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

Oncogenic Ki-ras inhibits the expression of interferon-responsive genes through inhibition of STAT1 and STAT2 expression.

The Journal of biological chemistry - 21 Nov 2003

Klampfer Lidija, Huang Jie, Corner Georgia, Mariadason John, Arango Diego, Sasazuki Takehiko, Shirasawa Senji, Augenlicht Leonard

Abstract excerpt

Endogenous interferon gamma (IFNgamma) promotes the host response to primary tumors, and IFNgamma-insensitive tumors display increased tumorigenicity and can evade tumor surveillance mechanisms. Here we demonstrate that activating mutations of Ki-ras are sufficient to inhibit the expression of STAT1 and STAT2, transcription factors required for signaling by IFNs, providing a potential mechanism for the...

Read the complete abstract on PubMed

Topics

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

Share to Colonic Neoplasms
Share to Gene Expression Profiling

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Expression Regulation, Neoplastic

Share to Genes, ras

Share to Interferon-gamma

Share to Oncogene Protein p21(ras)

Share to STAT1 Transcription Factor

Share to Trans-Activators

Source

Identifiers

PMID: 12972432
DOI: 10.1074/jbc.M304721200

Genes

STAT1
STAT2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Oncogenic Ki-ras inhibits the expression of interferon-responsive genes through inhibition of STAT1 and STAT2 expression.PMID 12972432Read ↗

Deficiency of interferon-gamma or its receptor promotes colorectal cancer development.Semantic proximity Read ↗

Suppression of IFN-Induced Transcription Underlies IFN Defects Generated by Activated Ras/MEK in Human Cancer CellsSemantic proximity Read ↗

Stat1 Phosphorylation Determines Ras Oncogenicity by Regulating p27Kip1Semantic proximity Read ↗

Suppression of interferon gene expression overcomes resistance to MEK inhibition in KRAS-mutant colorectal cancerSemantic proximity Read ↗

STAT1 is essential for the inhibition of hepatitis C virus replication by interferon-λ but not by interferon-αSemantic proximity Read ↗

Elevated type I interferon signaling defines the proliferative advantage of ARF and p53 mutant tumor cellsSemantic proximity Read ↗

Tumor-Suppressive Activity of the Cell Death Activator GRIM-19 on a Constitutively Active Signal Transducer and Activator of Transcription 3Semantic proximity Read ↗

Elevated Type I Interferon Signaling Defines the Proliferative Advantage of ARF and p53 Mutant Tumor Cells.Semantic proximity Read ↗

Activated Ki-Ras suppresses 12-O-tetradecanoylphorbol-13-acetate-induced activation of the c-Jun NH2-terminal kinase pathway in human colon cancer cells.Semantic proximity Read ↗

TAK1 inhibition promotes apoptosis in KRAS-dependent colon cancers.Semantic proximity Read ↗

Histone deacetylase inhibitors induce cell death selectively in cells that harbor activated kRasV12: The role of signal transducers and activators of transcription 1 and p21.Semantic proximity Read ↗

Microarray analysis of the differential transformation mediated by Kirsten and Harvey Ras oncogenes in a human colorectal adenocarcinoma cell line.Semantic proximity Read ↗

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