Area of research
Molecular Biology · Cancer Research
Research interest
Research focused on Ubiquitin ligase and Cancer research, with related work in Prostate cancer, Ubiquitin, Bromodomain. Notable publications include 'Intrinsic BET inhibitor resistance in SPOP-mutated prostate cancer is mediated by BET protein stabilization and AKT–mTORC1 activation', 'Prostate Cancer-associated SPOP mutations enhance cancer cell survival and docetaxel resistance by upregulating Caprin1-dependent stress granule assembly', and 'Dysregulation of INF2-mediated mitochondrial fission in SPOP-mutated prostate cancer'.
FBXL4 mutations cause excessive mitophagy via BNIP3/BNIP3L accumulation leading to mitochondrial DNA depletion syndrome
Excessive BNIP3- and BNIP3L-dependent mitophagy underlies the pathogenesis of FBXL4-mutated mitochondrial DNA depletion syndrome
The SET oncoprotein promotes estrogen-induced transcription by facilitating establishment of active chromatin
SPOP mutations promote tumor immune escape in endometrial cancer via the IRF1–PD-L1 axis
SPOP mutation induces DNA methylation via stabilizing GLP/G9a
Prostate cancer-associated SPOP mutations lead to genomic instability through disruption of the SPOP–HIPK2 axis
Prostate Cancer-associated SPOP mutations enhance cancer cell survival and docetaxel resistance by upregulating Caprin1-dependent stress granule assembly
CRL3–SPOP ubiquitin ligase complex suppresses the growth of diffuse large B-cell lymphoma by negatively regulating the MyD88/NF-κB signaling
SPOP promotes ATF2 ubiquitination and degradation to suppress prostate cancer progression
ARRDC1 and ARRDC3 act as tumor suppressors in renal cell carcinoma by facilitating YAP1 degradation.
PubMed 2018cited by 52position: middle
Assessing effects of different processing procedures on the yield of Treponema pallidum DNA from blood
Intrinsic BET inhibitor resistance in SPOP-mutated prostate cancer is mediated by BET protein stabilization and AKT–mTORC1 activation
Dysregulation of INF2-mediated mitochondrial fission in SPOP-mutated prostate cancer
RNF12 promotes p53-dependent cell growth suppression and apoptosis by targeting MDM2 for destruction
Endometrial cancer-associated mutants of SPOP are defective in regulating estrogen receptor-α protein turnover
Stabilization of MCRS1 by BAP1 prevents chromosome instability in renal cell carcinoma
ASPP1/2-PP1 complexes are required for chromosome segregation and kinetochore-microtubule attachments
Destruction of DDIT3/CHOP Protein by Wild-Type SPOP but Not Prostate Cancer-Associated Mutants
The Nedd4-like ubiquitin E3 ligases target angiomotin/p130 to ubiquitin-dependent degradation