USP11 Antibody
- Known as:
- USP11 Antibody
- Catalog number:
- 35115
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- USP11 Antibody
Related genes to: USP11 Antibody
- Gene:
- USP11 NIH gene
- Name:
- ubiquitin specific peptidase 11
- Previous symbol:
- -
- Synonyms:
- UHX1
- Chromosome:
- Xp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-01
- Date modifiied:
- 2016-10-05
Related products to: USP11 Antibody
Related articles to: USP11 Antibody
- Intestinal ischemia/reperfusion (I/R) injury is a life-threatening clinical condition associated with high mortality and limited therapeutic options. Ferroptosis, an iron-dependent form of regulated cell death driven by excessive lipid peroxidation, has emerged as a critical contributor to intestinal I/R injury. Nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy promotes ferroptosis by increasing intracellular iron availability; however, the upstream mechanisms governing this process remain poorly understood. Beclin-1 is a key initiator of autophagy, whereas ubiquitin-specific protease 11 (USP11) regulates protein stability through deubiquitination. Whether USP11 modulates NCOA4-mediated ferritinophagy via Beclin-1 during intestinal I/R injury remains unknown. Here, we investigated the role of the USP11/Beclin-1/NCOA4 signaling axis using a murine intestinal I/R model and an oxygen-glucose deprivation/reoxygenation (OGD/R)-induced IEC-6 cell injury model. Bioinformatic analysis, co-immunoprecipitation (CO-IP), gene knockdown, and rescue experiments were performed to characterize ferritinophagy and ferroptosis. Intestinal I/R injury and OGD/R treatment markedly induced NCOA4-mediated ferritinophagy, accompanied by enhanced lipid peroxidation and characteristic mitochondrial damage, whereas these alterations were reversed by the autophagy inhibitor 3-methyladenine (3-MA) and ferroptosis-specific inhibitor Ferrostatin-1 (Fer-1). Beclin-1 was identified as a critical interacting partner of NCOA4, and its knockdown suppressed ferritinophagy, ferroptosis, and intestinal injury. Mechanistically, USP11 expression was significantly upregulated following intestinal I/R injury and stabilized Beclin-1 through deubiquitination. Conversely, USP11 knockdown enhanced Beclin-1 ubiquitination, reduced its stability, and consequently inhibited NCOA4-mediated ferritinophagy and ferroptosis. Consistently, inhibition of USP11 markedly alleviated intestinal injury both in vivo and in vitro. Collectively, our findings reveal a previously unrecognized USP11/Beclin-1/NCOA4 signaling axis that drives ferritinophagy-dependent ferroptosis during intestinal I/R injury. By promoting Beclin-1 deubiquitination and stabilization, USP11 facilitates NCOA4-mediated ferritinophagy and subsequent ferroptotic cell death, highlighting USP11 as a promising therapeutic target for intestinal I/R injury. - Source: PubMed
Publication date: 2026/09/22
Han XiaoxiaMa XiaojieHou MinXing YangWang XinrunLi XiaoxiLiu JieZhou JiaLyu JipengLeng Yufang - Maternal immune activation (MIA) during pregnancy is a recognized risk factor for neurodevelopmental and neurodegenerative disorders, including Alzheimer's disease. Although the long-term consequences of prenatal inflammation have been extensively investigated, the influence of biological sex on age-related behavioral and hippocampal alterations remains insufficiently understood. MIA was induced in pregnant Wistar rats by the intraperitoneal administration of lipopolysaccharide (100 μg/kg) on gestational day 17. Male and female offspring were examined at 12 months of age. Behavioral patterns were assessed using the Morris water maze and elevated plus maze. Hippocampal neuronal morphology and microglial and astrocytic phenotypes were evaluated by histology and IHC, while the expression of genes associated with inflammation, neurodegeneration, neuroplasticity, oxidative stress, and neurogenesis was determined by RT-qPCR. Prenatal LPS exposure produced persistent behavioral alterations in both sexes but with distinct phenotypes. Both male and female offspring exhibited increased anxiety-like behavior, whereas females showed reduced exploratory activity during spatial memory testing. Female offspring demonstrated more pronounced hippocampal pathology, including an increased relative number of pyknotic hyperchromic neurons, a reduced ramified-to-amoeboid microglia ratio, decreased , and selective upregulation of and , potentially indicating enhanced susceptibility to neurodegenerative processes. In contrast, males maintained predominantly ramified microglia morphology and showed increased expression of the neuronal progenitor gene , possibly suggesting the activation of compensatory mechanisms. Both sexes exhibited hippocampal upregulation of , , , , and , consistent with chronic pro-inflammatory background accompanied by adaptive antioxidant and anti-inflammatory responses. Prenatal immune activation induces long-lasting behavioral, morphological, and molecular alterations that persist into middle age and exhibit marked sexual dimorphism. Female offspring appear more vulnerable to pro-neurodegenerative changes, whereas male offspring activate compensatory neuroprotective pathways that might partially preserve hippocampal function despite sustained pro-inflammatory reactions. These findings highlight sex as a critical biological variable in the long-term consequences of prenatal inflammation and may facilitate the identification of early biomarkers and therapeutic targets for MIA-associated neuropsychiatric and neurodegenerative disorders. - Source: PubMed
