Results 131 to 140 of about 109,331 (244)
Chemotherapy leverages tumor‐cell autophagy to reshape the colorectal cancer immune microenvironment. Autophagy degrades FBXW2 to promote C/EBPβ‐mediated TIMP‐2 transcription and MMP‐9 suppression, driving intra‐tumoral CD8+ T‐cell infiltration. Targeting MMP‐2/9 or restoring TIMP‐2 overcomes chemo‐resistance in autophagy‐deficient tumors. ABSTRACT The
Bing Cheng +12 more
wiley +1 more source
The combination of radiation therapy and immunotherapy has become a cornerstone of modern clinical cancer treatment. However, the inherent radiation resistance of tumors and complex immune evasion mechanisms remain major bottlenecks limiting their long ...
Qian Yang +8 more
doaj +1 more source
Small molecule modulators of RING-type E3 ligases: MDM and cullin families as targets
© 2018 Bulatov, Zagidullin, Valiullina, Sayarova and Rizvanov. Ubiquitin-proteasome system (UPS) is a primary signaling pathway for regulation of intracellular protein levels.
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GSTM4 enhances the interaction between ACLY and the E3 ubiquitin ligase TRIM27, thereby increasing K48‐linked ubiquitination at the K554 site of ACLY and promoting its degradation. Consequently, GSTM4 regulates lipid synthesis, as well as the proliferation and metastasis of PCa cells, by modulating ACLY stability.
Kang‐Ping Xiong +11 more
wiley +1 more source
Uhrf1‐mediated PKM2 ubiquitination and degradation repressed the nuclear translocation of PKM2, and EPT served as a molecular glue capable of targeting the Uhrf1–PKM2 complex to alleviate the IBD course, suggesting that the Uhrf1–PKM2 axis was a previously unrecognized strategy for treating IBD.
Juan Zhang +9 more
wiley +1 more source
OAF Blocks SIAH1‐Mediated Degradation of SCPX, a Therapeutic Strategy for MASLD
This study shows OAF directly binds to SCPX and inhibits its interaction with the E3 ligase SIAH1, thereby protecting SCPX from ubiquitin‐dependent degradation and stabilizing its levels. This OAF‐SCPX axis represents a novel pathway in lipid homeostasis, highlighting OAF as a promising therapeutic candidate for MASLD.
Zongxi Li +11 more
wiley +1 more source
BNC2 exhibits context‐dependent opposing functions across multiple cancer types. This study reveals BNC2 as an oncogenic driver of melanoma proliferation and metastasis through transcriptional activation of PIK3CA. The natural compound TSN simultaneously degrades BNC2 and its oncogenic partner SMAD3 via CRBN‐dependent ubiquitination.
Hui Dai +7 more
wiley +1 more source
AI‑guided single‑cell transcriptomics identifies OGT as a key regulator enriched in rheumatoid arthritis fibroblast‑like synoviocytes (RA‐FLSs). Inflammatory stimuli activate the OGT–SAP130 axis, which modulates the H3K27ac/H3K27me3 balance and epigenetically silences BTG2, promoting aggressive transformation of RA‑FLSs.
Duoli Xie +14 more
wiley +1 more source
Temozolomide treatment activates GSK3β, driving DNMT1 phosphorylation, destabilization, and CD47 promoter hypomethylation in glioblastoma. This epigenetic shift upregulates CD47, enabling TMZ‐treated GBM cells to evade macrophage phagocytosis, survive chemotherapy, and acquire resistance.
Jie Li +11 more
wiley +1 more source
Deubiquitination of Vangl by USP6 and USP32 Regulates Planar Cell Polarity Signaling
Compartment‐specific deubiquitination controls Vangl dosage and planar cell polarity signaling. USP6 and USP32 regulate distinct subcellular pools of Vangl by removing distinct ubiquitin modifications from Vangl proteins. This regulatory mechanism safeguards PCP‐dependent embryonic morphogenesis, while aberrant USP32‐dependent stabilization of VANGL ...
Fangzi Zha +13 more
wiley +1 more source

