Jian Jun Jin

The paper shows RAF/MEK glues enable full-dose combination with pan-RAF inhibitors, enhancing tumor-selective MAPK inhibition and tumor regression in RAS-mutant models.

The paper identifies a DNA-histone methylation axis that drives KMT2A amplifications and rearrangements in leukemia, revealing therapeutic targets.

The paper introduces dubTAGs, small molecules that stabilize proteins tagged with FKBP12F36V by recruiting deubiquitinases, enabling tunable and reversible control of protein levels.

This study identifies PRMT7 as a negative regulator of CD8+ T cell immunity and demonstrates a PROTAC degrader (MS54) that enhances anti-tumor responses by activating the NF-κB pathway.

The paper identifies a new four-membered-ring chemotype that selectively binds OTUB1, expands its ligandable chemical space, and enables the development of next-generation DUBTACs.

This paper develops MINDS, a multispecific nanobody-Fc platform that co-depletes membrane receptors and delivers diverse payloads, showing improved antitumor activity in cancer models.

This paper identifies the ENL-USP7 complex as a host factor that stabilizes BRD4 to maintain HIV-1 latency and shows that disrupting this complex reactivates latent HIV.

The paper identifies AMI-1 as an inhibitor of NMNAT1, shows its effect on NAD+ levels and cancer cell viability, and determines its binding mechanism via cryo-EM.

The paper identifies a hydrophobic funnel in BAX that binds 2t-hexadecenal, enhancing BAX activation with BIM, and shows proline 168 regulates this interaction.

This study investigates BCL11A DNA binding mechanisms, epigenetic regulation, and small-molecule effects on its expression in human erythrocyte precursor cells.

This study shows that loss of MHC Class II in BRAF-mutant anaplastic thyroid cancers leads to resistance to MAPK inhibitors by reducing CD4+ T-cell activation.

This study shows YY1 enhances p300 acetyltransferase activity in CRPC, promoting histone acetylation and oncogenic gene expression, and identifies a potential therapeutic target for overcoming drug resistance.

This paper identifies G9a's role in SARS-CoV-2-induced pathogenesis by regulating translation of viral and host proteins, showing that G9a inhibitors can reverse disease-related proteomic changes.

The paper identifies a kinase-independent role of MEK1/2 in stabilizing and maturing CRAF through direct binding, independent of catalytic activity.

This study shows PRMT1 promotes leukemogenesis by enhancing glycolysis and reducing fatty acid oxidation in AMKL cells.

This study shows that inhibiting PRMT1 reduces cardiac fibrosis by blocking fibroblast-to-myofibroblast transition through transcriptional regulation and disruption of FBL activity.

This paper discovers a first-in-class PROTAC degrader for G9a/GLP, showing effective degradation and superior anticancer activity compared to existing inhibitors.

This study identifies G9a's noncanonical role in promoting translation of genes involved in hyperinflammation and lymphopenia in COVID-19, revealing therapeutic targets that counteract viral effects.

This study uses a generative deep learning framework to design new KOR antagonists, which are prioritized for synthesis and validated through experimental assays.

This paper develops cell-based assays to monitor PROTAC degradation kinetics and ternary complex formation, revealing that ternary complex stability is critical for PROTAC efficiency.

The paper identifies small molecules that inhibit proteotoxicity and inflammation in Alzheimer's Disease models, revealing mechanisms linking glycolysis to neuroinflammation and suggesting new therapeutic targets.

The paper characterizes two MOR PAMs that enhance opioid antinociception without increasing adverse effects in mouse models.

This paper introduces deschloroclozapine (DCZ), a potent and selective DREADD agonist that rapidly modulates neuronal activity and behavior in mice and monkeys.

This study identifies molecular networks and key regulators in Alzheimer’s Disease using integrative genomics and experimental validation.