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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

V-raf murine sarcoma viral oncogene homolog B1

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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: KRAS, CAN, Raf, HAD, MAPK
Papers using BRAF antibodies
Induction of autophagy and inhibition of melanoma growth in vitro and in vivo by hyperactivation of oncogenic BRAF
Pal Soumitro, In PLoS ONE, 2009
... All primary antibodies were purchased from Cell Signaling Technology except the following: anti-BRAF from Santa Cruz Biotechnology, anti-CRAF from BD Biosciences, ...
RET/PTC rearrangements in thyroid nodules: studies in irradiated and not irradiated, malignant and benign thyroid lesions in children and adults
LiVolsi Virginia A et al., In CytoJournal, 2000
... The amplified products were electrophoresed on a 1.2% gel at 110 V for 1.5 hours and the BRAF bands (~220 bp) were cut using sterile blade and purified using Qiagen Gel Extraction Kit (Hilden, ...
A specific inhibitor of phosphatidylinositol 3-kinase, 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002)
Brinker Achim et al., In Current Chemical Genomics, 1993
... Unconjugated B-Raf antibody was from Santa Cruz Biotechnology (sc-5284), pMEK1/2 antibody from ...
Papers on BRAF
Common BRAF(V600E)-directed pathway mediates widespread epigenetic silencing in colorectal cancer and melanoma.
Green et al., Worcester, United States. In Proc Natl Acad Sci U S A, Feb 2016
We have recently described an epigenetic silencing pathway, directed by the oncogenic B-Raf proto-oncogene (BRAF) variant BRAF(V600E), that mediates widespread epigenetic silencing in colorectal cancer (CRC).
p53 Reactivation by PRIMA-1(Met) (APR-246) sensitises (V600E/K)BRAF melanoma to vemurafenib.
Ghanem et al., Brussels, Belgium. In Eur J Cancer, Feb 2016
UNASSIGNED: Intrinsic and acquired resistance of metastatic melanoma to (V600E/K)BRAF and/or MEK inhibitors, which is often caused by activation of the PI3K/AKT survival pathway, represents a major clinical challenge.
Melanoma: the intersection of molecular targeted therapy and immune checkpoint inhibition.
McArthur et al., Melbourne, Australia. In Curr Opin Immunol, Feb 2016
Although responses to molecularly targeted therapy is largely from blockade of oncogenic pathways, evidence is emerging of the immunomodulatory effects from BRAF inhibition.
TERT promoter mutations in thyroid cancer.
Xing et al., Baltimore, United States. In Endocr Relat Cancer, Feb 2016
TERT promoter mutations are associated with aggressive thyroid tumor characteristics, tumor recurrence, and patient mortality as well as BRAF V600E mutation.
Combination therapy with BRAF and MEK inhibitors for melanoma: latest evidence and place in therapy.
Ribas et al., Tampa, United States. In Ther Adv Med Oncol, Jan 2016
Treatment with BRAF inhibitors such as vemurafenib or dabrafenib in patients with advanced BRAFV600 mutated melanoma has shown objective tumor responses in approximately half of the patients.
Managing Cutaneous Side Effects From Targeted Molecular Inhibitors for Melanoma and Nonmelanoma Skin Cancer.
Ratner et al., New York City, United States. In Dermatol Surg, Jan 2016
MATERIALS AND METHODS: A comprehensive literature search related to the side effects and management of these side effects from vemurafenib, dabrafenib, trametinib (BRAF inhibitors), pembrolizumab (antiprogrammed-death-receptor-1 antibody), imatinib (tyrosine kinase inhibitor), ipilimumab (anticytotoxic T-lymphocyte antigen-4 antibody), cetuximab (epidermal growth factor receptor inhibitor), sorafenib (multikinase inhibitor), and vismodegib (smoothened receptor inhibitor).
Phase II Pilot Study of Vemurafenib in Patients With Metastatic BRAF-Mutated Colorectal Cancer.
Saltz et al., Houston, United States. In J Clin Oncol, Jan 2016
PURPOSE: BRAF V600E mutation is seen in 5% to 8% of patients with metastatic colorectal cancer (CRC) and is associated with poor prognosis.
(Secondary) solid tumors in thyroid cancer patients treated with the multi-kinase inhibitor sorafenib may present diagnostic challenges.
Morreau et al., Leiden, Netherlands. In Bmc Cancer, Dec 2015
BACKGROUND: Sorafenib is an orally active multikinase tyrosine kinase inhibitor (TKI) that targets B-type Raf kinase (BRAF), vascular endothelial growth factor receptors (VEGFR) 1 and 2, and rearranged during transfection (RET), inducing anti-angiogenic and pro-apoptotic actions in a wide range of solid tumors.
