Ask about this productRelated genes to: ZBTB7B antibody
- Gene:
- ZBTB7B NIH gene
- Name:
- zinc finger and BTB domain containing 7B
- Previous symbol:
- ZFP67
- Synonyms:
- ZBTB15, c-Krox, hcKrox, ZNF857B
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-23
- Date modifiied:
- 2016-10-05
Related products to: ZBTB7B antibody
Related articles to: ZBTB7B antibody
- Lung adenocarcinoma, the predominant type of non-small cell lung cancer, is associated with poor survival outcomes due to late-stage diagnosis, resistance to therapy, and lack of effective metabolic-targeted strategies. Increased glycolysis is a hallmark of LUAD progression, yet the upstream transcriptional and post-translational regulators of glycolytic enzymes remain incompletely defined. This study aims to clarify the molecular mechanisms through which transcription factors and ubiquitin ligases coordinate glycolytic activation and tumor progression in LUAD. We identified ZBTB7B as a transcriptional activator of the non-canonical glycolytic enzyme ADPGK. ZBTB7B expression was significantly increased in LUAD tissues and cell lines, associated with poor prognosis, and enhanced proliferation, migration, and glycolytic flux in an ADPGK-dependent manner. Mechanistically, the E3 ubiquitin ligase NEDD4 directly interacted with ZBTB7B, mediating its ubiquitination at K450 and proteasomal degradation, thereby suppressing ADPGK expression and glycolysis. NEDD4 overexpression suppressed LUAD growth both in vitro and in vivo, effects that were reversed by ZBTB7B restoration. Collectively, this work reveals a novel NEDD4/ZBTB7B/ ADPGK axis that integrates transcriptional and post-translational regulation of glycolysis, offering potential therapeutic targets for metabolic intervention in LUAD. - Source: PubMed
Publication date: 2026/03/11
Liu Fang-PengHuang TingYang Hai-YanZha Jian-HuaXu ChuanQiu Cheng-PengWang XingLu ZhuoWang Tao - MHC-I- and MHC-II-selected CD4CD8 precursor thymocytes differentiate into cytotoxic CD8 and helper CD4 lineage T cells, during which suppression of Cd4 and Thpok genes by Runx-dependent-silencers in those genes is crucial to segregate the two lineages. However, how TCR signals are linked to cytotoxic-lineage-specific Cd4-Thpok silencing remains unclear. Here we show that the terminal Y residue within the evolutionarily conserved C-terminal WRPY motif in Runx1, which is essential for interacting with TLE co-repressor proteins, was phosphorylated more in CD4CD8 thymocytes than in CD4CD8 thymocytes, inducing an interaction with TLE co-repressors for cytotoxic-lineage specific Cd4-Thpok silencing. Non-receptor tyrosine kinases Lck and Zap70 interacted with Runx in the cytoplasm more in MHC-I-signaled CD4CD8 thymocytes than in CD4CD8 thymocytes. Collectively, these findings reveal that differential phosphorylation states at the terminal tyrosine residue in Runx connect MHC restriction with the helper versus cytotoxic T cell lineage choice. - Source: PubMed
Publication date: 2026/02/19
Ogawa ChihiroOkuyama KazukiKojo SatoshiNishino KoheiMachiyama HiroakiPadhi Aditya KTakahashi HirotakaEbihara TakashiTenno MariZhizhen QinMuroi SawakoIto KoseiSawasaki TatsuyaZhang Kam Y JXue Hai-HuiYokosuka TadashiKosako HidetakaTaniuchi Ichiro - During development, blood generation begins in the yolk sac with the differentiation of haemato-endothelial mesoderm forming haematopoietic progenitors. This study aims to identify the crucial molecular regulators of haemato-endothelial mesoderm formation and to extend our knowledge of the process in an unbiased way. We employ a murine embryonic stem cell model that recapitulates embryonic blood development, and perform targeted CRISPR-Cas9 knock out screens focusing on transcription factors and chromatin regulators. We identify the transcription factors ETV2, LDB1, SMAD1, SIX4 and ZBTB7b as regulators of haemato-endothelial mesoderm commitment. Embryonic stem cells lacking these regulators give rise to mesodermal subsets with a defined lineage differentiation bias, while transcriptome analysis of these cells uncovers the precise impact of each factor on gene expression in the developing mesoderm. Our study reveals molecular pathways governing mesodermal development crucial to allow endothelial and haematopoietic lineage specification and paves the way for future advances in haematopoietic stem cell applications. - Source: PubMed
Publication date: 2025/12/13
Teske MichaelWertheimer TobiasButz StefanZwicky PascaleMallona IzaskunNopper Svenja LMünz ChristianElling UlrichLancrin ChristopheBecher BurkhardGrosso Ana RitaBaubec TuncaySchmolka Nina - Though ZBTB7B is overexpressed in breast and prostate cancers and dysregulates CD8 T cell response, there is no report on the close relationship between ZBTB7B and androgen receptor (AR) yet. This study aimed to investigate the molecular interaction between ZBTB7B and AR and to determine its role in prostate cancer progression. - Source: PubMed
Publication date: 2025/11/26
Im EunjiPark Su-YeonSim Deok-YongCho Ah ReumKil Bum JuKim BongleeShim Bum-SangKim Sung-Hoon - The transcription factor ZBTB7B has been identified as a potential tumor suppressor through a CRISPR-Cas9-based functional screen of tumor-associated genes, as overexpression of ZBTB7B could significantly suppress tumor growth in the models of breast cancer brain metastasis, which prompted our further exploration of its inhibitory role in glioma. To elucidate the underlying mechanisms of this suppressive effect, lentiviral-mediated ZBTB7B overexpression was established in U118 and GL261 glioma cell lines, and systematic evaluation of tumorigenic capacity was performed through in vitro and xenograft assays. The results showed that ZBTB7B transcriptionally activated GPR17 expression, which suppressed protein kinase A phosphorylation, amplified mitochondrial reactive oxygen species generation, and triggered Caspase3-dependent apoptosis. Meanwhile, ZBTB7B upregulated CXCL10 secretion, which markedly enhanced CD4+ and CD8+ T cell accumulation. Clinical validation through multiplex immunofluorescence staining on a tissue microarray of 129 glioma samples revealed a progressive loss of ZBTB7B protein expression across WHO grades II to IV, inversely correlating with tumor malignancy. These findings demonstrate ZBTB7B as a dual-function tumor suppressor that concurrently induces intrinsic apoptosis and remodels the tumor immune microenvironment in glioma toward a 'hot' phenotype. Therefore, we propose ZBTB7B reactivation as a novel therapeutic strategy for glioma. - Source: PubMed
Zhang LinmeiZhang HaozheWang ChenxiJiang AoxinZhao FeiYang SifanLei HongYu XuelanRen JuanTang ChengfangWang XiaofeiChen Yanke