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

V-raf murine sarcoma 3611 viral oncogene homolog

A-Raf, ARAF1
This proto-oncogene belongs to the RAF subfamily of the Ser/Thr protein kinase family, and maybe involved in cell growth and development. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Jan 2012] (from NCBI)
Top mentioned proteins: Raf, BRAF, ERK, ACID, CAN
Papers on A-Raf
Purification and characterization of a novel polysaccharide-peptide complex from Clinacanthus nutans Lindau leaves.
Sun et al., Zhenjiang, China. In Carbohydr Polym, Mar 2016
Its side chain might be composed of 1-linked Araf, 1,6-linked Galp and 1-linked Rhap residues.
Genetics, Transcriptional Profiles, and Catalytic Properties of the UDP-Arabinose Mutase Family from Barley.
Fincher et al., Adelaide, Australia. In Biochemistry, Feb 2016
The UDP-l-Arap → UDP-l-Araf reaction, which is essential for the generation of the UDP-Araf substrate for arabinoxylan, arabinogalactan protein, and pectic polysaccharide biosynthesis, is thermodynamically unfavorable and has an equilibrium constant of 0.02.
c-Raf promotes angiogenesis during normal growth plate maturation.
Demay et al., Boston, United States. In Development, Feb 2016
Ablation of both A-Raf (Araf) and B-Raf (Braf) in chondrocytes does not alter growth plate maturation.
Treatment of Langerhans cell histiocytosis: role of BRAF/MAPK inhibition.
Weitzman et al., Toronto, Canada. In Hematology Am Soc Hematol Educ Program, Jan 2016
The recent discovery of somatic mutations in ARAF and in MAP2K1, which lead to activation of the RAS-RAF-MEK -ERK pathway in the setting of wild-type BRAF, as well as the finding that activating mutation in MAP2K1 are relatively insensitive to MEK inhibitors, suggest that a more detailed understanding of this pathway in LCH may be necessary for the development of more effective targeted therapies.
Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms.
Abdel-Wahab et al., Kettering, United States. In Cancer Discov, Dec 2015
Through combined whole exome and transcriptome sequencing, we identified recurrent kinase fusions involving BRAF, ALK, and NTRK1, as well as recurrent, activating MAP2K1 and ARAF mutations in BRAFV600E-wildtype, non-LCH patients.
A-Raf: A new star of the family of raf kinases.
Xu et al., Glasgow, United Kingdom. In Crit Rev Biochem Mol Biol, Nov 2015
The Raf family kinases (A-Raf, B-Raf and C-Raf) have been intensively studied since being identified in the early 1980s as retroviral oncogenes, especially with respect to the discovery of activating mutations of B-Raf in a large number of tumors which led to intensified efforts to develop drugs targeting Raf kinases.
Comprehensive investigation of oncogenic driver mutations in Chinese non-small cell lung cancer patients.
Chen et al., Shanghai, China. In Oncotarget, Nov 2015
In lung adenocarcinoma cases "pan-negative" for the seven above-mentioned driver mutations, we also detected two oncogenic EGFR extracellular domain mutations (A289D and R324L), two HER2 extracellular and transmembrane domain mutations (S310Y and V659E), one ARAF S214C mutation and two CD74-NRG1 fusions.
Inhibition of RAF Isoforms and Active Dimers by LY3009120 Leads to Anti-tumor Activities in RAS or BRAF Mutant Cancers.
Flynn et al., Indianapolis, United States. In Cancer Cell, Oct 2015
Biochemical and cellular analyses revealed that LY3009120 inhibits ARAF, BRAF, and CRAF isoforms with similar affinity, while vemurafenib or dabrafenib have little or modest CRAF activity compared to their BRAF activities.
Exploring azole antifungal drug resistance in Aspergillus fumigatus with special reference to resistance mechanisms.
Meis et al., Delhi, India. In Future Microbiol, 2013
The high mortality rates observed in patients with invasive aspergillosis caused by azole-resistant A. fumigatus (ARAF) isolates pose serious challenges to the clinical microbiologist for timely identification of resistance and appropriate therapeutic interventions.
Phase I/II RAF kinase inhibitors in cancer therapy.
Larkin et al., London, United Kingdom. In Expert Opin Investig Drugs, 2013
BRAF is the only RAF family member that is commonly mutated, whilst CRAF and ARAF play important roles in the signal transduction from mutant RAS.
PRR5L degradation promotes mTORC2-mediated PKC-δ phosphorylation and cell migration downstream of Gα12.
Wu et al., New Haven, United States. In Nat Cell Biol, 2012
The late phase is mediated by Gα(12), which specifically activates ARAF, leading to upregulation of the RFFL E3 ubiquitin ligase and subsequent ubiquitylation and degradation of the PRR5L subunit of mTORC2.
Novel small molecule Raf kinase inhibitors for targeted cancer therapeutics.
Sim et al., Seoul, South Korea. In Arch Pharm Res, 2012
B-Raf is most attractive drug target out of three Raf isoforms (A-Raf, B-Raf and C-Raf) because it exhibits high kinase activity due to frequent mutations in human tumors.
[Regulation of cell survival by RAF kinases].
Ezzoukhry et al., Amiens, France. In Med Sci (paris), 2010
The RAF proteins (A-RAF, B-RAF et C-RAF) are a family of kinases that play a key role in the regulation of various aspects of cell physiology, among which cell proliferation, differentiation and survival.
Heterogeneous nuclear ribonucleoprotein H blocks MST2-mediated apoptosis in cancer cells by regulating A-Raf transcription.
Gires et al., München, Germany. In Cancer Res, 2010
hnRNP H blocks MST2-mediated apoptosis in cancer cells by regulating A-Raf transcription.
A transposon in Comt generates mRNA variants and causes widespread expression and behavioral differences among mice.
Williams et al., Memphis, United States. In Plos One, 2009
Expression of Araf in the mouse nucleus accumbens is modulated by a sequence variant (B2 SINE indel) in the 3' UTR of Comt (catechol-O-methyltransferase).
Positive regulation of A-RAF by phosphorylation of isoform-specific hinge segment and identification of novel phosphorylation sites.
Rapp et al., Würzburg, Germany. In J Biol Chem, 2008
Positive regulation of A-RAF by phosphorylation of isoform-specific hinge segment and identification of novel phosphorylation sites.
Cell wall modifications in Arabidopsis plants with altered alpha-L-arabinofuranosidase activity.
Goffner et al., Solomon Islands. In Plant Physiol, 2008
Arabinan-containing pectins are potential in vivo substrates.
Cortical migration defects in mice expressing A-RAF from the B-RAF locus.
Rapp et al., Würzburg, Germany. In Mol Cell Biol, 2006
These data reveal that B-RAF is an important mediator of neuronal survival, migration, and dendrite formation and that A-RAF cannot fully compensate for these functions.
Endothelial apoptosis in Braf-deficient mice.
Zimmer et al., Bethesda, United States. In Nat Genet, 1997
However, genetic studies of C. elegans and Drosophila, as well as the targeted mutagenesis of the murine Araf gene, have failed to support such a role.
Mammalian Ras interacts directly with the serine/threonine kinase Raf.
Cooper et al., Seattle, United States. In Cell, 1993
Approximately 50% of the clones identified encoded portions of the c-Raf and A-Raf serine/threonine kinases.
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