Human Engineered Cardiac Tissues Created Using Induced Pluripotent Stem Cells Reveal Functional Characteristics of BRAF-Mediated Hypertrophic Cardiomyopathy.
Costa et al., New York City, United States. In Plos One, Dec 2015
The hECTs were created using human cardiomyocytes obtained by directed differentiation of induced pluripotent stem cells derived from a patient with CFCS due to an activating BRAF mutation.
The mutational landscape of cutaneous T cell lymphoma and Sézary syndrome.
Palomero et al., New York City, United States. In Nat Genet, Dec 2015
Mutation analysis identified a broad spectrum of somatic mutations in key genes involved in epigenetic regulation (TET2, CREBBP, KMT2D (MLL2), KMT2C (MLL3), BRD9, SMARCA4 and CHD3) and signaling, including MAPK1, BRAF, CARD11 and PRKG1 mutations driving increased MAPK, NF-κB and NFAT activity upon T cell receptor stimulation.
Geldanamycin induces apoptosis in human gastric carcinomas by affecting multiple oncogenic kinases that have synergic effects with TNF-related apoptosis-inducing ligand.
Pan et al., Fuzhou, China. In Oncol Lett, Dec 2015
GA treatment inhibits proliferation, migration and invasion, and induces apoptosis in human gastric cancer SGC-7901 cells, most likely by decreasing the expression of B-RAF and by phosphorylation of protein kinase B (AKT) and ERK.
The Genetic Evolution of Melanoma from Precursor Lesions.
Bastian et al., Australia. In N Engl J Med, Dec 2015
Unequivocally benign lesions harbored BRAF V600E mutations exclusively, whereas those categorized as intermediate were enriched for NRAS mutations and additional driver mutations.
RAF inhibitors that evade paradoxical MAPK pathway activation.
Bollag et al., Berkeley, United States. In Nature, Nov 2015
Oncogenic activation of BRAF fuels cancer growth by constitutively promoting RAS-independent mitogen-activated protein kinase (MAPK) pathway signalling.
Comparison of dabrafenib and trametinib combination therapy with vemurafenib monotherapy on health-related quality of life in patients with unresectable or metastatic cutaneous BRAF Val600-mutation-positive melanoma (COMBI-v): results of a phase 3, open-label, randomised trial.
Robert et al., Marseille, France. In Lancet Oncol, Oct 2015
BACKGROUND: In the COMBI-v trial, patients with previously untreated BRAF Val600Glu or Val600Lys mutant unresectable or metastatic melanoma who were treated with the combination of dabrafenib and trametinib had significantly longer overall and progression-free survival than those treated with vemurafenib alone.
Overview of fundamental study of pazopanib in cancer.
Zhou et al., Tianjin, China. In Thorac Cancer, 2014
In an vitro study, pazopanib exerted anti-tumor effect through mechanisms including the Raf-MAPK/ERK (MEK)-extracellular signal-regulated kinase (ERK) pathway, and directly targeted on v-raf murine sarcoma viral oncogene homolog B (B-raf) as well.
The intermediate-activity (L597V)BRAF mutant acts as an epistatic modifier of oncogenic RAS by enhancing signaling through the RAF/MEK/ERK pathway.
Pritchard et al., Leicester, United Kingdom. In Genes Dev, 2012
endogenous expression of (L597V)Braf leads to approximately twofold elevated Braf kinase activity and weak activation of the Mek/Erk pathway
BRAF duplications and MAPK pathway activation are frequent in gliomas of the optic nerve proper.
Eberhart et al., Baltimore, United States. In J Neuropathol Exp Neurol, 2012
The results of this study supported an important role for BRAF duplication and MAPK pathway activation in gliomas of the optic nerve proper.
BRAF mutation in papillary thyroid cancer and its value in tailoring initial treatment: a systematic review and meta-analysis.
Xing et al., Baltimore, United States. In Medicine (baltimore), 2012
Thus, in this meta-analysis, the BRAF mutation in PTC was significantly associated with PTC recurrence, lymph node metastasis, extrathyroidal extension, and advanced stage AJCC III/IV.
KRAS and BRAF mutations in Serbian patients with colorectal cancer.
Jankovic et al., Belgrade, Serbia. In J Buon, 2012
the spectrum and frequency distribution of the identified KRAS and BRAF mutations in Serbian patient with colorectal cancer are in good accordance with literature data.
A cardio-facio-cutaneous syndrome case with tight Achilles tendons.
Ozkinay et al., İzmir, Turkey. In Genet Couns, 2011
Cardio-facio-cutaneous syndrome is caused by heterogeneous mutations in BRAF gene.
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