Ask about this productRelated genes to: USP37 antibody
- Gene:
- USP37 NIH gene
- Name:
- ubiquitin specific peptidase 37
- Previous symbol:
- -
- Synonyms:
- KIAA1594
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-04
- Date modifiied:
- 2015-08-26
Related products to: USP37 antibody
Related articles to: USP37 antibody
- - Source: PubMed
- The long-chain acyl-CoA synthetase (ACSL) family has been associated with tumor progression across various cancer types. However, the function of the ACSL family in gastric cancer (GC) remains poorly understood. Comprehensive investigations employing in vivo and in vitro experiments demonstrate that ACSL3 suppresses ferroptosis and drives GC progression. Mechanistically, ACSL3 facilitated YY1 nuclear translocation, triggering endoplasmic reticulum (ER) stress and subsequent activation of the unfolded protein response (UPR). Genome-wide binding analysis revealed that YY1 directly binds to the USP37 promoter, enhancing its transcriptional activation. Furthermore, a novel interaction was identified between USP37 and PERK, a pivotal UPR regulator, wherein USP37 mediates K29-linked deubiquitination of PERK. PERK stabilization upregulated SLC7A11 expression, thereby inhibiting ferroptosis and promoting tumor progression. Collectively, the findings establish a molecular cascade wherein ACSL3 mediates ER stress-mediated UPR activation through the YY1/USP37/PERK axis, suppressing ferroptosis and accelerating GC progression, identifying ACSL3 as a potential therapeutic target for GC treatment. - Source: PubMed
Publication date: 2026/07/07
Wang HongleiJiao JieYang WenshuoSun DanpingWei MengSun GuoruiYan ZhiboLiang YizeCheng ZeweiYan YongqiWang MenghuiLi YangjiaCui XiaohanYu Wenbin - USP37 plays a pivotal role in cell cycle regulation, oncogenesis and metastasis. So far, the precise mechanisms and function of USP37 in hepatocellular carcinoma (HCC) remain unclear. In this study, we found USP37 expression was significantly elevated in HCC tissues compared to adjacent normal tissues and high expression was negatively correlated with patient prognosis. Functional assays including CCK-8, EdU staining, colony formation assays, patient derived organoids, transwell assays, wound healing, and in vivo models demonstrated that USP37 significantly promoted proliferation and migration of HCC cells. Mechanistically, USP37 interacted with RAF1, enhancing its protein stability and activating the ERK signaling pathway. This study identifies a novel mechanism by which USP37 promotes HCC cell proliferation through stabilizing RAF1 and activating the RAF-ERK signaling pathway. These findings highlight USP37 as a potential therapeutic target for HCC. - Source: PubMed
Publication date: 2026/06/24
Wang YumingDing RuidongWang YilinCai XianghengShan Jijun - Cellular senescence, a state of permanent cell cycle arrest, contributes to tissue dysfunction and aging through the accumulation of apoptosis-resistant senescent cells. Although the transcription factor FOXO4 is known to enhance senescent cell survival, the mechanisms regulating its stability have remained unclear. Here, we identify a DNA damage response (DDR)-driven CHK2-USP37-FOXO4 axis essential for maintaining the apoptotic resistance of senescent cells. We demonstrate that FOXO4 protein stability is elevated in stress-induced senescent cells, resulting from reduced ubiquitin-proteasomal degradation. A deubiquitinase screen identified USP37 as the key enzyme stabilizing FOXO4 through direct interaction and removal of K48-linked polyubiquitin chains. Depletion of USP37 destabilizes FOXO4 and sensitizes senescent cells to apoptosis. Mechanistically, persistent DDR signaling during senescence activates CHK2, which phosphorylates USP37 at Thr589, thereby enhancing its binding to FOXO4. Importantly, ablation of USP37 in senescent cells increases the rate of apoptosis, a phenotype that is rescued by FOXO4 reexpression. Together, our work unveils USP37 as a CHK2-regulated stabilizer of FOXO4 that maintains the apoptotic resistance of senescent cells, suggesting the CHK2-USP37-FOXO4 axis as a therapeutic target for age-related pathologies. - Source: PubMed
Publication date: 2026/04/14
Sun JiahuiGeng AnkeSong ZhiweiChen LingjiangZhang Zhen-NingJiang YingMao Zhiyong - In aged humans and mice, hypobranched glycogen aggregates, known as polyglucosan bodies (PGBs), accumulate in hippocampal astrocytes. While PGBs are linked to cognitive decline in neurological diseases, they remain largely unstudied in the context of typical aging. We show that PGBs arise in autophagy-dysregulated astrocytes in the aged hippocampus, with substantial variation among 32 inbred BXD mouse strains. Genetic mapping through quantitative trait locus analysis identified a major locus (Pgb1) that modulates hippocampal PGB burden. Extensive transcriptomic and proteomic datasets were produced for the aged hippocampus of the BXD family to investigate the mechanism by which the Pgb1 locus modulates PGB burden. We identified that Pgb1 contains allelic Smarcal1 and Usp37 variants and influences PGB burden through trans-regulation of mRNA and protein expression levels, including abundance of glycogen-mobilizing factor PYGB. Furthermore, comprehensive phenome-wide association scans, transcriptomic analyses, and direct behavioral testing demonstrated that cognition remains intact despite age-related PGB burden. A record of this paper's transparent peer review process is included in the supplemental information. - Source: PubMed
Publication date: 2026/02/02
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