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

Heterozygous deletion of the PU.1 locus in human AML.

Blood - 14 Jan 2010

Bonadies Nicola, Pabst Thomas, Mueller Beatrice U

Abstract excerpt

The transcription factor PU.1 is essential for myeloid development. Targeted disruption of an upstream regulatory element (URE) decreases PU.1 expression by 80% and leads to acute myeloid leukemia (AML) in mice. Here, we sequenced the URE sequences of PU.1 in 120 AML patients. Four polymorphisms (single nucleotide polymorphisms [SNPs]) in the URE were observed, with homozygosity in all SNPs in 37 patients. Among...

Read the complete abstract on PubMed

Topics

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

Share to Gene Expression Regulation, Leukemic
Share to Heterozygote
Share to Leukemia, Myeloid, Acute

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Loss of Heterozygosity

Share to Proto-Oncogene Proteins

Share to Quantitative Trait Loci

Share to Sequence Deletion

Share to Trans-Activators

Source

Identifiers

PMID: 19890096
DOI: 10.1182/blood-2009-03-212225

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.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Heterozygous deletion of the PU.1 locus in human AML.PMID 19890096Read ↗

Heterozygous PU.1 mutations are associated with acute myeloid leukemia.Semantic proximity Read ↗

A distal single nucleotide polymorphism alters long-range regulation of the PU.1 gene in acute myeloid leukemia.Semantic proximity Read ↗

Mutations of the transcription factor PU.1 are not associated with acute lymphoblastic leukaemia.Semantic proximity Read ↗

PU.1 is regulated by NF-kappaB through a novel binding site in a 17 kb upstream enhancer element.Semantic proximity Read ↗

One hundred thirty-four germ line PU.1 variants and the agammaglobulinemic patients carrying themSemantic proximity Read ↗

Identification and functional analysis of acute myeloid leukemia susceptibility associated single nucleotide polymorphisms at non-protein coding regions of RUNX1.Semantic proximity Read ↗

PU.1-Dependent Enhancer Inhibition Separates Tet2 -Deficient Hematopoiesis from Malignant TransformationSemantic proximity Read ↗

Mutations of the PU.1 Ets domain are specifically associated with murine radiation-induced, but not human therapy-related, acute myeloid leukaemia.Semantic proximity Read ↗

Leukemogenesis in heterozygous PU.1 knockout mice.Semantic proximity Read ↗

Pharmacological inhibition of the transcription factor PU.1 in leukemiaSemantic proximity Read ↗

Down-regulation of Notch-1 expression decreases PU.1-mediated myeloid differentiation signaling in acute myeloid leukemia.Semantic proximity Read ↗

The myeloid master regulator transcription factor PU.1 is inactivated by AML1-ETO in t(8;21) myeloid leukemiaSemantic proximity Read ↗

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