Zbtb9 antibody - C-terminal region (ARP31669_P050)
- Known as:
- Zbtb9 (anti-) - C-terminal region (ARP31669_P050)
- Catalog number:
- arp31669_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Zbtb9 antibody - C-terminal region (ARP31669_P050)
Related genes to: Zbtb9 antibody - C-terminal region (ARP31669_P050)
- Gene:
- ZBTB9 NIH gene
- Name:
- zinc finger and BTB domain containing 9
- Previous symbol:
- -
- Synonyms:
- MGC23166, ZNF919
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-23
- Date modifiied:
- 2016-10-05
Related products to: Zbtb9 antibody - C-terminal region (ARP31669_P050)
Related articles to: Zbtb9 antibody - C-terminal region (ARP31669_P050)
- Peroxisome proliferator-activated receptor-γ (PPARγ) is a nuclear hormone receptor that is a master regulator of adipocyte differentiation and function. ZBTB9 is a widely expressed but poorly studied transcription factor that was predicted to interact with PPARγ based on large-scale protein-protein interaction experiments. In addition, genome-wide association studies (GWAS) revealed associations between ZBTB9 and BMI, T2D risk, and HbA1c levels. Here we show that Zbtb9 deficiency in mature adipocytes decreased PPARγ activity and protein level, and thus acts as a positive regulator of PPARγ signaling. In contrast, Zbtb9 deficiency in 3T3-L1 and human preadipocytes increased PPARγ levels and enhanced adipogenesis. Transcriptomic and transcription factor binding site analyses of Zbtb9 deficient preadipocytes revealed that the E2F pathway, controlled by the E2F family of transcription factors that are classically associated with cell cycle regulation, was among the most upregulated pathways. E2F1 positively regulates adipogenesis by promoting Pparg expression, independent of its cell cycle role, via direct binding to the Pparg promoter early during adipogenesis. RB phosphorylation (pRB), which regulates E2F activity, was also upregulated in Zbtb9 deficient preadipocytes. Critically, an E2F1 inhibitor blocked the effects of Zbtb9 deficiency on adipogenesis. Collectively, these results demonstrate that Zbtb9 inhibits adipogenesis as a negative regulator of Pparg expression via pRB-E2F signaling. Our findings reveal cell-state dependent roles of ZBTB9 in adipocytes, identifying a new molecule that regulates adipocyte biology as both a positive and negative regulator of PPARγ signaling depending on the cellular context, and thus may be important in the pathogenesis of obesity and T2D. - Source: PubMed
Publication date: 2024/11/13
Xu XuanCharrier AlyssaCongrove SunnyOckunzzi JeremiahBuchner David A - Adipocytes play a critical role in metabolic homeostasis. Peroxisome proliferator-activated receptor- (PPAR ) is a nuclear hormone receptor that is a master regulator of adipocyte differentiation and function. ZBTB9 was predicted to interact with PPAR based on large-scale protein interaction experiments. In addition, GWAS studies in the type 2 diabetes (T2D) Knowledge Portal revealed associations between Z and both BMI and T2D risk. Here we show that ZBTB9 positively regulates PPAR activity in mature adipocytes. Surprisingly Z knockdown (KD) also increased adipogenesis in 3T3-L1 cells and human preadipocytes. activity was increased and E2F downstream target genes were upregulated in -KD preadipocytes. Accordingly, RB phosphorylation, which regulates E2F activity, was enhanced in -KD preadipocytes. Critically, an E2F1 inhibitor blocked the effects of deficiency on adipogenic gene expression and lipid accumulation. Collectively, these results demonstrate that inhibits adipogenesis as a negative regulator of expression via altered RB-E2F1 signaling. Our findings reveal complex cell-state dependent roles of ZBTB9 in adipocytes, identifying a new molecule that regulates adipogenesis and adipocyte biology as both a positive and negative regulator of PPAR signaling depending on the cellular context, and thus may be important in the pathogenesis and treatment of obesity and T2D. - Source: PubMed
Publication date: 2024/03/06
Xu XuanCharrier AlyssaCongrove SunnyBuchner David A - Zinc finger and bric-a-brac/tramtrack/broad (ZBTB) domain-containing proteins have been reported to be associated with many tumors' development. However, in tumor initiation and progression, the role of ZBTB9, one of the protein family, and its prognostic value were yet to be elucidated in Liver Hepatocellular Carcinoma (LIHC). - Source: PubMed
Publication date: 2022/12/15
Zhang ZhenshanWu LeileiLi JuanChen JiayanYu QiYao HuiXu YapingLiu Liang - Protein-protein interaction (PPI) analysis is a key process to understand protein functions. Recently, we constructed a human protein array (20 K human protein beads array) consisting of 19,712 recombinant human proteins produced by a wheat cell-free protein production system. Here, we developed a cell-free protein array technology for proximity biotinylation-based PPI identification (CF-PPiD). The proximity biotinylation enzyme AirID-fused TP53 and -IκBα proteins each biotinylated specific interacting proteins on a 1536-well magnetic plate. In addition, AirID-fused cereblon was shown to have drug-inducible PPIs using CF-PPiD. Using the human protein beads array with AirID-IκBα, 132 proteins were biotinylated, and then selected clones showed these biological interactions in cells. Although ZBTB9 was not immunoprecipitated, it was highly biotinylated by AirID-IκBα, suggesting that this system detected weak interactions. These results indicated that CF-PPiD is useful for the biochemical identification of directly interacting proteins. - Source: PubMed
Publication date: 2022/06/22
Sugiyama ShuseiYamada KohdaiDenda MiwakoYamanaka SatoshiOzawa SatoshiMorishita RyoSawasaki Tatsuya - To identify potential causative markers involved in the development of early-onset myasthenia gravis (EOMG) in the MHC and non-MHC regions that may interact with the HLA-B*08:01 allele. - Source: PubMed
Publication date: 2017/10/14
Varade JezabelWang NingLim Che KangZhang TaoZhang YuanweiLiu XiaominPiehl FredrikMatell RitvaCao HongzhiXu XunHammarström Lennart