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

Complementation of defective colony-stimulating factor 1 receptor signaling and mitogenesis by Raf and v-Src.

Molecular and cellular biology - 1 Feb 1999

Aziz N, Cherwinski H, McMahon M

Abstract excerpt

Ras-activated signal transduction pathways are implicated in the control of cell proliferation, differentiation, apoptosis, and tumorigenesis, but the molecular mechanisms mediating these diverse functions have yet to be fully elucidated. Conditionally active forms of Raf, v-Src, and MEK1 were used to identify changes in gene expression that participate in oncogenic transformation, as well as in normal growth...

Read the complete abstract on PubMed

Topics

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

Share to 3T3 Cells
Share to Cell Division
Share to Enzyme Activation

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

Share to Gene Expression Regulation

Share to Genetic Complementation Test

Share to Mutation

Share to Protein Serine-Threonine Kinases

Source

Open in PubMed Open full text

Identifiers

PMID: 9891045
DOI: 10.1128/MCB.19.2.1101
PMCID: PMC116040

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

Complementation of defective colony-stimulating factor 1 receptor signaling and mitogenesis by Raf and v-Src.PMID 9891045Read ↗

Transactivation of c-fos and beta-actin genes by raf as a step in early response to transmembrane signals.Semantic proximity Read ↗

Transcriptional and translational control of ornithine decarboxylase during Ras transformation.Semantic proximity Read ↗

Serum-, TPA-, and Ras-induced expression from Ap-1/Ets-driven promoters requires Raf-1 kinase.Semantic proximity Read ↗

Transformation by Raf and other oncogenes renders cells differentially sensitive to growth inhibition by a dominant negative c-jun mutant.Semantic proximity Read ↗

Induction of cell cycle progression and acceleration of apoptosis are two separable functions of c-Myc: transrepression correlates with acceleration of apoptosis.Semantic proximity Read ↗

Complementation of growth factor receptor-dependent mitogenic signaling by a truncated type I phosphatidylinositol 4-phosphate 5-kinase.Semantic proximity Read ↗

Constitutive modulation of Raf-1 protein kinase is associated with differential gene expression of several known and unknown genes.Semantic proximity Read ↗

Myc rescue of a mutant CSF-1 receptor impaired in mitogenic signalling.Semantic proximity Read ↗

Activation of c-fos gene expression by a kinase-deficient epidermal growth factor receptor.Semantic proximity Read ↗

Reversible regulation of the transformed phenotype of ornithine decarboxylase- and ras-overexpressing cells by dominant-negative mutants of c-Jun.Semantic proximity Read ↗

Stimulation of B-Raf increases c-Jun and c-Fos expression and upregulates AP-1-regulated gene transcription in insulinoma cells.Semantic proximity Read ↗

Oncogenic Met receptor induces cell-cycle progression in Xenopus oocytes independent of direct Grb2 and Shc binding or Mos synthesis, but requires phosphatidylinositol 3-kinase and Raf signaling.Semantic proximity Read ↗

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