USP11 Pre-design Chimera RNAi
- Known as:
- USP11 Pre-design Chimera RNAi
- Catalog number:
- H00008237-R01
- Product Quantity:
- 10 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- USP11 Pre-design Chimera RNAi
Related genes to: USP11 Pre-design Chimera RNAi
- 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 Pre-design Chimera RNAi
Related articles to: USP11 Pre-design Chimera RNAi
- 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 - Pathological cardiac hypertrophy is a key precursor to heart failure. Protein ubiquitination and deubiquitination are crucial mechanisms controlling cardiomyocyte signaling homeostasis. USP11, a ubiquitin-specific protease, has been implicated in multiple cellular regulatory processes, but its cardiac function remains unknown. Here, we investigated whether USP11 modulates cardiac hypertrophy and explored its downstream molecular mechanisms. - Source: PubMed
Publication date: 2026/06/18
Wang XijiaZong WenzheZhou DiJi XiaoyangAn XiaogeLiu ZiheKong LingyaoWang YihuanFang YudongGao LuLi YueZheng ZheLiu GangqiongFan Siyuan - To explore the role and mechanism of X-linked USP11 in mitochondrial dysfunction associated with depression. - Source: PubMed
Feng YuqiLi NingyuanZhang LingfengWang WeiDuan HaoSun SiqiLi RuilingZhang YuhuiSong XinhuaZhang YingyueZhang HonghanNie ZhaowenYan HanchunWang ChaoLiu Zhongchun