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BRAF alternative splicing is differentially regulated in vertebrates. Exon 9b is present in all vertebrates, including Xenopus, but exon 8b is present only in eutherians.
Gene expression studies nominated TWIST2 (show TWIST2 ELISA Kits) as a key effector downstream of BRAF.
BRAF alternative splicing is differentially regulated in vertebrates. Exon 9b is present in all vertebrates, including Danio rerio, but exon 8b is present only in eutherians.
BRAF activation is sufficient for f-nevus formation, and is among the primary events in melanoma development.
BRAF alternative splicing is differentially regulated in rodent and primates. Exon 9b is present in vertebrates but exon 8b is present only in eutherians.
Mechanistically, BRAF and RAF1 (show RAF1 ELISA Kits) operate independently to balance MAPK (show MAPK1 ELISA Kits) signaling: BRAF promotes ERK (show EPHB2 ELISA Kits) activation, while RAF1 (show RAF1 ELISA Kits) dims stress kinase activation.
Mass spectrometry based screening for potential interaction partners revealed that BRAF interacts and phosphorylates PAX3 (show PAX3 ELISA Kits).
Using a conditional allele for Braf(V600E) , a mutation observed in clinical cases of GIST, authors observed that Braf(V600E) activation was sufficient to drive ICC hyperplasia but not GIST tumorigenesis.
This study detected the BrafV637E mutation by whole-exome analysis in 4/4 hepatic tumors induced by neonatal treatment with diethylnitrosamine (DEN) in male B6C3F1 mice.
a critical threshold for inhibition of MAPK (show MAPK1 ELISA Kits) signaling is required to optimally restore expression of thyroid differentiation genes in thyroid cells and in mice with BrafV600E-induced thyroid cancer.
A- and B-Raf ablation in chondrocytes does not alter skeletal development, whereas ablation of C-Raf decreases hypertrophic chondrocyte apoptosis and impairs vascularization of the growth plate. However, ablation of C-Raf does not impair phosphate-induced ERK1/2 phosphorylation in vitro, but leads to rickets by decreasing VEGF protein stability.
these contrasting signatures precisely match those proposed to confer bias toward Hras (show HRAS ELISA Kits)(CAA61CTA) versus Braf(GTG636GAG) mutations in the original tumor sets. Our findings highlight a novel mechanism whereby exposure history acts through strand-biased mutagenesis to specify activation of preferred oncogenes
these results suggest that the activation of 5-HT1D receptors selectively enhanced IA via the Gbetagamma of the Go-protein, PKA, and the sequential B-Raf (show SNRPE ELISA Kits)-dependent p38 MAPK (show MAPK14 ELISA Kits) signaling cascade.
BRAF V600E inhibition stimulates AMP-activated protein kinase (show PRKAA2 ELISA Kits)-mediated autophagy in colorectal cancer cells.
these data confirm the existence of a negative feedback pathway by which BRAF protein stability is regulated by ERK (show EPHB2 ELISA Kits).
FZR1 inhibits BRAF oncogenic functions via both APC-dependent proteolysis and APC-independent disruption of BRAF dimers, whereas hyperactivated ERK and CDK4 reciprocally suppress APC(FZR1) E3 ligase activity
BRAF mutation is associated with melanoma.
Mutations in KRAS, NRAS (show NRAS ELISA Kits), and BRAF together occur in more than half of all colorectal cancer cases and are often associated with negative responses to the EGFR (show EGFR ELISA Kits) inhibitors cetuximab and panitumumab.guideline is clear that we should not be giving EGFR (show EGFR ELISA Kits) inhibitors to patients with RAS mutations and that patients with BRAF V600E mutations have a much worse prognosis
These findings identify a dynamic interplay between FZR1 and BRAF with strong implications for cell-fate determination and the tumor suppressor role of FZR1
KIT knockdown increased RAS/MAPK (show MAPK1 ELISA Kits) pathway activation in a BRAF(V600E)-mutant melanoma cell line.
Data show that the the RET (show RET ELISA Kits) receptor (RET/PTC (show RET ELISA Kits)), Ras and BRAF function along a linear oncogenic signaling cascade in which RET/PTC (show RET ELISA Kits) induces RAS-dependent BRAF activation and RAS- and BRAF-dependent ERK (show EPHB2 ELISA Kits) activation.
Although BRAF(non-V600E) mutations identified were a rare and unestablished molecular subtype, certain BRAF(non-V600E) mutations might contribute to a lesser benefit of anti-EGFR (show EGFR ELISA Kits) monoclonal antibody treatment in patients with metastatic colorectal cancer
ARMC10 (show ARMC10 ELISA Kits)-BRAF fusion is associated with melanoma.
BRAF gene mutation is confirmed by several studies found in malignant melanoma of the skin. The histopathology findings in our group did not confirmed our theory, that since the uveal melanoma itself has the similar origin as skin melanoma, should also contain a BRAF mutation.
BRAF mutation is not associated with response to chemotherapy in Melanoma.
This gene encodes a protein belonging to the raf/mil family of serine/threonine protein kinases. This protein plays a role in regulating the MAP kinase/ERKs signaling pathway, which affects cell division, differentiation, and secretion. Mutations in this gene are associated with cardiofaciocutaneous syndrome, a disease characterized by heart defects, mental retardation and a distinctive facial appearance. Mutations in this gene have also been associated with various cancers, including non-Hodgkin lymphoma, colorectal cancer, malignant melanoma, thyroid carcinoma, non-small cell lung carcinoma, and adenocarcinoma of lung. A pseudogene, which is located on chromosome X, has been identified for this gene.
94 kDa B-raf protein
, B-Raf proto-oncogene serine/threonine-protein kinase (p94)
, murine sarcoma viral (v-raf) oncogene homolog B1
, proto-oncogene B-Raf
, serine/threonine-protein kinase B-raf
, v-raf murine sarcoma viral oncogene homolog B1
, B-Raf proto-oncogene serine/threonine-protein kinase
, proto-oncogene c-Rmil
, rmil serine/threonine-protein kinase
, serine/threonine kinase
, serine/threonine-protein kinase Rmil
, serine/threonine protein kinase BRAF
, serine/threonine-protein kinase B-raf-like
, B-raf protein
, uncharacterized protein LOC561722