Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Tumor suppressor ASXL1 is essential for the activation of INK4B expression in response to oncogene activity and anti-proliferative signals.

Cell research - 1 Nov 2015

Wu Xudong, Bekker-Jensen Ida Holst, Christensen Jesper, Rasmussen Kasper Dindler, Sidoli Simone, Qi Yan, Kong Yu, Wang Xi, Cui Yajuan, Xiao Zhijian, Xu Guogang, Williams Kristine, Rappsilber Juri, Sønderby Casper Kaae, Winther Ole, Jensen Ole N, Helin Kristian

Abstract excerpt

ASXL1 mutations are frequently found in hematological tumors, and loss of Asxl1 promotes myeloid transformation in mice. Here we present data supporting a role for an ASXL1-BAP1 complex in the deubiquitylation of mono-ubiquitylated lysine 119 on Histone H2A (H2AK119ub1) in vivo. The Polycomb group proteins control the expression of the INK4B-ARF-INK4A locus during normal development, in part through catalyzing...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Proliferation
Share to Cyclin-Dependent Kinase Inhibitor p15

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Histones

Share to Polycomb-Group Proteins

Share to Repressor Proteins

Share to Tumor Suppressor Proteins

Share to Ubiquitin-Specific Proteases

Share to Ubiquitin Thiolesterase

Source

Open in PubMed Open full text

Identifiers

PMID: 26470845
DOI: 10.1038/cr.2015.121
PMCID: PMC4650424

Genes

ASXL1
BAP1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Tumor suppressor ASXL1 is essential for the activation of INK4B expression in response to oncogene activity and anti-proliferative signals.PMID 26470845Read ↗

Mutant ASXL1 cooperates with BAP1 to promote myeloid leukaemogenesis.Semantic proximity Read ↗

The BAP1/ASXL2 Histone H2A Deubiquitinase Complex Regulates Cell Proliferation and Is Disrupted in CancerSemantic proximity Read ↗

Cancer-associated ASXL1 mutations may act as gain-of-function mutations of the ASXL1-BAP1 complex.Semantic proximity Read ↗

Reducing hyperactivated BAP1 attenuates mutant ASXL1-driven myeloid malignancies in human haematopoietic cells.Semantic proximity Read ↗

Tumor-derived neomorphic mutations in ASXL1 impairs the BAP1-ASXL1-FOXK1/K2 transcription network.Semantic proximity Read ↗

Structural basis of histone H2A lysine 119 deubiquitination by Polycomb Repressive Deubiquitinase BAP1/ASXL1Semantic proximity Read ↗

Modeling ASXL1 mutation revealed impaired hematopoiesis caused by derepression of p16Ink4a through aberrant PRC1-mediated histone modification.Semantic proximity Read ↗

Histone H2AK119 Mono-Ubiquitination is Essential for Polycomb-Mediated Transcriptional RepressionSemantic proximity Read ↗

Human ASXL1-Mutant Hematopoiesis Is Driven by a Truncated Protein Associated with Aberrant Deubiquitination of H2AK119.Semantic proximity Read ↗

Chromatin regulator Asxl1 loss and Nf1 haploinsufficiency cooperate to accelerate myeloid malignancySemantic proximity Read ↗

Loss of the Tumor Suppressor BAP1 Causes Myeloid TransformationSemantic proximity Read ↗

Molecular Regulation of the Polycomb Repressive-Deubiquitinase.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.