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Articles by Chenji Wang
TRAF7 mutations stabilize K/NRAS and hyperactivate MAPK signaling to cause CAFDADD neurodevelopmental defects
Abstract INTRODUCTION RESULTS DISCUSSION MATERIALS AND METHODS Acknowledgments Supplementary Materials REFERENCES Information & Authors Metrics & Citations View Options References Figures Tables Media Share This article has 0 eLetter . Abstract The MAPK-ERK1/2 pathway plays a crucial role in neurodevelopment during embryogenesis, and the hyperactivation of this signaling cascade serves as a pathological hallmark for various neurodevelopmental disorders.
TSC22D4 drives clear cell renal cell carcinoma progression and therapy resistance by stabilizing NRF2 through KEAP1 disruption
Abstract Clear cell renal cell carcinoma (ccRCC), the most common form of kidney cancer, is highly aggressive and difficult to manage due to its intrinsic resistance to oxidative stress. Nuclear factor erythroid 2-related factor 2 (NRF2), a master regulator of oxidative stress responses, is frequently overexpressed in ccRCC and is associated with poor prognosis.
DPP9 inhibition boosts antitumor immunity by disrupting BRISC-mediated PD-L1 expression in clear cell renal cell carcinoma
Abstract Programmed cell death protein 1 (PD-1) and its ligand programmed cell death ligand-1 (PD-L1) are key mediators of immune checkpoint blockade therapy in clear cell renal cell carcinoma (RCC). However, immune evasion and primary resistance often limit their efficacy, highlighting the need for improved strategies. Here, we identified dipeptidyl peptidase 9 (DPP9) as a critical regulator of PD-L1 expression in ccRCC.
SIRT7 regulates T-cell antitumor immunity through modulation BCAA and fatty acid metabolism - Cell Death & Differentiation
Abstract SIRT7, one of the least studied members of the Sirtuins family, is an NAD+-dependent lysine deacetylase and desuccinylase. While previous studies using affinity enrichment and quantitative proteomics identified numerous lysine-deacetylated substrates of SIRT7, its lysine-desuccinylated substrates remain underexplored, limiting our understanding of its role in cellular homeostasis.
FBXL4 mutation-caused mitochondrial DNA depletion syndrome is driven by BNIP3/BNIP3L-dependent excessive mitophagy
Footnotes 3 These authors contributed equally to this work. Affiliations State Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, China
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