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

Pim-1 expression is sufficient to induce cytokine independence in murine hematopoietic cells, but is dispensable for BCR-ABL-mediated transformation.

Experimental hematology - 1 Jul 2002

Nosaka Tetsuya, Kitamura Toshio

Abstract excerpt

OBJECTIVE: BCR-ABL is a unique oncoprotein of which sole expression can cause cancer. A number of signaling molecules were shown to be activated by BCR-ABL. One of the important molecules that contributes to BCR-ABL-mediated cell proliferation is signal transducer and activator of transcription (STAT) 5. To elucidate the mechanism of BCR-ABL-mediated leukemogenesis, a role of pim-1, one of the important target...

Read the complete abstract on PubMed

Topics

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

Share to Cell Transformation, Neoplastic
Share to Fusion Proteins, bcr-abl

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

Share to Gene Dosage

Share to Hematopoietic Stem Cells

Share to Interleukin-3

Share to Milk Proteins

Share to Protein Isoforms

Share to STAT5 Transcription Factor

Source

Identifiers

PMID: 12135666
DOI: 10.1016/s0301-472x(02)00808-1

Genes

BCR

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

Pim-1 expression is sufficient to induce cytokine independence in murine hematopoietic cells, but is dispensable for BCR-ABL-mediated transformation.PMID 12135666Read ↗

Targeting PIM kinases impairs survival of hematopoietic cells transformed by kinase inhibitor-sensitive and kinase inhibitor-resistant forms of Fms-like tyrosine kinase 3 and BCR/ABL.Semantic proximity Read ↗

The direct Myc target Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomasSemantic proximity Read ↗

Pim-1 is up-regulated by constitutively activated FLT3 and plays a role in FLT3-mediated cell survival.Semantic proximity Read ↗

Abnormal hematopoietic phenotypes in Pim kinase triple knockout mice.Semantic proximity Read ↗

Lymphocyte Transformation by Pim-2 Is Dependent on Nuclear Factor-κB ActivationSemantic proximity Read ↗

Cutting edge: Transcriptional activity of NFATc1 is enhanced by the Pim-1 kinase.Semantic proximity Read ↗

Pim and Akt oncogenes are independent regulators of hematopoietic cell growth and survivalSemantic proximity Read ↗

Genetic Modeling of PIM Proteins in Cancer: Proviral Tagging and Cooperation with Oncogenes, Tumor Suppressor Genes, and CarcinogensSemantic proximity Read ↗

Suppression of interferon (IFN)-inducible genes and IFN-mediated functional responses in BCR-ABL-expressing cells.Semantic proximity Read ↗

The serine/threonine kinase Pim-2 is a transcriptionally regulated apoptotic inhibitor.Semantic proximity Read ↗

STAT5 activation contributes to growth and viability in Bcr/Abl-transformed cells.Semantic proximity Read ↗

Distinct GAB2 signaling pathways are essential for myeloid and lymphoid transformation and leukemogenesis by BCR-ABL1.Semantic proximity Read ↗

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