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

Apoptotic and mitogenic stimuli inactivate Rb by differential utilization of p38 and cyclin-dependent kinases.

Oncogene - 4 Sept 2003

Nath Niharika, Wang Sheng, Betts Vicki, Knudsen Erik, Chellappan Srikumar

Abstract excerpt

Inactivation of the retinoblastoma (Rb) tumor suppressor protein is essential for the G1/S transition during mammalian cell cycle progression. Although Rb is inactivated by phosphorylation by cyclins D and E and their associated kinases during cell cycle progression, we find that Rb is inactivated upon apoptotic stimulation by Fas through the mediation of p38 kinase, independent of cyclins and cyclin-dependent...

Read the complete abstract on PubMed

Topics

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

Share to Culture Media, Serum-Free
Share to Cyclin D
Share to E2F Transcription Factors

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

Share to fas Receptor

Share to Jurkat Cells

Share to Mitogens

Share to p38 Mitogen-Activated Protein Kinases

Share to Retinoblastoma Protein

Source

Identifiers

PMID: 12955077
DOI: 10.1038/sj.onc.1206843

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

Apoptotic and mitogenic stimuli inactivate Rb by differential utilization of p38 and cyclin-dependent kinases.PMID 12955077Read ↗

Distinct Mechanisms for Regulating the Tumor Suppressor and Antiapoptotic Functions of RbSemantic proximity Read ↗

Direct binding of apoptosis signal-regulating kinase 1 to retinoblastoma protein: novel links between apoptotic signaling and cell cycle machinery.Semantic proximity Read ↗

Non-Classical P38 Map Kinase Functions: Cell Cycle Checkpoints and SurvivalSemantic proximity Read ↗

Phosphorylation site mutated RB exerts contrasting effects on apoptotic response to different stimuli.Semantic proximity Read ↗

RB1 dual role in proliferation and apoptosis: Cell fate control and implications for cancer therapySemantic proximity Read ↗

Loss of Rb-E2F repression results in caspase-8-mediated apoptosis through inactivation of focal adhesion kinase.Semantic proximity Read ↗

Rb at the Interface Between Cell Cycle and Apoptotic DecisionsSemantic proximity Read ↗

Sequential Cdk1 and Plk1 phosphorylation of caspase-8 triggers apoptotic cell death during mitosis.Semantic proximity Read ↗

SerpinB2 protection of retinoblastoma protein from calpain enhances tumor cell survival.Semantic proximity Read ↗

An E2F1-dependent gene expression program that determines the balance between proliferation and cell death.Semantic proximity Read ↗

Constitutive phosphorylation mutation in Fas-associated death domain (FADD) results in early cell cycle defects.Semantic proximity Read ↗

Activation of retinoblastoma protein in mammary gland leads to ductal growth suppression, precocious differentiation, and adenocarcinoma.Semantic proximity Read ↗

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