ZBTB7A antibody - N-terminal region (ARP37762_P050)
- Known as:
- ZBTB7A (anti-) - N-terminal region (ARP37762_P050)
- Catalog number:
- arp37762_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZBTB7A antibody - N-terminal region (ARP37762_P050)
Related genes to: ZBTB7A antibody - N-terminal region (ARP37762_P050)
- Gene:
- ZBTB7A NIH gene
- Name:
- zinc finger and BTB domain containing 7A
- Previous symbol:
- ZBTB7
- Synonyms:
- FBI-1, LRF, DKFZp547O146, pokemon, ZNF857A
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-16
- Date modifiied:
- 2014-11-19
Related products to: ZBTB7A antibody - N-terminal region (ARP37762_P050)
Related articles to: ZBTB7A antibody - N-terminal region (ARP37762_P050)
- [This retracts the article DOI: 10.2147/CMAR.S257419.]. - Source: PubMed
Publication date: 2026/05/13
- COUP-TFII encoded by the gene, is an orphan nuclear receptor highly expressed during embryonic development in several tissues. In erythropoiesis, COUP-TFII is active in yolk sac-derived cells prior to the switch to adult globin expression. Its broad expression pattern suggests a complex transcriptional regulation involving multiple, yet poorly defined, regulatory elements. Using integrative and chromatin accessibility analyses, here we identified an erythroid-specific enhancer located 52Kb upstream of the transcription start site. This element shows epigenetic features of an active enhancer in K562 erythroid cells. Notably, in subclones derived from adult HUDEP2 erythroid progenitor cells that spontaneously re-express fetal gamma globin, is reactivated, concomitantly with the opening of the -52Kb enhancer. We also identify the transcription factor ZBTB7A as a repressor of , as knock-out of in HUDEP2 cells restores expression and active chromatin marks at the -52Kb region Our findings uncover a novel distal enhancer controlling expression in erythroid cells. - Source: PubMed
Publication date: 2026/04/01
Pastori ValentinaLabedz AgataSimanovich Maria AFabiano MartinaFrigo CarlottaVerheul ThijsProietti LudovicaGrebien FlorianCitterio ElisabettaPhilipsen SjaakRonchi Antonella Ellena - Ovarian cancer (OV) remains the most lethal gynecological malignancy, owing to late‑stage diagnosis, high metastatic potential and limited therapeutic efficacy. Although the transcription factor zinc finger and BTB domain‑containing 7A (ZBTB7A) has been implicated in several types of cancer, its role in OV has not yet been systematically characterized. The present study comprehensively investigated the expression pattern, prognostic relevance, functional role and downstream mechanisms of ZBTB7A in OV progression. Multi‑cohort transcriptomic analyses across independent public datasets revealed consistent upregulation of ZBTB7A in OV tissues, and high expression predicted a significantly poor prognosis. Single‑cell RNA sequencing demonstrated that ZBTB7A‑high tumor cells were enriched in proliferative, migratory and epithelial‑mesenchymal transition‑related programs, accompanied by activation of oncogenic pathways such as Wnt/β‑catenin and Hippo‑YAP. Functional assays using overexpression and RNA interference demonstrated that ZBTB7A enhanced malignant phenotypes, including increased cell proliferation, DNA synthesis, clonogenic survival and migration. Further analyses identified cytokine receptor‑like factor 1 (CRLF1) as a key downstream effector of ZBTB7A. ZBTB7A overexpression elevated CRLF1 transcription, whereas CRLF1 knockdown abrogated ZBTB7A‑induced proliferation and migration, defining a functional ZBTB7A/CRLF1 oncogenic axis. Collectively, these findings establish ZBTB7A as an important transcriptional driver of OV aggressiveness and highlight the ZBTB7A/CRLF1 regulatory pathway as a potential prognostic biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/03/27
Hao XiaobaiChen Yu - Fetal hemoglobin (HbF) plays a central role in mitigating the pathophysiological effects of sickle cell disease (SCD). Understanding the genetic determinants influencing HbF expression is essential for identifying the factors contributing to its modulation. This review provides an updated synthesis of evidence on HbF modulation, focusing on β haplotypes and their molecular characterization through Sanger sequencing, polymorphisms consistently associated with HbF levels in genome-wide association studies (GWAS), and recent advances in gene editing targeting HbF expression. An integrative review (2016-2025) was conducted using PubMed/MEDLINE, Scopus, and Web of Science, encompassing original research, experimental studies, systematic reviews, and genomic analyses. Key regulatory loci such as BCL11A, HBS1L-MYB (HMIP), and the HBB cluster explain a significant proportion of HbF variability across populations. Furthermore, additional variants in KLF1, NFIX, BACH2, and ZBTB7A have emerged as potential modulators in specific cohorts. Regarding advances in γ-globin editing, "prime editing", although still in the experimental phase, has recently emerged as an innovative approach capable of introducing multiple HPFH-like mutations within γ-globin promoters, expanding future therapeutic possibilities in SCD. This review also provides a comparative overview of prime editing and other gene-editing strategies for HbF modulation, such as CRISPR-Cas9 and Base editing. Collectively, this work outlines the current landscape of HbF modulation and provides an informative basis for future research aimed at advancing precision-oriented therapeutic strategies in sickle cell disease. - Source: PubMed
Publication date: 2026/01/27
Márquez-Benitez YusselfyOsorio-Garzón Valeria IsabelaBernal-Villegas Jaime EduardoBriceño-Balcázar Ignacio - Inactivation of tumor suppressor genes (TSGs) imparts a cellular fitness in cancers, including in acute myeloid leukemia (AML). The detection of silenced TSGs without direct mutations presents challenges in designing targeted cancer treatments, yet it also opens a therapeutic opportunity to restore their function. In this study, we identified the transcriptional repressor as a TSG that is down-regulated in samples from patients with AML and is associated with poor survival outcomes. Loss of ZBTB7A amplifies TNF signaling, driving a dysfunctional inflammatory state that accelerates AML progression in vivo. Mechanistically, the mRNA decay factor ZFP36L2 binds to the 3' untranslated region (3'UTR) of , promoting its transcript degradation in human AML cells. To identify therapeutic targets, we developed a CRISPR-based screening approach coupled with fluorescence in situ hybridization and flow cytometry (FISH-Flow), pinpointing the KDM4 family of histone demethylases as a vulnerability to restore ZBTB7A function. Pharmacologic inhibition of KDM4 up-regulated ZBTB7A expression, promoted terminal differentiation in patient-derived xenograft models, and demonstrated broad antileukemic efficacy across AML subtypes as well as preserved normal hematopoiesis. These findings reveal regulatory mechanisms of ZBTB7A and support epigenetic therapy as a promising strategy to reactivate its tumor suppressor function in hematologic cancers. - Source: PubMed
Publication date: 2026/02/25
Arnuk AlexanderHan CuijuanLawal Abimbola EWang BofeiKarma SadikZhang ZhipingYassouf Mhd YousufRajendran Sakthi HariniChandok HarshpreetEller Madeline LSajedi SogandMcKenna MerylHerman EveHagen LouisaNadorp BettinaMo ZengshuoOrellana HectorTsirigos AristotelisMiura PedroAbbas Hussein AAifantis IannisWang Eric