Results 101 to 110 of about 13,489 (251)
Ubiquilin (UBQLN), like many other human proteins, contains both well‐folded and disordered regions. Here, we show that intramolecular interactions between disordered regions and folded domains modulate between open and closed topologies of UBQLN proteins, altering their structure and function.
Jessica K. Niblo +4 more
wiley +1 more source
CCT2 Promotes Prostate Cancer Progression Through EIF3F‐Dependent Stabilization of FASN
ABSTRACT Prostate cancer (PCa) is increasingly recognized to be driven by dysregulated lipid metabolism. Although fatty acid synthase (FASN) is highly expressed in PCa, the mechanisms governing FASN protein stability and its functional integration into oncogenic lipid metabolism remain poorly defined.
Shun Xu +13 more
wiley +1 more source
Why cancer cells disproportionately accumulate polyubiquitinated proteotoxic proteins despite high proteasomal activity is an outstanding question. While mis-regulated ubiquitination is a contributing factor, here we show that a structurally-perturbed ...
Rangapriya Sundararajan +5 more
doaj +1 more source
PDIA6–SCD1 Axis Rewires Lipid Metabolism to Drive Gastric Cancer Progression
Protein disulfide isomerase A6 (PDIA6) is identified as an oncogenic driver in gastric cancer. PDIA6 directly binds and stabilizes SCD1 by limiting its ubiquitin–proteasome‐mediated degradation, thereby sustaining monounsaturated fatty acid (MUFA)‐enriched lipid homeostasis and lipid metabolic reprogramming.
Zhen Tian +13 more
wiley +1 more source
Host‐specific compatibility between RNF138‐like proteins and flavivirus NS5 determines NS5 stability. Mammalian RNF138 but not arthropod homologs recognizes and induces conserved NS5/RdRp K48‐linked ubiquitination and proteasomal degradation, thereby restricting viral replication. Ectopic RNF138 in mice attenuates TBEV‐induced pathogenesis. (Created in
Jialiang Sun +6 more
wiley +1 more source
In the pathological state of PD induced by MPP+, the upregulated PRMT9 in dopaminergic neurons translocates into mitochondrion and interacts with DUSP26 and catalyzes its arginine methylation, leading to the ubiquitin‐proteasomal degradation of DUSP26 mediated by Trim32.
Tengfei Liu +13 more
wiley +1 more source
We introduced genetically encodable, receptor‐independent nanobody‐CPP chimeras, termed endobodies, as robust and modular membrane protein degraders. Additionally, proteasome‐targeting domain (PTD)‐tethered endobody demonstrates further enhanced degradation potency.
Chengjian Zhou +3 more
wiley +1 more source
In response to hypertrophic stimuli, increased c‑JUN phosphorylation upregulates RNF115, leading to SPTBN1 ubiquitination and degradation. which promotes F‑actin depolymerization and YAP activation, driving cardiac hypertrophy. The RNF115 inhibitor DTD effectively suppresses SPTBN1 ubiquitination and cardiac hypertrophy.
Yan Zu +12 more
wiley +1 more source
Decoding the secrets: how conformational and structural regulators inhibit the human 20S proteasome. [PDF]
Fernandes PMP +4 more
europepmc +1 more source
Upon JEV infection, ZNF33B recruits METTL14 to stabilize the METTL3‐METTL14 m6A methyltransferase complex, leading to increased m6A modification of host transcripts, including Trim25 mRNA. ZNF33B selectively binds m6A‐modified sites on Trim25 mRNA and accelerates its decay, resulting in reduced TRIM25 protein abundance.
Jian Du +9 more
wiley +1 more source

