ZhengMing Wu

ORCID: 0000-0002-3738-4605
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Prostate Cancer Treatment and Research
  • Adipose Tissue and Metabolism
  • Cancer, Hypoxia, and Metabolism
  • Cancer, Stress, Anesthesia, and Immune Response
  • Hippo pathway signaling and YAP/TAZ
  • Immune Cell Function and Interaction
  • Estrogen and related hormone effects
  • CAR-T cell therapy research
  • Cancer, Lipids, and Metabolism
  • Wnt/β-catenin signaling in development and cancer
  • Ubiquitin and proteasome pathways
  • Sirtuins and Resveratrol in Medicine
  • Biochemical effects in animals
  • PARP inhibition in cancer therapy
  • T-cell and B-cell Immunology
  • Cancer-related Molecular Pathways
  • Protein Kinase Regulation and GTPase Signaling
  • Social Robot Interaction and HRI
  • High-Voltage Power Transmission Systems
  • FOXO transcription factor regulation
  • Education and Work Dynamics
  • Bioactive Compounds and Antitumor Agents
  • Tunneling and Rock Mechanics
  • Epigenetics and DNA Methylation
  • Signaling Pathways in Disease

University of California, San Diego
2018-2023

Guangzhou Automobile Group (China)
2023

Moores Cancer Center
2018-2019

Fudan University
2019

Shanghai Medical College of Fudan University
2015-2018

Shanxi Science and Technology Department
2013

Yancheng Institute of Technology
2008

Taixing People's Hospital
2006

Second Military Medical University
2003

Small cell lung cancer (SCLC) is highly lethal due to its prevalent metastasis. Most SCLCs have inactivating mutations in TP53 and RB1. We find that loss of YAP expression key for SCLC cells acquire rapid ameboid migration high metastatic potential. functions through target genes CCN1/CCN2 inhibit migration. RB1 mutation contributes transcriptional silencing via E2F7, which recruits the RCOR co-repressor complex promoter. discover benzamide family HDAC inhibitors stimulate by inhibiting...

10.1038/s41467-023-41585-z article EN cc-by Nature Communications 2023-09-22

Highlights•Sirt5+ subset in wild-type Kras colorectal tumors determines multidrug resistance•Sirt5-mediated demalonylation and inactivation of SDHA lead to succinate accumulation•Succinate binds activates TrxR2 maintain chemotherapy resistance•Succinate inhibits aKG-dependent dioxygenases regulate cetuximab resistanceSummaryA major obstacle for successful management patients with carcinoma (CRC) is resistance anti-cancer cytotoxic treatments. Here, we identified a mechanism CRCs based on the...

10.1016/j.celrep.2018.02.037 article EN cc-by-nc-nd Cell Reports 2018-03-01

Autonomous cars are indispensable when humans go further down the hands-free route. Although existing literature highlights that acceptance of autonomous car will increase if it drives in a human-like manner, sparse research offers naturalistic experience from passenger's seat perspective to examine humanness current cars. The present study tested whether AI driver could create ride for passengers based on 69 participants' feedback real-road scenario. We designed experience-based version...

10.1109/taffc.2023.3279311 article EN IEEE Transactions on Affective Computing 2023-05-23

Oncogenic mutations in the KRAS gene are very common human cancers, resulting cells with well-characterized selective advantages. For more than three decades, development of effective therapeutics to inhibit KRAS-driven tumorigenesis has proved a formidable challenge and was considered 'undruggable'. Therefore, multi-targeted therapy may provide reasonable strategy for treatment cancers. Here, we assess efficacy mechanistic rationale combining HASPIN mTOR inhibition as potential cancers...

10.1016/j.tranon.2022.101540 article EN cc-by-nc-nd Translational Oncology 2022-09-14

Cytokine-inducible SH2-containing protein (CIS, encoded by the gene CISH) is a key negative regulator of IL-15 signaling in natural killer (NK) cells. Here, we developed human CISH knockout (CISH-/-) NK cells using an induced pluripotent stem cell-derived cell (iPSC-NK cell) platform. CISH-/- iPSC-derived demonstrate increased mediated JAK-STAT pathway activity. Consequently iPSC-NK exhibit improved expansion and cytotoxic activity against multiple tumor lines when maintained at low cytokine...

10.2139/ssrn.3544410 article EN SSRN Electronic Journal 2020-01-01

<p>Figure S2 shows increased GAD65 enzymatic activity caused by phosphorylation at serine 6</p>

10.1158/0008-5472.22421264.v1 preprint EN cc-by 2023-03-31
Coming Soon ...