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Muscle RAS oncogene homolog

MRAs, R-Ras3
This gene encodes a member of the Ras family of small GTPases. These membrane-associated proteins function as signal transducers in multiple processes including cell growth and differentiation, and dysregulation of Ras signaling has been associated with many types of cancer. The encoded protein may play a role in the tumor necrosis factor-alpha and MAP kinase signaling pathways. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene. [provided by RefSeq, Nov 2011] (from NCBI)
Top mentioned proteins: CAN, p21, Angiotensin II, HAD, Raf
Papers on MRAs
Mineralocorticoid Receptor Antagonists in End-Stage Renal Disease: Efficacy and Safety.
Bomback, New York City, United States. In Blood Purif, Feb 2016
UNASSIGNED: Mineralocorticoid receptor antagonists (MRAs) that block aldosterone's effects on both epithelial and non-epithelial receptors have become a mainstay of therapy for chronic heart failure.
Clinical Outcomes in Dialysis Patients: Prospects for Improvement with Aldosterone Receptor Antagonists.
Middleton et al., Durham, United States. In Semin Dial, Jan 2016
Therapy with mineralocorticoid receptor antagonists (MRAs) effectively reduces cardiac risk in discrete populations.
Mineralocorticoid receptor antagonists and atrial fibrillation: a meta-analysis.
Li et al., Tianjin, China. In Europace, Jan 2016
We, therefore, conducted a meta-analysis of randomized clinical trials (RCTs) and observational studies in order to examine the protective role of mineralocorticoid receptor antagonists (MRAs) on AF.
Effects of mineralocorticoid receptor antagonists in patients with hypertension and diabetes mellitus: a systematic review and meta-analysis.
Yokoyama et al., Tokyo, Japan. In J Hum Hypertens, Jan 2016
The objective of this study was to evaluate the antihypertensive effects of mineralocorticoid receptor antagonists (MRAs) as add-on therapy to renin-angiotensin system (RAS) inhibitor(s) in patients with hypertension and DM.
Mineralocorticoid Receptor Antagonists and Clinical Outcomes in Primary Aldosteronism: As Good as Surgery?
Catena et al., Udine, Italy. In Horm Metab Res, Dec 2015
Treatment with mineralocorticoid receptor antagonists (MRAs) is currently recommended for PA patients with bilateral adrenal disease, but these agents effectively decrease blood pressure also in patients with unilateral disease, although concern remains for possible sex-related side effects.
Spot urine sodium excretion as prognostic marker in acutely decompensated heart failure: the spironolactone effect.
Rossignol et al., Vandœuvre-lès-Nancy, France. In Clin Res Cardiol, Dec 2015
Mineralocorticoid receptor antagonists (MRAs) in natriuretic doses may improve spot urine sodium excretion and outcomes.
Comparison of eplerenone and spironolactone for the treatment of primary aldosteronism.
Takeda et al., Kanazawa, Japan. In Hypertens Res, Dec 2015
Fifty-four patients with PA were treated with one of two MRAs, EPL (25-100 mg daily, n=27) or SPL (12.5-100 mg daily, n=27) for 12 months.
Molecular mechanisms of skeletal muscle development, regeneration, and osteogenic conversion.
Endo, Chiba, Japan. In Bone, Nov 2015
The small GTPase M-Ras is likely to participate in the ectopic calcification and ossification, as well as in osteogenesis during development.
Spironolactone for Management of Heart Failure with Preserved Ejection Fraction: Whither to After TOPCAT?
Shah et al., Chicago, United States. In Curr Atheroscler Rep, Nov 2015
Mineralocorticoid receptor antagonists (MRAs) represent an attractive class of drugs for the treatment of heart failure with preserved ejection fraction (HFpEF) because of the deleterious cardiovascular effects of aldosterone and because MRAs combat myocardial fibrosis and improve cardiac structure/function and vascular health.
