Area of research
Molecular Biology · Oncology
Research interest
Research interests include DNA Repair Mechanisms, PARP inhibition in cancer therapy, Ubiquitin and proteasome pathways, and Cancer-related Molecular Pathways.
GCN5-ERK lactylation-phosphorylation loop amplifies lactate-driven cancer progression.
RAD51 succinylation regulates homologous recombination and contributes to the chemosensitivity in cancer
USP25 aggravates liver cancer development and impairs chemosensitivity by limiting LATS1 activation.
A cGAS-mediated mechanism in naked mole-rats potentiates DNA repair and delays aging
Human HDAC6 senses valine abundancy to regulate DNA damage.
Lactylation of XLF promotes non-homologous end-joining repair and chemoresistance in cancer
Lactylation of XLF promotes non-homologous end-joining repair and chemoresistance in cancer
NUFIP1 integrates amino acid sensing and DNA damage response to maintain the intestinal homeostasis
A cGAS-mediated mechanism in naked mole-rats potentiates DNA repair and delays aging.
Lactylation Enhances the Activity of Lactate Dehydrogenase A and Promotes the Chemoresistance to Cisplatin Through Facilitating DNA Nonhomologous End Junction in Lung Adenocarcinoma
Cathepsin D promotes acute myeloid leukemia progression through stabilization of the anti-apoptotic proteins.
Author Correction: Human HDAC6 senses valine abundancy to regulate DNA damage.
Histone H1 deamidation: new insight into chromatin relaxation and DNA damage repair
Metabolic regulation of homologous recombination repair by MRE11 lactylation
Activation and antitumor immunity of CD8 <sup>+</sup> T cells are supported by the glucose transporter GLUT10 and disrupted by lactic acid
Activation and antitumor immunity of CD8<sup>+</sup> T cells are supported by the glucose transporter GLUT10 and disrupted by lactic acid.
USP25 Elevates SHLD2-Mediated DNA Double-Strand Break Repair and Regulates Chemoresponse in Cancer.
Synergistic anticancer effect by targeting CDK2 and EGFR-ERK signaling.
Identification and validation of calcium extrusion-related genes prognostic signature in colon adenocarcinoma
Germline Mutations of Holliday Junction Resolvase Genes in Multiple Primary Malignancies Involving Lung Cancer Lead to PARP Inhibitor Sensitization.
Lactate accelerates cancer progression through the ERK-GCN5 lactylation-phosphorylation feedback cascade
Supplementary Figure S7 from Germline Mutations of Holliday Junction Resolvase Genes in Multiple Primary Malignancies Involving Lung Cancer Lead to PARP Inhibitor Sensitization
Supplementary Figure S3 from Germline Mutations of Holliday Junction Resolvase Genes in Multiple Primary Malignancies Involving Lung Cancer Lead to PARP Inhibitor Sensitization
Supplementary Table S2 from Germline Mutations of Holliday Junction Resolvase Genes in Multiple Primary Malignancies Involving Lung Cancer Lead to PARP Inhibitor Sensitization
Supplementary Figure S3 from Germline Mutations of Holliday Junction Resolvase Genes in Multiple Primary Malignancies Involving Lung Cancer Lead to PARP Inhibitor Sensitization
Supplementary Table S2 from Germline Mutations of Holliday Junction Resolvase Genes in Multiple Primary Malignancies Involving Lung Cancer Lead to PARP Inhibitor Sensitization
Supplementary Figure S2 from Germline Mutations of Holliday Junction Resolvase Genes in Multiple Primary Malignancies Involving Lung Cancer Lead to PARP Inhibitor Sensitization
Supplementary Figure S4 from Germline Mutations of Holliday Junction Resolvase Genes in Multiple Primary Malignancies Involving Lung Cancer Lead to PARP Inhibitor Sensitization
Supplementary Figure S5 from Germline Mutations of Holliday Junction Resolvase Genes in Multiple Primary Malignancies Involving Lung Cancer Lead to PARP Inhibitor Sensitization
Supplementary Figure S7 from Germline Mutations of Holliday Junction Resolvase Genes in Multiple Primary Malignancies Involving Lung Cancer Lead to PARP Inhibitor Sensitization