Their Collaborators Published in Nature Reviews Cancer

        The research team led by Dr. Jian Jin, the Mount Sinai Endowed Professor in Therapeutics Discovery and Director of the Mount Sinai Center for Therapeutics Discovery, and Dr. Yue Xiong, William R. Kenan Jr. Distinguished Professor at University of North Carolina at Chapel Hill, has published a review article entitled “Advancing Targeted Protein Degradation for Cancer Therapy” in Nature Reviews Cancer (https://www.nature.com/articles/s41568-021-00365-x). Dr. Jin’s lab is a pioneer and leader in discovering and characterizing first-in-class small-molecule degraders (also known as proteolysis targeting chimeras (PROTACs)) that target oncogenic proteins and developing novel technologies for advancing the targeted protein degradation field. The Jin lab’s work in this area has been published in high impact journals such as Nature Chemical Biology, Science Advances, Nature Cancer, and Journal of The American Chemical Society.

                • Drs. He Chen, H. Ümit Kaniskan and Jian Jin and Their Collaborators Published a Research Article Entitled “TF-PROTACs Enable Targeted Degradation of Transcription Factors” in Journal of American Chemical Society

        The research team led by Dr. Jian Jin, the Mount Sinai Endowed Professor in Therapeutics Discovery and Director of the Mount Sinai Center for Therapeutics Discovery, and Dr. Wenyi Wei, a Professor at Harvard Medical School, developed a novel technology, termed as TF-PROTACs, for degrading transcription factors (TFs) by hijacking the cellular ubiquitin-proteasome system (https://pubs.acs.org/doi/10.1021/jacs.1c03852). This technology provides a generalizable platform to achieve selective degradation of TFs, many of which are oncogenic proteins, and a universal strategy for targeting most “undruggable” TFs.

                • Drs. He Chen, H. Ümit Kaniskan and Jian Jin and Their Collaborators Published a Research Article Entitled “Cancer Selective Target Degradation by Folate-Caged PROTACs” in Journal of American Chemical Society

        The research team led by Dr. Jian Jin, the Mount Sinai Endowed Professor in Therapeutics Discovery and Director of the Mount Sinai Center for Therapeutics Discovery, and Dr. Wenyi Wei, a Professor at Harvard Medical School, developed a novel folate-caging technology as a generalizable platform for selective targeting cancer cells over normal cells by proteolysis targeting chimeras (PROTACs), a new class of promising therapeutic modalities (https://pubs.acs.org/doi/10.1021/jacs.1c00451). Prior to this discovery, the same research team developed a novel caging strategy, termed as “opto-PROTACs”, that enables the degradation of protein targets in a spatiotemporal manner by photo uncaging. The work was published in Science Advances in 2020 (https://advances.sciencemag.org/content/6/8/eaay5154). These novel technologies provide generalizable platforms for enabling PROTACs to be precision medicines.

                • Dr. Jian Jin Has Received a New Multiple-PI R01 Grant from NCI to Develop Novel Therapeutics for Treating MLL-rearranged Leukemias

        Dr. Jian Jin (the contact PI), the Mount Sinai Endowed Professor in Therapeutics Discovery and Director of the Mount Sinai Center for Therapeutics Discovery, and Dr. Hong Wen (the MPI), an Associate Professor at Van Andel Research Institute, have received a new five-year multiple-PI R01 grant from the National Cancer Institute of the National Institutes of Health. The mixed-lineage leukemia (MLL) gene rearrangements account for approximately 80% of infant acute lymphoblastic leukemia and 35-50% of infant acute myeloid leukemia. Patients bearing rearrangements of the MLL gene are associated with dismal prognosis. The research team led by Drs. Jin and Wen will target ENL, an MLL fusion partner, which functions as a reader of histone acetylation and is essential for growth and survival of the MLL-rearranged leukemic cells. Dr. Jin’s laboratory is a pioneer and leader in discovering novel heterobifunctional small-molecule degraders (also known as proteolysis targeting chimeras (PROTACs)) targeting oncogenic proteins. Using the PROTAC technology, the research team will develop first-in-class PROTAC degraders of ENL as a novel therapeutic strategy for treating MLL-rearranged leukemias.

                • Dr. Jian Jin’s Laboratory Received a Major Grant from DARPA to Create Novel and Safe Psychiatric Medications

        Dr. Jian Jin, the Mount Sinai Endowed Professor in Therapeutics Discovery and Director of the Mount Sinai Center for Therapeutics Discovery, is part of a team of internationally acclaimed scientists who has received a four-year, $26,975,142 cooperative agreement from the U.S. Defense Advanced Research Project Agency (DARPA) to generate novel and safe medications for rapidly and effectively treating psychiatric disorders such as depression, anxiety and substance abuse. The research team led by Dr. Bryan Roth at University of North Carolina at Chapel Hillalso includes Drs. Brian Shoichet and Nevan Kroganat University of California at San Francisco, Drs. Georgios Skiniotis and Ron Dror at Stanford University, and Dr. William Wetsel at Duke University. The team has developed innovative methods and technologies and will utilize them to create and advance novel biased agonists of G protein-coupled receptors as drug candidates.

                • Drs. Jian Jin and H. Ümit Kaniskan Published in Nature Reviews Drug Discovery

        Dr. Jian Jin, the Mount Sinai Endowed Professor in Therapeutics Discovery and Director of the Mount Sinai Center for Therapeutics Discovery, and Dr. H. Ümit Kaniskan, Associate Professor of Pharmacological Sciences and Associate Director of the Mount Sinai Center for Therapeutics Discovery, along with their collaborators Drs. Or Gozani and Kamakoti P. Bhat at Stanford University have published a review article entitled “Epigenetics and beyond: targeting writers of protein lysine methylation to treat disease” in Nature Reviews Drug Discovery (https://www.nature.com/articles/s41573-020-00108-x). Dr. Jin’s lab is a pioneer and leader in discovering selective small-molecule inhibitors of protein lysine methyltransferases (KMTs, also known as histone lysine methyltransferases), an important class of epigenetic enzymes that play critical roles in human diseases including cancer. The Jin lab has discovered numerous novel, potent and selective small-molecule inhibitors of KMTs including EZH2, G9a/GLP and SETD8 since 2008.

                • Kwang-Su Park, Ph.D. received 2019-2020 Postdoctoral Award for Excellence in Mentoring

        The Office of Postdoctoral Affairs and the Postdoc Executive Committee at the Icahn School of Medicine at Mount Sinai (ISMMS) announced award winner for “The Excellence in Mentoring Award” as Kwang-Su Park, Ph.D., Postdoctoral fellow in Dr. Jian Jin Lab.