CIMR-Yaping Huang

Research Group

Yaping Huang

hypiwl(at)163.com

Junior Investigator

hypiwl(at)163.com

B.S. in Biology, Wuhan University, China

Ph.D. in Biology, Tsinghua University, China

Work Experience

2024.6

Junior Investigator, Chinese Institutes for Medical Research, Beijing, China

2018.12-2024.5

Postdoctoral Fellow, University of Texas Southwestern Medical Center, USA

Research Direction

The Huang laboratory at CIMR mainly studies the physiological functions of heat shock protein 40s (HSP40s) in critical biological pathways including genome maintenance, innate immunity and glucose metabolism, and their implications in pathogenesis of human diseases, such as cancer, autoimmune disease and metabolic disorder.

Major Research Projects

Decoding the functions and functional mechanisms of HSP40 in critical biological pathways including genome maintenance, innate immunity and glucose metabolism.

2. Exploring the functions of HSP40 in the pathology and treatment of human disease, such as cancer, autoimmune disease and metabolic disorder.

3. Developing HSP40-based therapeutics for human diseases.

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 (Manuscript in preparation)

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

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, Li GM. DNA mismatch repair preferentially safeguards actively transcribed genes. DNA Repair (Amst), 2018, 71: 82-86. DOI: 10.1016/j.dnarep.2018.08.010

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