USP11 Control Peptide antibody /CP
- Known as:
- USP11 Control Peptide (anti-) /CP
- Catalog number:
- 'AP12021CP-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- USP11 Control Peptide antibody /
Related genes to: USP11 Control Peptide antibody /CP
- 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 Control Peptide antibody /CP
Related articles to: USP11 Control Peptide antibody /CP
- Luminal breast cancers account for 70%-80% of total breast cancer cases. More than half of luminal breast cancers either relapse after treatment or lose their luminal features, resulting in poorly differentiated cancers with enhanced invasiveness and metastasis, yet the mechanisms remain largely elusive. In this study, we demonstrated that USP11 suppresses the proliferation and migration of luminal epithelial and tumor cells in vitro, but not basal-like tumor cells. Consistently, USP11 inhibits luminal tumorigenesis and metastasis, but promotes basal-like tumorigenesis in vivo. Mechanistically, USP11 positively regulates GATA3, p27, and ERα in a deubiquitinase activity-dependent manner. USP11 deubiquitinates GATA3, which subsequently binds to and transcriptionally activates CDKN1B (encoding p27). USP11 stimulates CDKN1B and ESR1 (encoding ERα) transcription in a GATA3-dependent manner. GATA3 knockdown reverses the increase in p27 and ERα and the decrease in cell proliferation and migration induced by USP11 overexpression, and p27 knockdown rescues the proliferative inhibition induced by USP11 or GATA3 overexpression in luminal tumorigenesis. USP11 overexpression sensitizes luminal breast cancer cells to tamoxifen treatment. The expression levels of USP11, GATA3, p27, and ERα are positively correlated with each other in human breast tumors and cell lines. We thus identify a novel USP11-GATA3 axis that governs luminal cell fate and restrains luminal cell proliferation and migration during mammary tumor development and metastasis. - Source: PubMed
Publication date: 2026/07/28
Qian TaoLiu XiongBai FengHe QiyueXu YipeiZhang JiayiZhang ShiwenYe ShaolingWang YuchanPeng BinGulnara KapanovaRizaev JasurZhu Wei-GuoXu XingzhiPei Xin-Hai - Emerging evidence has established that renal tubular epithelial cell (TEC) senescence is an essential driver of renal fibrosis, while the activation of p53/p21 pathway plays a key role in initiating TEC senescence. However, the upstream regulatory mechanisms of p53/p21 pathway activation remain unclear, hindering the development of targeted anti-fibrotic therapies for chronic kidney disease (CKD). This study aimed to reveal the upstream regulator of the p53/p21 pathway and investigate its role in renal fibrosis. Here, we report that unilateral ureteral ligation (UUO) and folic acid (FA)-induced fibrotic mouse kidneys exhibited a marked senescent phenotype and activated p53/p21 pathway, accompanied by significant upregulation of ubiquitin-specific protease 11 (USP11). These changes were further verified in angiotensin II (Ang II)-stimulated HK-2 cells. Both Usp11 knockout and pharmacological inhibition with mitoxantrone (MTX) significantly alleviated UUO-induced p53/p21 pathway activation, tubular senescence and renal fibrosis. Mechanistically, USP11 directly interacted with p53 and protected it from ubiquitin-dependent degradation, thereby promoting tubular cell senescence and fibrosis. Furthermore, we identified Krüppel-like factor 4 (KLF4) as the upstream transcription factor that directly bound to the USP11 promoter and enhanced its transcription under pathological conditions. Our findings demonstrate that the KLF4-USP11-p53 axis drives tubular senescence and renal fibrosis, representing a highly promising therapeutic target for CKD. - Source: PubMed
Publication date: 2026/07/14
Wang XinNing MingWang HengminLi JingyaoXie XinXie HongyanLi LuxinSun Xi'angLu LiZhang YitaoZhou LiXu ChenShen QianLu LiminXu Hong - Ubiquitin-specific protease 11 (USP11) is a deubiquitinating enzyme implicated in diverse disease-related signaling pathways, yet well-characterized chemical probes for this target remain limited. Here, we report a structure-activity relationship (SAR) study of a pyrrolo-phenylamidine scaffold as a chemotype for USP11 inhibition. A focused library of analogues was designed and synthesized to define key binding determinants, revealing the pyrrolo-amidine moiety as an essential element, while the terminal phenyl group primarily contributes to hydrophobic stabilization. These SAR trends were supported by molecular docking and molecular dynamics simulations. Representative compounds exhibited low micromolar USP11 inhibitory activity, with a modest preference over the closely related USP15, and reduced TGF-β-induced transcription in a cellular reporter assay at non-cytotoxic concentrations, consistent with their enzymatic potency; higher concentrations were associated with cytotoxicity. Together, these findings identify a promising chemical scaffold for the development of USP11-directed chemical tools and provide a basis for future structure-based optimization. - Source: PubMed
Publication date: 2026/07/07
Kang SoominYoon JihwanHurh SunghoonShin YulimHa JiyoonMin WoongjinKhan Rasel AhmedLee HobinHwang Jong-IkKim Hong-Rae - Intracerebral haemorrhage (ICH) is a subtype of stroke, with resulting long-term disability determined by secondary brain injury. The prevailing biphasic model of neuroinflammation, which conceptualizes a temporal transition from acute to chronic stages, fails to reconcile persistent clinical trial failures or to explain the mechanisms underpinning the progression to chronic neurological deficits. We propose that the core pathology is the failure of acute inflammation to resolve in a timely manner owing to a functional collapse of physiological pro-resolution programmes, governed by dysregulation at critical molecular checkpoints such as the USP11-p53 axis. This failure locks the microenvironment into a destructive, non-resolving state, perpetuating immune-mediated damage. We discuss the evidence for a causal link between this checkpoint failure and the defining chronic sequelae: progressive white matter injury, inhibitory gliosis and large-scale network disconnection. We conceptualize the long-term motor, cognitive and affective impairments as a cohesive clinical entity, which we term post-ICH sequelae. This framework calls for a therapeutic reorientation from broad immunosuppression towards precision pro-resolution strategies such as USP11 inhibitors guided by biomarker-based immune staging. This Perspective provides a theoretical foundation, currently supported predominantly by preclinical evidence, and a translational roadmap for improving long-term recovery after ICH. - Source: PubMed
Publication date: 2026/06/23
Cao LiangZhao WangZhang YanjunPi WenjunYong V WeeXue Mengzhou - An accumulation of evidence underscores the critical importance of both hypoxia and the immune microenvironment in driving the progression of osteosarcoma. Despite advancements in therapeutic strategies, osteosarcoma continues to pose a formidable challenge due to its aggressive nature and high metastatic potential. Nonetheless, the identification of reliable gene signatures that combine information on hypoxia and immune status to predict osteosarcoma prognosis remains an unmet need. - Source: PubMed
Publication date: 2026/06/20
Xie ShangfangYu WenyaoLin RunyeXin Songjian