MRAS gene marker rs9818870 is not associated with acute
coronary syndrome in the Czech population and does not
predict mortality in males after acute coronary syndrome

Hubacek, Jaroslav A.; Staněk, Vladimír; Gebauerová, M; Češka, Richard; Adámková, Věra; Lánská, Věra; Piťha, Jan

doi:10.17219/acem/67460

Cited by 3 publications

(2 citation statements)

References 20 publications

(34 reference statements)

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“…Nonetheless, a similar study in a Czech population found that MRAS SNP variants were not associated with acute coronary syndrome or cardiovascular disease mortality, supporting the idea that the associations observed in initial studies are ancestry-dependent. 43 Further study of these associations in additional populations is merited.…”

Section: Cardiovascular Systemmentioning

confidence: 99%

The Role of R-Ras Proteins in Normal and Pathologic Migration and Morphologic Change

Weber¹,

Carroll²

2021

The American Journal of Pathology

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The contributions that the R-Ras subfamily [R-Ras, R-Ras2/teratocarcinoma 21 (TC21), and M-Ras] of small GTP-binding proteins make to normal and aberrant cellular functions have historically been poorly understood. However, this has begun to change with the realization that all three R-Ras subfamily members are occasionally mutated in Noonan syndrome (NS), a RASopathy characterized by the development of hematopoietic neoplasms and abnormalities affecting the immune, cardiovascular, and nervous systems. Consistent with the abnormalities seen in NS, a host of new studies have implicated R-Ras proteins in physiological and pathologic changes in cellular morphology, adhesion, and migration in the cardiovascular, immune, and nervous systems. These changes include regulating the migration and homing of mature and immature immune cells, vascular stabilization, clotting, and axonal and dendritic outgrowth during nervous system development. Dysregulated R-Ras signaling has also been linked to the pathogenesis of cardiovascular disease, intellectual disabilities, and human cancers. This review discusses the structure and regulation of R-Ras proteins and our current understanding of the signaling pathways that they regulate. It explores the phenotype of NS patients and their implications for the R-Ras subfamily functions. Next, it covers recent discoveries regarding physiological and pathologic R-Ras functions in key organ systems. Finally, it discusses how R-Ras signaling is dysregulated in cancers and mechanisms by which this may promote neoplasia.

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Section: Cardiovascular Systemmentioning

confidence: 99%

The Role of R-Ras Proteins in Normal and Pathologic Migration and Morphologic Change

Weber¹,

Carroll²

2021

The American Journal of Pathology

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“…In Czeck Slavonic population, rs9818870 was not associated with acute coronary syndrome or mortality 51 . Furthermore, in Pakistani populations, no associations were detected between this Single Nucleotide Polymorphism (SNP) and CAD or lipid parameters 52 …”

Section: Introductionmentioning

confidence: 99%

MRAS in coronary artery disease—Unchartered territory

Shah,

Reinberger,

Hashmi

et al. 2024

IUBMB Life

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Genome‐wide association studies (GWAS) have identified coronary artery disease (CAD) susceptibility locus on chromosome 3q22.3. This locus contains a cluster of several genes that includes muscle rat sarcoma virus (MRAS). Common MRAS variants are also associated with CAD causing risk factors such as hypertension, dyslipidemia, obesity, and type II diabetes. The MRAS gene is an oncogene that encodes a membrane‐bound small GTPase. It is involved in a variety of signaling pathways, regulating cell differentiation and cell survival (mitogen‐activated protein kinase [MAPK]/extracellular signal‐regulated kinase and phosphatidylinositol 3‐kinase) as well as acute phase response signaling (tumor necrosis factor [TNF] and interleukin 6 [IL6] signaling). In this review, we will summarize the role of genetic MRAS variants in the etiology of CAD and its comorbidities with the focus on tissue distribution of MRAS isoforms, cell type/tissue specificity, and mode of action of single nucleotide variants in MRAS associated complex traits. Finally, we postulate that CAD risk variants in the MRAS locus are specific to smooth muscle cells and lead to higher levels of MRAS, particularly in arterial and cardiac tissue, resulting in MAPK‐dependent tissue hypertrophy or hyperplasia.

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The influence of MRAS gene variants on ischemic stroke and serum lipid levels in Chinese Han population

Song¹,

Zhang³

2019

Medicine

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Previous studies have indicated that muscle RAS oncogene homolog (MRAS) gene played an important role in cardiovascular diseases. However, the effect of MRAS genetic variations on ischemic stroke (IS) is still not clear. The aim of the current study was to investigate the association between the MRAS polymorphism and IS risk in Han populations. Three SNPs (rs40593, rs751357, rs6782181) at MRAS were selected for genotyping in a sample of 240 IS patients and 430 controls. Logistic regression was performed to evaluate the association of 3 SNPs with IS and IS subgroups. No association of MRAS SNPs with IS risk was observed, while G allele of rs40593 was associated with increased risk of cerebral infarction area. Compared with carriers of the AA genotype, the risk of carriers of the AG+GG genotype increased, with an OR (95%CI) of 2.337 (1.175–4.647), P = .016. In relation to lipid profile, rs40593, rs751357, rs6782181 were associated with increased total cholesterol (TC) levels. Summarily, this study suggested that MRAS rs40593 may contribute to the increased risk of area of cerebral infarction of IS in Han population. rs40593, rs751357, and rs6782181 were associated with higher serum TC levels.

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MRAS gene marker rs9818870 is not associated with acute coronary syndrome in the Czech population and does not predict mortality in males after acute coronary syndrome

Abstract: Background. Genome-wide association studies (GWAs) focused on cardiovascular diseases reveal variants within genes which have not been analyzed through the pre-GWAs era, and whose function is often unknown. One of them is variant rs9818870 at the MRAS gene locus.

Cited by 3 publications

References 20 publications

The Role of R-Ras Proteins in Normal and Pathologic Migration and Morphologic Change

The Role of R-Ras Proteins in Normal and Pathologic Migration and Morphologic Change

MRAS in coronary artery disease—Unchartered territory

The influence of MRAS gene variants on ischemic stroke and serum lipid levels in Chinese Han population

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