ZBTB26 antibody - N - terminal region (OAAB13826)
- Known as:
- ZBTB26 (anti-) - N - terminal region (OAAB13826)
- Catalog number:
- oaab13826
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZBTB26 antibody - terminal region (OAAB13826)
Related genes to: ZBTB26 antibody - N - terminal region (OAAB13826)
- Gene:
- ZBTB26 NIH gene
- Name:
- zinc finger and BTB domain containing 26
- Previous symbol:
- ZNF481
- Synonyms:
- -
- Chromosome:
- 9q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-14
- Date modifiied:
- 2016-10-05
Related products to: ZBTB26 antibody - N - terminal region (OAAB13826)
Related articles to: ZBTB26 antibody - N - terminal region (OAAB13826)
- The Integrator complex is primarily known to attenuate transcription by inducing premature termination of paused RNA polymerase II (RNAPII) and restraining pause release through its endonuclease and phosphatase activities. However, the mechanisms that govern Integrator recruitment to chromatin and direct gene-specific transcriptional programs in response to external stimuli and diverse biological contexts remain poorly understood. In particular, the regulatory functions of the Integrator auxiliary or arm module (INTS10/13/14/15) are the least characterized. Here, we identify ZBTB26 as an interactor of the Integrator auxiliary module via INTS10 and INTS13, demonstrate its ability to directly bind a specific DNA motif, and show that it co-occupies select promoters and enhancers with Integrator and active histone markers across the genome. We demonstrate that ZBTB26 is required for the recruitment of Integrator to its target loci, including genes involved in stimulus response, development, and differentiation. Importantly, the ZBTB26-Integrator axis sustains the active state of specific promoters and enhancers and drives defined gene transcriptional programs. Our findings reveal a transcription factor-like mechanism of targeted gene regulation mediated by ZBTB26-Integrator binding, extending the functional paradigm of Integrator beyond its canonical catalytic roles. - Source: PubMed
Yu DingdangChen GuoyuLin FolanCheng XinQiao ZijunZhu PingHu Shibin - Genome-wide association studies (GWAS) have identified over 60 susceptibility loci for lung cancer, yet the biological mechanisms underlying these associations remain largely unknown, particularly for lung squamous cell carcinoma (LUSC). Here, we integrated data from 3890 LUSC cases and 13 328 controls of Chinese descent, and performed a conditional analysis to explore independent genetic variants and analyzed the interaction between the genetic variants and smoking. Our study was the first to identify a specific association between genetic variants in the 9q33.2 region and increased risk of LUSC in smokers. After adjusting for the tag SNP rs4573350 in 9q33.2, no additional significant genetic variants were found. However, significant additive (RERI = 1.66, 95% CI: 1.17-2.22, AP = 0.26, 95% CI: 0.19-0.33) and multiple interactions (OR = 1.30, 95% CI: 1.08-1.56, P = 5.40 × 10-3) were observed between rs4573350 and smoking. Compared to nonsmokers with the CC genotype, smokers with the CT/TT genotype showed an increased risk of 6.29-fold (95% CI: 5.46-7.23, P = 2.00 × 10-16). Functional annotation identified rs4573350 as the strongest functional variant within the linkage disequilibrium block. Biological experiments confirmed that the combined exposure to the T allele of rs4573350 and cigarette smoke extract promotes the expression of the ZBTB26 by modulating the binding ability of the transcription factor FOXA1. Furthermore, ZBTB26 was found to regulate tumorigenesis of LUSC both in vitro and in vivo by affecting the expression of PCNA, which is involved in cell cycle and promotes tumorigenesis of LUSC. - Source: PubMed
Ma HuiminWang GuoqingMiao SunanJin ChenCai JiayingGe WenjingZhang ChangZhang ErbaoMa HongxiaZhu Meng - Emerging literature links the role of the renin-angiotensin-aldosterone system (RAAS) to the progression of cancers. However, the function of RAAS has not been verified in Clear-cell renal cell carcinoma (ccRCC). - Source: PubMed
Publication date: 2024/12/19
Yin LeiMao LixinYin RuiLv ChengxunShi XiaokaiYue ChuangChen YinLu ChaoWu ZonglinXu KaiCao Wei - The formation of dynamic protein filaments contributes to various biological functions by clustering individual molecules together and enhancing their binding to ligands. We report such a propensity for the BTB domains of certain proteins from the ZBTB family, a large eukaryotic transcription factor family implicated in differentiation and cancer. Working with Xenopus laevis and human proteins, we solved the crystal structures of filaments formed by dimers of the BTB domains of ZBTB8A and ZBTB18 and demonstrated concentration-dependent higher-order assemblies of these dimers in solution. In cells, the BTB-domain filamentation supports clustering of full-length human ZBTB8A and ZBTB18 into dynamic nuclear foci and contributes to the ZBTB18-mediated repression of a reporter gene. The BTB domains of up to 21 human ZBTB family members and two related proteins, NACC1 and NACC2, are predicted to behave in a similar manner. Our results suggest that filamentation is a more common feature of transcription factors than is currently appreciated. - Source: PubMed
Mance LucijaBigot NicolasZhamungui Sánchez EdisonCoste FranckMartín-González NataliaZentout SihamBiliškov MarinPukało ZofiaMishra AanchalChapuis CatherineArteni Ana-AndreeaLateur AxelleGoffinont StéphaneGaudon VirginieTalhaoui IbtissamCasuso IgnacioBeaufour MartineGarnier NorbertArtzner FranckCadene MartineHuet SébastienCastaing BertrandSuskiewicz Marcin Józef - Congenital primary hypothyroidism (CH; OMIM 218700) is characterized by an impaired thyroid development, or dyshormonogenesis, and can lead to intellectual disability and growth retardation if untreated. Most of the children with congenital hypothyroidism present thyroid dysgenesis, a developmental anomaly of the thyroid. Various genes have been associated with thyroid dysgenesis, but all known genes together can only explain a small number of cases. To identify novel genetic causes for congenital hypothyroidism, we performed trio whole-exome sequencing in an affected newborn and his unaffected parents. A predicted damaging de novo missense mutation was identified in the gene (Zinc Finger A and BTB Domain containing 26). An additional cohort screening of 156 individuals with congenital thyroid dysgenesis identified two additional gene variants of unknown significance. To study the underlying disease mechanism, morpholino knock-down of in was carried out, which demonstrated significantly smaller thyroid anlagen in knock-down animals at tadpole stage. Marker genes expressed in thyroid tissue precursors also indicated a specific reduction in the ortholog of human Paired-Box-Protein PAX8, a transcription factor required for thyroid development, which could be rescued by adding zbtb26. Pathway and network analysis indicated network links of to and other genes involved in thyroid genesis and function. GWAS associations of ZBTB26 were found with height. Together, our study added a novel genetic risk factor to the list of genes underlying congenital primary hypothyroidism and provides additional support that de novo mutations, together with inherited variants, might contribute to the genetic susceptibility to CH. - Source: PubMed
Publication date: 2021/11/24
Vick PhilippEberle BirgitChoukair DanielaWeiss BirgitRoeth RalphSchneider IsabelleParamasivam NagarajanBettendorf MarkusRappold Gudrun A