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

B-Raf(V600E) cooperates with alternative spliced Rac1b to sustain colorectal cancer cell survival.

Gastroenterology - 1 Sept 2008

Matos Paulo, Oliveira Carla, Velho Sérgia, Gonçalves Vânia, da Costa Luís Teixiera, Moyer Mary Pat, Seruca Raquel, Jordan Peter

Abstract excerpt

BACKGROUND & AIMS: In colorectal tumors, activating BRAF mutations occur alternative to KRAS oncogenic mutations, but in cell culture possess a much lower transforming capacity. Rac1b, a hyperactive Rac1 spliced variant, is over expressed in some colorectal tumors and activates the transcription factor nuclear factor-kappaB, which initiates a transcriptional response that promotes cell cycle progression and...

Read the complete abstract on PubMed

Topics

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

Share to Alternative Splicing
Share to Cell Cycle

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Death

Share to Cell Survival

Share to Genes, ras

Share to Proto-Oncogene Proteins B-raf

Share to rac1 GTP-Binding Protein

Share to RNA Interference

Source

Identifiers

PMID: 18602919
DOI: 10.1053/j.gastro.2008.05.052

Genes

KRAS
BRAF

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

B-Raf(V600E) cooperates with alternative spliced Rac1b to sustain colorectal cancer cell survival.PMID 18602919Read ↗

C-Raf inhibits MAPK activation and transformation by B-Raf(V600E).Semantic proximity Read ↗

Genetic targeting of B-RafV600E affects survival and proliferation and identifies selective agents against BRAF-mutant colorectal cancer cells.Semantic proximity Read ↗

BRAF and RAS oncogenes regulate Rho GTPase pathways to mediate migration and invasion properties in human colon cancer cells: a comparative studySemantic proximity Read ↗

LY3009120, a panRAF inhibitor, has significant anti-tumor activity in BRAF and KRAS mutant preclinical models of colorectal cancer.Semantic proximity Read ↗

B-Raf Inhibitors Induce Epithelial Differentiation in <i>BRAF</i> -Mutant Colorectal Cancer CellsSemantic proximity Read ↗

Colorectal cancer cells with the BRAF(V600E) mutation are addicted to the ERK1/2 pathway for growth factor-independent survival and repression of BIM.Semantic proximity Read ↗

Studying the function of the alternative spliced isoform Rac1b in colorectal cancerSemantic proximity Read ↗

Expression of endogenous oncogenic V600EB-raf induces proliferation and developmental defects in mice and transformation of primary fibroblasts.Semantic proximity Read ↗

RAC1b overexpression correlates with poor prognosis in KRAS/BRAF WT metastatic colorectal cancer patients treated with first-line FOLFOX/XELOX chemotherapy.Semantic proximity Read ↗

Cloning of a novel human Rac1b splice variant with increased expression in colorectal tumorsSemantic proximity Read ↗

Alternative splicing of BRAF transcripts and characterization of C-terminally truncated B-Raf isoforms in colorectal cancer.Semantic proximity Read ↗

Activation and involvement of Ral GTPases in colorectal cancer.Semantic proximity Read ↗

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