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USP8-EIF2S1 signaling enhances CML cell survival under TKI-induced stress.

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The FEBS journal 📖 저널 OA 39.4% 2024: 0/1 OA 2025: 3/10 OA 2026: 10/22 OA 2024~2026 2026 Vol.293(5) p. 1297-1301
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Mohan CG, Pavithran K

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CML is primarily driven by the oncogenic BCR-ABL fusion kinase; however, tyrosine kinase inhibitor (TKI) resistance remains a significant clinical challenge.

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APA Mohan CG, Pavithran K (2026). USP8-EIF2S1 signaling enhances CML cell survival under TKI-induced stress.. The FEBS journal, 293(5), 1297-1301. https://doi.org/10.1111/febs.70372
MLA Mohan CG, et al.. "USP8-EIF2S1 signaling enhances CML cell survival under TKI-induced stress.." The FEBS journal, vol. 293, no. 5, 2026, pp. 1297-1301.
PMID 41454439 ↗
DOI 10.1111/febs.70372

Abstract

CML is primarily driven by the oncogenic BCR-ABL fusion kinase; however, tyrosine kinase inhibitor (TKI) resistance remains a significant clinical challenge. A study by Zang et al. identified USP8 as a critical mediator of this resistance. USP8, a deubiquitinase, stabilizes the stress-response regulator EIF2S1 (eIF2α) by removing K48-linked ubiquitin chains. This stabilization sustains PERK-EIF2S1-mediated unfolded protein response (UPR) signaling. The UPR suppresses general protein translation while promoting the expression of adaptive stress-response genes, allowing CML cells to survive TKI-induced stress. Consequently, targeting the USP8-EIF2S1 axis is proposed as a key therapeutic strategy to overcome resistance and enhance patient outcomes.

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