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Data indicate that BRAF inhibitor (BRAFi) have unique paradoxical ERK (show EPHB2 ELISA Kits) activation profiles.
these data highlight the poor prognosis of patients with metastatic melanoma and BM, despite a targetable 'driver' oncogene (show RAB1A ELISA Kits) mutation(BRAFv600) and evidence of initial drug-responsiveness
BRAF-mutant advanced colorectal cancer ( aCRC) confers a markedly worse prognosis independent of associated clinicopathological features. Chemotherapy provides meaningful improvements in outcome throughout treatment lines. Post-progression survival is markedly worse and vigilance is required to ensure appropriate delivery of treatment after first-line progression
Case Reports: pediatric intracranial and cranial juvenile xanthogranuloma with BRAF V600E mutations.
Data indicate that BRAF, NRAS (show NRAS ELISA Kits) and C-KIT (show KIT ELISA Kits) melanomas constitute distinct clinico-pathological entities.
Mutant BRAF may, in part, drive the histologic progression of colorectal adenomas toward serrated histology
Case Reports: two cases of gliosarcoma harbouring the BRAF V600E mutation, of which one case appears to have arisen de novo, while the other likely arose from ganglioglioma.
MC1R (show MSHR ELISA Kits) genotype is associated with patient phenotypes with BRAF and NRAS (show NRAS ELISA Kits) mutations in melanoma
Our data suggest that KRAS, NRAS (show NRAS ELISA Kits), and BRAF mutations predict response to cetuximab treatment in metastatic colorectal cancer patients.
This study is the first to describe the BRAF (L597Q) mutation in malignant peripheral nerve sheath tumors and the first to implicate a BRAF mutation in neurofibroma biology
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.
TTM (show SLITRK1 ELISA Kits) reduces copper levels and MAPK (show MAPK1 ELISA Kits) signaling, thereby inhibiting BRAF(V600E)-driven melanoma tumor growth.
BRAF and ROKalpha (show ROCK2 ELISA Kits) form independent RAF1 (show RAF1 ELISA Kits) complexes in embryonic fibroblasts (MEFs) treated with epidermal growth factor (EGF (show EGF ELISA Kits)).
Braf(V600E) expression, coupled with simultaneous p53 (show TP53 ELISA Kits) ablation, permits bypass of senescence and progression to lung adenocarcinoma.
These results provide support for the role of BRAF(V600E) in metastasis.
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.
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