Effect of Mineralocorticoid Receptor Antagonists on Cardiac Structure and Function in Patients With Diastolic Dysfunction and Heart Failure With Preserved Ejection Fraction: A Meta-Analysis and Systematic Review.
Kumbhani et al., Boston, United States. In J Am Heart Assoc, Oct 2015
BACKGROUND: There has been an increasing interest in use of mineralocorticoid receptor antagonists (MRAs) in patients with heart failure with preserved ejection fraction (HFPEF).
A high-throughput platform for stem cell niche co-cultures and downstream gene expression analysis.
Magness et al., Chapel Hill, United States. In Nat Cell Biol, Mar 2015
We use MRAs to demonstrate that Paneth cells, a known ISC niche component, enhance organoid formation in a contact-dependent manner.
Mineralocorticoid Receptor Antagonists Therapy in Resistant Hypertension: Time to Implement Guidelines!
Rossi et al., Padova, Italy. In Front Cardiovasc Med, 2014
Based on these premises randomized clinical trials aimed at testing the efficacy of MR antagonists (MRAs) in RH patients have been completed.
Temporal Trends and Hospital Variation in Mineralocorticoid Receptor Antagonist Use in Veterans Discharged With Heart Failure.
Wu et al., Aurora, United States. In J Am Heart Assoc, 2014
BACKGROUND: Despite concerns about mineralocorticoid receptor antagonist therapies (MRAs) underuse and misuse in patients with heart failure, temporal and institutional variations of MRA prescription have not been reported.
Suppression of Rapidly Progressive Mouse Glomerulonephritis with the Non-Steroidal Mineralocorticoid Receptor Antagonist BR-4628.
Tesch et al., Australia. In Plos One, 2014
BACKGROUND/AIM: Steroidal mineralocorticoid receptor antagonists (MRAs) are effective in the treatment of kidney disease; however, the side effect of hyperkalaemia, particularly in the context of renal impairment, is a major limitation to their clinical use.
Critical roles of interactions among switch I-preceding residues and between switch II and its neighboring alpha-helix in conformational dynamics of the GTP-bound Ras family small GTPases.
Kataoka et al., Kōbe, Japan. In J Biol Chem, 2011
succeed in solving two crystal structures corresponding to state 1 and state 2 from a single Ras polypeptide, M-RasD41E, carrying an H-Ras-type substitution in residue 41
Structural basis for conformational dynamics of GTP-bound Ras protein.
Kataoka et al., Kōbe, Japan. In J Biol Chem, 2010
X-ray crystal structure analyses of a series of mutant H-Ras and M-Ras in complex with guanosine 5'-(beta,gamma-imido)triphosphate (GppNHp), representing various intermediate states of the transition, were determined.
M-Ras is activated by bone morphogenetic protein-2 and participates in osteoblastic determination, differentiation, and transdifferentiation.
Endo et al., Chiba, Japan. In Exp Cell Res, 2010
These results imply that M-Ras, induced and activated by BMP-2 signaling, participates in the osteoblastic determination, differentiation, and transdifferentiation under p38 MAPK and JNK regulation
Plexin-B1 is a GTPase activating protein for M-Ras, remodelling dendrite morphology.
Negishi et al., Kyoto, Japan. In Embo Rep, 2009
Plexin-B1 is a dual functional GTPase activating protein for R-Ras and M-Ras, remodelling axon and dendrite morphology, respectively.
New susceptibility locus for coronary artery disease on chromosome 3q22.3.
Schunkert et al., Lübeck, Germany. In Nat Genet, 2009
Identification of one new CAD risk locus on 3q22.3 in MRAS, and suggestive association with a locus on 12q24.31 near HNF1A-C12orf43.
Switch-of-function mutants based on morphology classification of Ras superfamily small GTPases.
Meyer et al., Stanford, United States. In Cell, 2003
The algorithm was validated by creating switch-of-function mutants for Rac1, CDC42, H-Ras, RalA, Rap2B, and R-Ras3.
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