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Last update 08 May 2025

ZBTB11

Last update 08 May 2025

Basic Info

Synonyms

ZBTB11, zinc finger and BTB domain containing 11, Zinc finger and BTB domain-containing protein 11

+ [2]

Introduction

May be involved in transcriptional regulation.

Drugs associated with ZBTB11

JWJ-01306

Target

ZBTB11

Mechanism

ZBTB11 inhibitors

Active Org.

University of California San Diego

Originator Org.

University of California San Diego

Active Indication

Pancreatic Ductal Adenocarcinoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ZBTB11

100 Translational Medicine associated with ZBTB11

0 Patents (Medical) associated with ZBTB11

Literatures (Medical) associated with ZBTB11

01 Sep 2024·Movement Disorders

Biallelic ZBTB11 Variants: A Neurodevelopmental Condition with Progressive Complex Movement Disorders

Article

Author: Strømme, Petter ; Tamim, Abdullah ; Azizimalamiri, Reza ; Hashem, Mais O. ; Veith, Regan ; Alvi, Javeria Raza ; Alkuraya, Fowzan S ; Alabdi, Lama ; Roze, Emmanuel ; Ruedy, Jessica ; Nicita, Francesco ; Galehdari, Hamid ; Ortigoza‐Escobar, Juan Darío ; Dorison, Nathalie ; Sadeghian, Saeid ; Zifarelli, Giovanni ; Houlden, Henry ; Tam, Allison ; Shariati, Gholamreza ; Bauer, Peter ; Ababneh, Faroug ; Bhambhani, Vikas ; Doummar, Diane ; Maroofian, Reza ; Morrow, Michelle M ; Zamani, Mina ; Efthymiou, Stephanie ; Leeuwen, Lisette ; Saberi, Alihossein ; Moreno‐De‐Luca, Andres ; Curry, Cynthia ; Zahraei, Seyed Mohammadsaleh ; Ojea Ponce, Núria ; d'Hardemare, Vincent ; Sultan, Tipu ; Travaglini, Lorena ; Burglen, Lydie

AbstractBackgroundBiallelic ZBTB11 variants have previously been associated with an ultrarare subtype of autosomal recessive intellectual developmental disorder (MRT69).ObjectiveThe aim was to provide insights into the clinical and genetic characteristics of ZBTB11‐related disorders (ZBTB11‐RD), with a particular emphasis on progressive complex movement abnormalities.MethodsThirteen new and 16 previously reported affected individuals, ranging in age from 2 to 50 years, with biallelic ZBTB11 variants underwent clinical and genetic characterization.ResultsAll patients exhibited a range of neurodevelopmental phenotypes with varying severity, encompassing ocular and neurological features. Eleven new patients presented with complex abnormal movements, including ataxia, dystonia, myoclonus, stereotypies, and tremor, and 7 new patients exhibited cataracts. Deep brain stimulation was successful in treating 1 patient with generalized progressive dystonia. Our analysis revealed 13 novel variants.ConclusionsThis study provides additional insights into the clinical features and spectrum of ZBTB11‐RD, highlighting the progressive nature of movement abnormalities in the background of neurodevelopmental phenotype.

14 Nov 2023·Blood Advances

Late fetal hematopoietic failure results from ZBTB11 deficiency despite abundant HSC specification

Article

Author: Amann-Zalcenstein, Daniela ; Keightley, M Cristina ; Lieschke, Graham J ; Cao, Benjamin ; Cao, Huimin ; Naik, Shalin H ; Nilsson, Susan K ; Salim, Agus ; Hickey, Peter

AbstractHematopoiesis produces diverse blood cell lineages to meet the basal needs and sudden demands of injury or infection. A rapid response to such challenges requires the expansion of specific lineages and a prompt return to balanced steady-state levels, necessitating tightly coordinated regulation. Previously we identified a requirement for the zinc finger and broad complex, tramtrak, bric-a-brac domain–containing 11 (ZBTB11) transcription factor in definitive hematopoiesis using a forward genetic screen for zebrafish myeloid mutants. To understand its relevance to mammalian systems, we extended these studies to mice. When Zbtb11 was deleted in the hematopoietic compartment, embryos died at embryonic day (E) 18.5 with hematopoietic failure. Zbtb11 hematopoietic knockout (Zbtb11hKO) hematopoietic stem cells (HSCs) were overabundantly specified from E14.5 to E17.5 compared with those in controls. Overspecification was accompanied by loss of stemness, inability to differentiate into committed progenitors and mature lineages in the fetal liver, failure to seed fetal bone marrow, and total hematopoietic failure. The Zbtb11hKO HSCs did not proliferate in vitro and were constrained in cell cycle progression, demonstrating the cell-intrinsic role of Zbtb11 in proliferation and cell cycle regulation in mammalian HSCs. Single-cell RNA sequencing analysis identified that Zbtb11-deficient HSCs were underrepresented in an erythroid-primed subpopulation and showed downregulation of oxidative phosphorylation pathways and dysregulation of genes associated with the hematopoietic niche. We identified a cell-intrinsic requirement for Zbtb11-mediated gene regulatory networks in sustaining a pool of maturation-capable HSCs and progenitor cells.

31 Mar 2023·Cardiovascular ResearchQ1 · MEDICINE

Spatial transcriptomics unveils ZBTB11 as a regulator of cardiomyocyte degeneration in arrhythmogenic cardiomyopathy

Q1 · MEDICINE

Article

Author: van Rooij, Eva ; de Jonge, Nicolaas ; Junker, Jan Philipp ; Vink, Aryan ; Versteeg, Danielle ; Perini, Ilaria ; van Oudenaarden, Alexander ; van Kampen, Sebastiaan J ; de Ruiter, Hesther ; Brodehl, Andreas ; van der Kraak, Petra ; Vértesy, Ábel ; Boogerd, Cornelis J ; Lacraz, Grégory P A ; Giacca, Mauro

AbstractAimsArrhythmogenic cardiomyopathy (ACM) is an inherited cardiac disorder that is characterized by progressive loss of myocardium that is replaced by fibro-fatty cells, arrhythmias, and sudden cardiac death. While myocardial degeneration and fibro-fatty replacement occur in specific locations, the underlying molecular changes remain poorly characterized. Here, we aim to delineate local changes in gene expression to identify new genes and pathways that are relevant for specific remodelling processes occurring during ACM.Methods and resultsUsing Tomo-Seq, genome-wide transcriptional profiling with high spatial resolution, we created transmural epicardial-to-endocardial gene expression atlases of explanted ACM hearts to gain molecular insights into disease-driving processes. This enabled us to link gene expression profiles to the different regional remodelling responses and allowed us to identify genes that are potentially relevant for disease progression. In doing so, we identified distinct gene expression profiles marking regions of cardiomyocyte degeneration and fibro-fatty remodelling and revealed Zinc finger and BTB domain-containing protein 11 (ZBTB11) to be specifically enriched at sites of active fibro-fatty replacement of myocardium. Immunohistochemistry indicated ZBTB11 to be induced in cardiomyocytes flanking fibro-fatty areas, which could be confirmed in multiple cardiomyopathy patients. Forced overexpression of ZBTB11 induced autophagy and cell death-related gene programmes in human cardiomyocytes, leading to increased apoptosis.ConclusionOur study shows the power of Tomo-Seq to unveil new molecular mechanisms in human cardiomyopathy and uncovers ZBTB11 as a novel driver of cardiomyocyte loss.

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