USP8-EIF2S1 signaling enhances CML cell survival under TKI-induced stress.
1/5 보강
CML is primarily driven by the oncogenic BCR-ABL fusion kinase; however, tyrosine kinase inhibitor (TKI) resistance remains a significant clinical challenge.
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 ↗
Abstract 한글 요약
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.
🏷️ 키워드 / MeSH 📖 같은 키워드 OA만
- Humans
- Leukemia
- Myelogenous
- Chronic
- BCR-ABL Positive
- Eukaryotic Initiation Factor-2
- Signal Transduction
- Unfolded Protein Response
- Cell Survival
- Protein Kinase Inhibitors
- Ubiquitin Thiolesterase
- Drug Resistance
- Neoplasm
- Fusion Proteins
- bcr-abl
- Endopeptidases
- eIF-2 Kinase
- TKI resistance drugs
- UPR signaling
- chronic myeloid leukemia
- deubiquitinating enzyme
- structure‐based drug design
- ubiquitin‐specific protease family
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