Ask about this productRelated genes to: ZBTB11 antibody
- Gene:
- ZBTB11 NIH gene
- Name:
- zinc finger and BTB domain containing 11
- Previous symbol:
- -
- Synonyms:
- ZNF-U69274, ZNF913
- Chromosome:
- 3q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-15
- Date modifiied:
- 2015-08-26
Related products to: ZBTB11 antibody
Related articles to: ZBTB11 antibody
- The aim of this study was to gain insight into the molecular spectrum of anophthalmia and microphthalmia (A/M) in the Egyptian population. - Source: PubMed
Publication date: 2026/01/20
Elmakkawy GehadNabil AmiraNabil KarimAmin Asmaa KenawyMaskill DavidAli ManirSchorderet DanielBayoumi NaderShakankiri NihalAbdalla Ebtesam - Hepatocellular carcinoma (HCC) is a heterogeneous liver cancer with limited treatment options and a poor prognosis in advanced stages. To identify novel biomarkers and therapeutic targets, we investigated the role of chromosome 1 open reading frame 50 (), a gene with a previously uncharacterized function in HCC. - Source: PubMed
Tanaka AtsushiOtani YusukeMaekawa MasakiRogachevskaya AnnaPeña TirsoChin Vanessa DToyooka ShinichiRoehrl Michael HFujimura Atsushi - PBK/TOPK is a mitotic kinase implicated in haematological and non-haematological cancers. Here we show that the key haemopoietic regulators Ikaros and Aiolos require PBK-mediated phosphorylation to dissociate from chromosomes in mitosis. Eviction of Ikaros is rapidly reversed by addition of the PBK-inhibitor OTS514, revealing dynamic regulation by kinase and phosphatase activities. To identify more PBK targets, we analysed loss of mitotic phosphorylation events in Pbk preB cells and performed proteomic comparisons on isolated mitotic chromosomes. Among a large pool of C2H2-zinc finger targets, PBK is essential for evicting the CCCTC-binding protein CTCF and zinc finger proteins encoded by Ikzf1, Ikzf3, Znf131 and Zbtb11. PBK-deficient cells were able to divide but showed altered chromatin accessibility and nucleosome positioning consistent with CTCF retention. Our studies reveal that PBK controls the dissociation of selected factors from condensing mitotic chromosomes and contributes to their compaction. - Source: PubMed
Publication date: 2025/09/23
Dimond AndrewGim Do HyeonIng-Simmons ElizabethWhilding ChadKramer Holger BDjeghloul DouniaMontoya AlexPatel BhavikCheriyamkunnel SherryBrown Karen EShliaha Pavel VVaquerizas Juan MMerkenschlager MatthiasFisher Amanda G - Rational optimization of molecular glue degraders (MGD) remains a challenging and lengthy process even after identification of a promising scaffold. Unlike proteolysis targeting chimeras (PROTAC), MGDs rely on induced protein-protein interactions as opposed to direct binding in order to target a protein of interest for degradation. Here, we report the synthesis of MGDs targeting the transcription factor ZBTB11 guided by protein complex modeling. Exploration of structure-activity-relationships yielded JWJ-01-306 with improved ZBTB11 degradation activity and potent antiproliferative effects against BRAF inhibitor-resistant melanoma cells. Our findings led to the discovery of a novel MGD that targets a previously undrugged transcription factor with the potential to address acquired resistance to cancer therapy. - Source: PubMed
Publication date: 2025/09/05
Jiang JieweiTran Nathan LSvendsen EmmaWang Eric SFerguson Fleur M - Over 95% of pancreatic ductal adenocarcinomas (PDACs) harbor oncogenic mutations in KRAS. However, upon treatment with KRAS inhibitors, PDAC cells undergo rapid metabolic reprogramming toward an oxidative phosphorylation (OXPHOS)-dependent, drug-resistant state. Here, we demonstrate that this metabolic shift is associated with upregulation of the transcription factor ZBTB11 and both the metabolic state and resistance to KRAS inhibitors can be attenuated by ZBTB11 depletion. We develop molecular glue degraders of ZBTB11 and demonstrate that they reprogram the aberrant transcriptome, proteome, metabolome and bioenergetics of KRAS inhibitor-resistant PDAC, resensitizing them to KRAS inhibition. ZBTB11 degradation leverages cell-type-specific and cell-state-specific differences in gene-regulatory mechanisms controlling OXPHOS pathway transcripts to selectively target the KRAS inhibitor-resistant state in PDAC while sparing neurons derived from human induced pluripotent stem cells. Together, this work establishes ZBTB11 as a druggable vulnerability in KRAS inhibitor-resistant PDAC and provides a suite of molecular glue degrader tool compounds to investigate its function. - Source: PubMed
Publication date: 2025/08/11
Tran Nathan LJiang JieweiMa MinGadbois Gillian EGulay Kevin C MVerano Alyssa LSchiavon Cara RRebollo ElenaZhou HaowenHuang Chun-TengMurad RabiScott David AManor UriBang Anne GTiriac HerveLowy Andrew MWang Eric SFerguson Fleur M