MRAS

Source: Wikipedia, the free encyclopedia.
MRAS
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
Ensembl
UniProt
RefSeq (mRNA)

NM_008624

RefSeq (protein)

NP_032650

Location (UCSC)Chr 3: 138.35 – 138.41 MbChr 9: 99.27 – 99.32 Mb
PubMed search[3][4]
Wikidata
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Ras-related protein M-Ras, also known as muscle RAS oncogene homolog and R-Ras3, is a

SNPs associated with increased risk of coronary artery disease.[13]

Structure

Gene

The MRAS gene resides on chromosome 3 at the band 3q22.3 and includes 10

Protein

M-Ras is a member of the

Gpp(NH)p). Of the two states M-Ras can switch between, M-Ras is predominantly found in its state 1 conformation, which does not bind Ras effectors.[15]

Function

The MRAS gene is expressed specifically in

TNF-alpha-stimulated and Rap1-mediated LFA-1 activation in splenocytes.[23] More generally, cells transfected with M-Ras exhibit dendritic appearances with microspikes, suggesting that M-Ras may participate in reorganization of the actin cytoskeleton.[16] In addition, it is reported that M-Ras forms a complex with SCRIB and SHOC2, a polarity protein with tumor suppressor properties, and may play a key role in tumorigenic growth.[24]

Clinical significance

In humans, other members of the Ras subfamilies carry mutations in human cancers.[25] Furthermore, the Ras proteins are not only involved in tumorigenesis but also in many developmental disorders.[25] For instance, the Ras-related proteins appear to be overexpressed in human carcinomas of the oral cavity, esophagus, stomach, skin, and breast, as well as in lymphomas.[26][27][28][29] More currently, Ras family members such as R-RAS, R-RAS2 and also R-RAS3 have also been implicated as main factors in triggering neural transformation, with R-RAS2 as the most significant element.[30]

Clinical marker

A multi-locus genetic risk score study based on a combination of 27 loci, including the MRAS gene, identified individuals at increased risk for both incidence and recurrent coronary artery disease events, as well as an enhanced clinical benefit from statin therapy. The study was based on a community cohort study (the Malmo Diet and Cancer study) and four additional randomized controlled trials of primary prevention cohorts (JUPITER and ASCOT) and secondary prevention cohorts (CARE and PROVE IT-TIMI 22).[31]

Interactions

MRAS has been shown to

interact with RASSF5[32] and RALGDS.[5][33]

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000158186Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000032470Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^
    PMID 9400994
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  7. ^ a b "Entrez Gene: MRAS muscle RAS oncogene homolog".
  8. ^ "BioGPS - your Gene Portal System". biogps.org. Retrieved 2016-10-10.[permanent dead link]
  9. S2CID 25048933
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  14. ^ a b "MRAS - Ras-related protein M-Ras precursor - Homo sapiens (Human) - MRAS gene & protein". www.uniprot.org. Retrieved 2016-10-10.
  15. PMID 15994326
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Further reading

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