CIMR-Yaping Huang

Research Group

Yaping Huang

huangyp(at)cimrbj.ac.cn

Junior Investigator

Heat Shock Protein, Immune Homeostasis,

Genomic Stability, Cancer Immunotherapy,

Inflammatory Diseases

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huangyp(at)cimrbj.ac.cn

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B.S. in Biology, Wuhan University, China

Ph.D. in Biology, Tsinghua University, China

Work Experience

2024.6-Present

Junior Investigator, Chinese Institute for Molecular and Cellular Therapeutics, Chinese Institutes for Medical Research, Beijing, China

2018.12-2024.5

Postdoctoral Fellow, University of Texas Southwestern Medical Center, USA

Research Interests

Huang Lab focuses on the non-canonical molecular functions of heat shock proteins (HSPs, also called molecular chaperones) in maintaining cellular and tissue homeostasis with particular interests in innate immunity and genome maintenance, and related human diseases, including cancer, infection, neurodegeneration and autoimmune disorders. Huang Lab is also interested in developing new HSP-based strategies for intervention of these human diseases on the basis of lab's discoveries.

Major Contributions

1. Discovering the functions of HSP40 protein DNAJA2 in genome maintenance and cancer immunotherapy (Nature Communications, 2023; Cell Discovery, 2023)

2. Demonstrating the functions of DNAJA2 in maintaining glucose homeostasis (Nature Communications, 2025)

3. Identification of novel genetic variants predisposing to familial oral cancer (Cell Discovery, 2019)

4. Revealing the mechanism by which histone modification H3K36me3 and histone mutation H3G34V/R/D regulate genome stability and tumorigenesis (JBC, 2018; PNAS, 2018)

Representative Publications *：Co-first author; #：Co-corresponding author

Qin Y*, Wu W*, Lin K, Davis AJ, and Huang Y. Heat shock protein DNAJA2 controls insulin signaling and glucose homeostasis by preventing spontaneous insulin receptor endocytosis. Nature Communications, 2025, 16: 9973. DOI: 10.1038/s41467-025-64948-0

Huang Y^*, Lu C^*, Wang H, Gu L, Fu YX^#, Li GM^#. DNAJA2 deficiency activates cGAS-STING pathway via the induction of aberrant mitosis and chromosome instability. Nature Communications, 2023, 14: 5246. DOI: 10.1038/s41467-023-40952-0

Huang Y, Gu L, Li GM. Heat shock protein DNAJA2 regulates transcription-coupled repair by triggering CSB degradation via chaperone-mediated autophagy. Cell Discovery, 2023, 9: 107. DOI: 10.1038/s41421-023-00601-8

Huang Y^*, Zhao J^*, Mao G, Lee GS, Zhang J, Bi L, Gu L, Chang Z, Valentino J^#, Li GM^#. Identification of novel genetic variants predisposing to familial oral squamous cell carcinomas. Cell Discovery, 2019, 5: 57. DOI: 10.1038/s41421-019-0126-6

Fang J^*, Huang Y^*, Mao G^*, Yang S, Rennert G, Gu L, Li H, Li GM. Cancer-driving H3G34V/R/D mutations block H3K36 methylation and H3K36me3-MutSα interaction. Proceedings of the National Academy of Science of the United States of America, 2018, 115: 9598-9603. DOI: 10.1073/pnas.1806355115

Huang Y, Li GM. DNA mismatch repair in the chromatin context: Mechanisms and therapeutic potential. DNA Repair (Amst), 2020, 93: 102918. DOI: 10.1016/j.dnarep.2020.102918

Huang Y, Gu L, Li GM. H3K36me3-mediated mismatch repair preferentially protects actively transcribed genes from mutation. Journal of Biological Chemistry, 2018, 293: 7811-7823. DOI: 10.1074/jbc.RA118.002839