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

The Mos/MAP kinase pathway stabilizes c-Fos by phosphorylation and augments its transforming activity in NIH 3T3 cells.

The EMBO journal - 16 Oct 1995

Okazaki K, Sagata N

Abstract excerpt

The c-mos proto-oncogene product, Mos, is a serine/threonine kinase that can activate ERK1 and 2 mitogen-activated protein (MAP) kinases by direct phosphorylation of MAPK/ERK kinase (MEK). ERK activation is essential for oncogenic transformation of NIH 3T3 cells by Mos. In this study, we examined how mitogenic and oncogenic signalling from the Mos/MEK/ERK pathway reaches the nucleus to activate downstream target...

Read the complete abstract on PubMed

Topics

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

Share to Amino Acid Sequence
Share to Cell Transformation, Neoplastic
Share to Cloning, Molecular

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

Share to Molecular Sequence Data

Share to Mutation

Share to Phosphorylation

Share to Recombinant Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 7588633
DOI: 10.1002/j.1460-2075.1995.tb00187.x
PMCID: PMC394608

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

The Mos/MAP kinase pathway stabilizes c-Fos by phosphorylation and augments its transforming activity in NIH 3T3 cells.PMID 7588633Read ↗

MAP kinase activation is essential for oncogenic transformation of NIH3T3 cells by Mos.Semantic proximity Read ↗

Evasion from proteasomal degradation by mutated Fos proteins expressed from FBJ-MSV and FBR-MSV osteosarcomatogenic retroviruses.Semantic proximity Read ↗

Constitutively active mitogen-activated protein kinase kinase 1 (MAPKK1) and MAPKK2 mediate similar transcriptional and morphological responses.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 ↗

Alteration of a cyclic AMP-dependent protein kinase phosphorylation site in the c-Fos protein augments its transforming potential.Semantic proximity Read ↗

What does mos do in oocytes and somatic cells?Semantic proximity Read ↗

Regulation of c-Fos gene transcription by stimulus-responsive protein kinases.Semantic proximity Read ↗

c-Fos proto-oncoprotein is degraded by the proteasome independently of its own ubiquitinylation in vivo.Semantic proximity Read ↗

Identification of a C-terminal tripeptide motif involved in the control of rapid proteasomal degradation of c-Fos proto-oncoprotein during the G(0)-to-S phase transition.Semantic proximity Read ↗

The transcription factor Fos: a Janus-type regulator in health and disease.Semantic proximity Read ↗

Degradation of cellular and viral Fos proteins.Semantic proximity Read ↗

c-Fos induces chondrogenic tumor formation in immortalized human mesenchymal progenitor cellsSemantic proximity Read ↗

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