Ask about this productRelated genes to: USP16 antibody
- Gene:
- USP16 NIH gene
- Name:
- ubiquitin specific peptidase 16
- Previous symbol:
- -
- Synonyms:
- Ubp-M
- Chromosome:
- 21q21
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-09
- Date modifiied:
- 2015-08-26
- Gene:
- USP21 NIH gene
- Name:
- ubiquitin specific peptidase 21
- Previous symbol:
- USP23
- Synonyms:
- USP16
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-08
- Date modifiied:
- 2016-10-05
Related products to: USP16 antibody
Related articles to: USP16 antibody
- Polycomb group proteins (PcGs) add repressive post translational histone modifications such as H2AK119ub1, and histone H2A deubiquitinases remove it. Mice lacking histone H2A deubiquitinases such as Usp16 and Bap1 die in embryonic stage, while mice lacking Usp3, Mysm1, Usp12, and Usp21 have been shown to be deficient in hematopoietic lineage differentiation, cell cycle regulation, and DNA repair. Thus, it is likely that histone deubiquitinases may also be required for human endothelial cell differentiation; however, there are no reports about the role of histone H2A deubiquitinase BAP1 in human endothelial cell development. We differentiated human pluripotent stem cells into the endothelial lineage which expressed stable inducible shRNA against BAP1. Our results show that BAP1 is required for human endothelial cell differentiation. - Source: PubMed
Publication date: 2024/07/08
Shastry ShrutiSamal DharitreePethe Prasad - Activating mutations in KRAS (KRAS*) are present in nearly all pancreatic ductal adenocarcinoma (PDAC) cases and critical for tumor maintenance. By using an inducible KRAS* PDAC mouse model, we identified a deubiquitinase USP21-driven resistance mechanism to anti-KRAS* therapy. USP21 promotes KRAS*-independent tumor growth via its regulation of MARK3-induced macropinocytosis, which serves to maintain intracellular amino acid levels for anabolic growth. The USP21-mediated KRAS* bypass, coupled with the frequent amplification of USP21 in human PDAC tumors, encourages the assessment of USP21 as a novel drug target as well as a potential parameter that may affect responsiveness to emergent anti-KRAS* therapy. - Source: PubMed
Publication date: 2021/09/16
Hou PingpingMa XingdiYang ZechengZhang QiangWu Chang-JiunLi JunTan LinYao WantongYan LiangZhou XinKimmelman Alec CLorenzi Philip LZhang JianhuaJiang ShanSpring DeniseWang Y AlanDePinho Ronald A - Skeletal muscle as a metabolic consumer determines systemic energy homeostasis by regulating myofibre type conversion and muscle mass control. Perturbation of the skeletal muscle metabolism elevates the risk of a variety of diseases including metabolic disorders. However, the regulatory pathways and molecules are not completely understood. The discovery of relevant responsible molecules and the associated network could be an attractive strategy to overcome diseases associated with muscle problems. - Source: PubMed
Publication date: 2021/09/15
Kim AyoungKoo Ja HyunJin XingKim WondongPark Shi-YoungPark SunghyoukRhee Eugene PChoi Cheol SooKim Sang Geon - The E3 deubiquitinating enzyme ubiquitin-specific proteolytic enzyme 21 (USP21) plays vital roles in physiological activities and is required for Treg-cell-mediated immune tolerance. Using a murine model infected with , we observed that there were more cercariae developed into adults and more eggs deposited in the livers of the USP21FOXP3 (KO) mice. However, immunohistochemistry showed that the degree of egg granuloma formation and liver fibrosis was reduced. In USP21FOXP3 mice, levels of IFN-gamma, IL-4, anti-soluble egg antigen (SEA) IgG and anti-soluble worm antigen preparation (SWAP) IgG increased in blood, as determined using ELISAs and multiplex fluorescent microsphere immunoassays, while the levels of IL-10, lL-17A, IL-23, IL-9, and anti-SEA IgM decreased. In addition, the levels of the USP21 protein and mRNA in the liver and spleen of KO mice decreased. We further observed increased Th1 responses amplified by Tregs (regulatory T cells) and compromised Th17 responses, which alleviated the liver immunopathology. We speculated that these changes were related to polarization of Th1-like Tregs. Our results revealed the roles of USP21 in Treg-cell-mediated regulation of immune interactions between and its host. USP21 may have potential for regulating hepatic fibrosis in patients with schistosomiasis. - Source: PubMed
Publication date: 2021/02/09
Zhang YouxiangXiong De-HuiLi YangyangXu GuinaZhang BaoxinLiu YangZhang ShanHuang QingChen SiminZeng FanshengGuo JingyiLi BinQin ZhiqiangZhang Zuping - The transcription factor FOXM1 contributes to cell cycle progression and is significantly upregulated in basal-like breast cancer (BLBC). Despite its importance in normal and cancer cell cycles, we lack a complete understanding of mechanisms that regulate FOXM1. We identified USP21 in an RNAi-based screen for deubiquitinases that control FOXM1 abundance. USP21 increases the stability of FOXM1, and USP21 binds and deubiquitinates FOXM1 in vivo and in vitro, indicating a direct enzyme-substrate relationship. Depleting USP21 downregulates the FOXM1 transcriptional network and causes a significant delay in cell cycle progression. Significantly, USP21 depletion sensitized BLBC cell lines and mouse xenograft tumors to paclitaxel, an anti-mitotic, frontline therapy in BLBC treatment. USP21 is the most frequently amplified deubiquitinase in BLBC patient tumors, and its amplification co-occurs with the upregulation of FOXM1 protein. Altogether, these data suggest a role for USP21 in the proliferation and potentially treatment of FOXM1-high, USP21-high BLBC. - Source: PubMed
Arceci AnthonyBonacci ThomasWang XianxiStewart KyleDamrauer Jeffrey SHoadley Katherine AEmanuele Michael J