Publication date: 2026/09/15
Sentyabreva Alexandra VLyamtsev Alexander SMelnikova Ekaterina AAliper Gleb MKosyreva Anna M - Myocardial ischemia/reperfusion (I/R) injury is closely associated with excessive oxidative stress and ferroptosis. (Sal), a major active component of Rhodiola, has demonstrated cardioprotective properties, yet its precise mechanisms in regulating ferroptosis remain unclear. The present study investigated whether Sal attenuates myocardial I/R injury by modulating ubiquitin‑specific protease 11 (USP11)‑mediated deubiquitination and stabilization of peroxiredoxin 2 (PRDX2). An H9c2 anoxia/reoxygenation (A/R) model and an rat I/R model were established. Sal significantly improved the viability of A/R‑injured H9c2 cells and reduced reactive oxygen species accumulation, ferrous iron overload and lipid peroxidation. Mechanistically, Sal upregulated the expression levels of USP11, glutathione peroxidase 4 and PRDX2 while suppressing prostaglandin‑endoperoxide synthase 2; notably, these effects were attenuated by USP11 silencing. Molecular docking and cellular thermal shift assay analyses suggested that USP11 may represent a potential molecular target involved in Sal‑mediated cardioprotection, thereby increasing its thermal stability and strengthening the USP11‑PRDX2 interaction. This may facilitate the USP11‑mediated stabilization of PRDX2, prolonging its half‑life and preserving cellular redox homeostasis. experiments further demonstrated that Sal pretreatment markedly reduced myocardial infarct size and improved cardiac contractile function, which was associated with the concurrent upregulation of the USP11‑PRDX2 axis. Collectively, these findings indicate that Sal confers robust cardioprotection against I/R injury by engaging USP11 and promoting the stabilization of PRDX2, thereby suppressing oxidative stress and ferroptosis. USP11 represents a promising therapeutic target for mitigating myocardial I/R injury. - Source: PubMed
Publication date: 2026/09/25
Qiu Zhi-CongLi Jian-NanLi Yi-ZhouWu Zi-MingLuo Xu-DongZeng Rui-YuanLai Song-QingZhao Shi-TaoWan Li - Calcific aortic valve disease (CAVD) lacks effective pharmacotherapies. Although small extracellular vesicles (sEVs) are established mediators of cellular communication, how they translate oscillatory shear stress (OSS) into pro-calcific signals through endothelial-interstitial crosstalk remains unknown. This study aimed to delineate a complete mechanosensitive pathway by which sEVs drive aortic valve calcification (AVC). - Source: PubMed
Publication date: 2026/09/16
Chen ShiqiShang XiaokeXu JianjunFan ZhengfengZhang ShaoshaoLi RuiLiu MingLiu ZhouFan LeileiLiu JunweiJin XinZhou Tingwen - Metastatic colon cancer remains a significant clinical challenge, often associated with poor patient prognosis. Recent studies have identified the secreted frizzled-related protein 2 (SFRP2) as a key player in this malignancy, showing its overexpression in metastatic cases. This research aimed to elucidate the molecular mechanisms by which SFRP2 influences colon cancer progression. We employed in vitro assays to assess the effects of SFRP2 on cell migration and invasion, revealing that SFRP2 significantly enhances these processes without affecting cell proliferation. Mechanistically, we found that SFRP2 interacts with Snai1, a transcription factor known to promote epithelial-mesenchymal transition (EMT), thereby stabilizing Snai1 protein levels. Furthermore, SFRP2 was shown to inhibit Snai1 ubiquitination through the deubiquitinase USP11, leading to increased Snai1 activity. Notably, Snai1 also positively regulates SFRP2 transcription, establishing a feedback loop that amplifies their expression. Our findings indicate that the SFRP2-Snai1 axis promotes colon cancer cell migration and invasion via the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signalling pathway. In vivo experiments further confirmed that the SFRP2-Snai1 interaction significantly enhances metastatic potential. Collectively, these results suggest that targeting the SFRP2-Snai1 signalling pathway may provide a novel therapeutic strategy for metastatic colon cancer. - Source: PubMed
Kuang YanshenLiu XinKe MuChang ZhijieJia BaoqingLi BingQian Honggang