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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Related RAS viral

RRAS, Ras-related protein R-ras
Top mentioned proteins: ACID, V1a, Interferon Regulatory Factor-3, Raf, POLYMERASE
Papers on RRAS
Recent advances in RASopathies.
Review
New
Matsubara et al., Sendai, Japan. In J Hum Genet, Nov 2015
Recently, novel gene variants, including RIT1, RRAS, RASA2, A2ML1, SOS2 and LZTR1, have been shown to be associated with RASopathies, further expanding the disease entity.
R-Ras Regulates Murine T Cell Migration and Intercellular Adhesion Molecule-1 Binding.
Chan et al., Hong Kong, Hong Kong. In Plos One, 2014
R-Ras is a member of the Ras-subfamily of small guanosine-5'-triphosphate-binding proteins and its role in T cell trafficking has been investigated in R-Ras null mice (Rras-/-).
miR-34/449 control apical actin network formation during multiciliogenesis through small GTPase pathways.
Marcet et al., Antibes, France. In Nat Commun, 2014
Protection of RRAS messenger RNA against miR-34/449 binding impairs actin cap formation and multiciliogenesis, despite a still active RhoA.
Activating mutations in RRAS underlie a phenotype within the RASopathy spectrum and contribute to leukaemogenesis.
Tartaglia et al., Düsseldorf, Germany. In Hum Mol Genet, 2014
We report on two germline mutations (p.Gly39dup and p.Val55Met) in RRAS, a gene encoding a small monomeric GTPase controlling cell adhesion, spreading and migration, underlying a rare (2 subjects among 504 individuals analysed) and variable phenotype with features partially overlapping Noonan syndrome, the most common RASopathy.
An increase in tolerogenic dendritic cell and natural regulatory T cell numbers during experimental autoimmune encephalomyelitis in Rras-/- mice results in attenuated disease.
Dittel et al., Milwaukee, United States. In J Immunol, 2014
We used Rras-deficient mice to study the mechanism whereby R-Ras contributes to autoimmunity using experimental autoimmune encephalomyelitis (EAE), a mouse model of the CNS autoimmune disease multiple sclerosis.
Aberrant microRNA expression likely controls RAS oncogene activation during malignant transformation of human prostate epithelial and stem cells by arsenic.
Waalkes et al., United States. In Toxicol Sci, 2014
Reduced miR-143, miR-34c-5p, and miR-205 in As-CSC correlated with increased target RAN mRNA, and KRAS, NRAS, and RRAS proteins.
A polymorphism linked to RRAS, SCAF1, IRF3 and BCL2L12 genes is associated with cirrhosis in hepatitis C virus carriers.
Pineda et al., Sevilla, Spain. In Liver Int, 2014
RESULTS: Only the SNP rs12104272, linked to RRAS, SCAF1, IRF3 and BCL2L12 genes, was associated with cirrhosis.
The disparate twins: a comparative study of CXCR4 and CXCR7 in SDF-1α-induced gene expression, invasion and chemosensitivity of colon cancer.
Allgayer et al., Osnabrück, Germany. In Clin Cancer Res, 2014
Expressions of AKR1C3, AXL, C5, IGFBP7, IL24, RRAS, and TNNC1 were confirmed by quantitative real-time PCR.
Computational simulation of ligand docking to L-type pyruvate kinase subunit.
Järv et al., Tartu, Estonia. In Comput Biol Chem, 2014
Computational blind docking approach was used for mapping of possible binding sites in L-type pyruvate kinase subunit for peptides, RRASVA and the phosphorylated derivative RRAS(Pi)VA, which model the phosphorylatable N-terminal regulatory domain of the enzyme.
Interaction of non-phosphorylated liver pyruvate kinase with fructose 1,6-bisphosphate and peptides that mimic the phosphorylatable N-terminus of the enzyme.
Järv et al., Tartu, Estonia. In Protein Pept Lett, 2013
The phosphorylation site analogue peptides RRASVA and RRAAVA had no effect on the activity of the enzyme, while the phosphorylated peptide RRAS(Pi)VA reversibly inhibited the enzyme and this process was characterised by the Ki value 47 μM.
α5β1 integrin induces the expression of noncartilaginous procollagen gene expression in articular chondrocytes cultured in monolayers.
Fukui et al., In Arthritis Res Ther, 2012
Elated RAS viral (r-ras) oncogene homolog (RRAS) was considered to regulate the progression of dedifferentiation by modulating the affinity and avidity of α5β1 integrin to ligands.
R-RAS2 overexpression in tumors of the human central nervous system.
Cubelos et al., Madrid, Spain. In Mol Cancer, 2012
The RAS-related subfamily of GTPases is that which is most closely related to classical Ras and it currently contains 3 members: RRAS, RRAS2 and RRAS3.
Small GTPase R-Ras regulates integrity and functionality of tumor blood vessels.
Impact
GeneRIF
Komatsu et al., Orlando, United States. In Cancer Cell, 2012
These findings identify R-Ras as a critical regulator of vessel integrity and function during tumor vascularization.
Tracking the excitation dynamics in the Mn:Ge(111) metallic interface by resonant electron spectroscopy.
Morgante et al., Brescia, Italy. In J Phys Condens Matter, 2012
The switching from the resonant Raman Auger (RRAS) to the normal Auger regime is found about 2 eV below the Mn L(3) absorption edge.
Gene expression profiles of the NCI-60 human tumor cell lines define molecular interaction networks governing cell migration processes.
Pommier et al., Bethesda, United States. In Plos One, 2011
From a cluster rich in genes associated with GO categories related to cell migration, we extracted 15 genes that were highly cross-correlated; prominent among them were RRAS, AXL, ADAM9, FN14, and integrin-beta1.
A genome-scale RNA-interference screen identifies RRAS signaling as a pathologic feature of Huntington's disease.
Hughes et al., Novato, United States. In Plos Genet, 2011
In addition to established mechanisms, the screen identified multiple components of the RRAS signaling pathway as loss-of-function suppressors of mutant huntingtin toxicity in human and mouse cell models.
R-Ras interacts with filamin a to maintain endothelial barrier function.
GeneRIF
Matter et al., Honolulu, United States. In J Cell Physiol, 2011
Maintaining endothelial barrier function is dependent upon active R-Ras and association between R-Ras and FLNa.
RRAS: A key regulator and an important prognostic biomarker in biliary atresia.
GeneRIF
Zheng et al., Shanghai, China. In World J Gastroenterol, 2011
Data suggest that the RRAS gene is an important regulatory module in the pathogenesis of biliary atresia (BA), which may serve as a novel prognostic marker for BA.
Semaphorin 3E initiates antiangiogenic signaling through plexin D1 by regulating Arf6 and R-Ras.
GeneRIF
Gutkind et al., Bethesda, United States. In Mol Cell Biol, 2010
Sema3E acts on plexin D1 to initiate a two-pronged mechanism involving R-Ras inactivation and Arf6 stimulation, which affect the status of activation of integrins and their intracellular trafficking, respectively.
R-Ras regulates migration through an interaction with filamin A in melanoma cells.
GeneRIF
Matter et al., Honolulu, United States. In Plos One, 2009
data support a model in which R-Ras functionally associates with FLNa and thereby regulates integrin-dependent migration
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