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

Generation of rac3 null mutant mice: role of Rac3 in Bcr/Abl-caused lymphoblastic leukemia.

Molecular and cellular biology - 1 Jul 2005

Cho Young Jin, Zhang Bin, Kaartinen Vesa, Haataja Leena, de Curtis Ivan, Groffen John, Heisterkamp Nora

Abstract excerpt

Numerous studies indirectly implicate Rac GTPases in cancer. To investigate if Rac3 contributes to normal or malignant cell function, we generated rac3 null mutants through gene targeting. These mice were viable, fertile, and lacked an obvious external phenotype. This shows Rac3 function is dispensable for embryonic development. Bcr/Abl is a deregulated tyrosine kinase that causes chronic myelogenous leukemia and...

Read the complete abstract on PubMed

Topics

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

Share to Lymphoma
Share to Cell Culture Techniques

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Lineage

Share to Gene Expression Regulation, Leukemic

Share to Gene Targeting

Share to Genes, abl

Share to Leukemia, Experimental

Share to rac GTP-Binding Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 15964830
DOI: 10.1128/MCB.25.13.5777-5785.2005
PMCID: PMC1157002

Genes

BCR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Generation of rac3 null mutant mice: role of Rac3 in Bcr/Abl-caused lymphoblastic leukemia.PMID 15964830Read ↗

Vav3 collaborates with p190-BCR-ABL in lymphoid progenitor leukemogenesis, proliferation, and survivalSemantic proximity Read ↗

Rac guanosine triphosphatases represent integrating molecular therapeutic targets for BCR-ABL-induced myeloproliferative disease.Semantic proximity Read ↗

BCR/ABL P190 transgenic mice develop leukemia in the absence of Crkl.Semantic proximity Read ↗

Rac2 GTPase deficiency depletes BCR-ABL+ leukemic stem cells and progenitors in vivoSemantic proximity Read ↗

BCR/ABL-mediated leukemogenesis requires the activity of the small GTP-binding protein Rac.Semantic proximity Read ↗

Crkl enhances leukemogenesis in BCR/ABL P190 transgenic mice.Semantic proximity Read ↗

Association of Bcr-Abl with the Proto-oncogene Vav Is Implicated in Activation of the Rac-1 PathwaySemantic proximity Read ↗

A BCR-ABLp190 Fusion Gene Made by Homologous Recombination Causes B-Cell Acute Lymphoblastic Leukemias in Chimeric Mice With Independence of the Endogenous bcr ProductSemantic proximity Read ↗

G-protein coupled receptor 34 activates Erk and phosphatidylinositol 3-kinase/Akt pathways and functions as alternative pathway to mediate p185Bcr-Abl-induced transformation and leukemogenesis.Semantic proximity Read ↗

Reduced oncogenicity of p190 Bcr/Abl F-actin-binding domain mutants.Semantic proximity Read ↗

Genetic and structural studies of RABL3 reveal an essential role in lymphoid development and function.Semantic proximity Read ↗

Examination of clinically-derived p210 BCR/ABL1 RhoGEF mutations in a murine bone marrow transplantation model of CML.Semantic proximity Read ↗

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