USP11 polyclonal antibody (A01)
- Known as:
- USP11 pab (anti-) (A01)
- Catalog number:
- H00008237-A01
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- USP11 polyclonal antibody (A01)
Related genes to: USP11 polyclonal antibody (A01)
- Gene:
- ABRAXAS2 NIH gene
- Name:
- abraxas 2, BRISC complex subunit
- Previous symbol:
- KIAA0157, FAM175B
- Synonyms:
- Em:AC068896.4, ABRO1
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-16
- Date modifiied:
- 2017-04-27
- Gene:
- AKR1C3 NIH gene
- Name:
- aldo-keto reductase family 1 member C3
- Previous symbol:
- HSD17B5
- Synonyms:
- KIAA0119, DDX, HAKRB, PGFS
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-29
- Date modifiied:
- 2016-10-05
- Gene:
- ARHGAP4 NIH gene
- Name:
- Rho GTPase activating protein 4
- Previous symbol:
- -
- Synonyms:
- KIAA0131, C1, p115, RhoGAP4, SrGAP4
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-28
- Date modifiied:
- 2015-09-11
- Gene:
- ARHGEF7 NIH gene
- Name:
- Rho guanine nucleotide exchange factor 7
- Previous symbol:
- -
- Synonyms:
- KIAA0142, PIXB, DKFZp761K1021, Nbla10314, DKFZp686C12170, BETA-PIX, COOL1, P85SPR, P85, P85COOL1, P50BP, PAK3, P50
- Chromosome:
- 13q34
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-21
- Date modifiied:
- 2016-10-05
- Gene:
- BCLAF1 NIH gene
- Name:
- BCL2 associated transcription factor 1
- Previous symbol:
- -
- Synonyms:
- KIAA0164, BTF
- Chromosome:
- 6q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-13
- Date modifiied:
- 2017-06-09
Related products to: USP11 polyclonal antibody (A01)
Related articles to: USP11 polyclonal antibody (A01)
- 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 - To explore the regulatory role of SENP1 in ferroptosis of differentiated thyroid cancer cells and its molecular mechanism. - Source: PubMed
Zhu FeifeiYan NaYang JiwenChen XiaoleiWang Yingying