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Gene Review

MRAS  -  muscle RAS oncogene homolog

Homo sapiens

Synonyms: M-RAs, R-RAS3, RRAS3, Ras-related protein M-Ras, Ras-related protein R-Ras3
 
 
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Disease relevance of MRAS

  • Patients of protocol I with persistent MRAS for 7 days showed lowest weight gain and a tendency for a further increase in urinary aldosterone and nitrogen excretion [1].
  • During a 50 month period, 452 low birth-weight infants were screened for spontaneous development of incipient late metabolic acidosis (ILMA), an early stage during the development of retention acidosis, characterized by maximum renal acid stimulation (MRAS, urine-pH < 5.4) on two consecutive days but still compensated systemic acid-base status [1].
  • The biological significance of R-Ras3 in inducing Akt kinase activity is evidenced by the ability of an activated R-Ras3 to confer cell survival in the rat pheochromocytoma cell line, PC12 [2].
  • The differential diagnosis between malignancy-related ascites (MRAs) and nonmalignant ascites (NMAs) has remained an essential problem in clinical practice [3].
  • Regarding subgroups of MRAs, the telomerase activity and cytological examination demonstrated a sensitivity of 81.3% and 56.3%, respectively, in peritoneal carcinomatosis and a sensitivity of 66.7% and 11.1%, respectively, in HCC-associated ascites [3].
 

Psychiatry related information on MRAS

 

High impact information on MRAS

  • The algorithm was validated by creating switch-of-function mutants for Rac1, CDC42, H-Ras, RalA, Rap2B, and R-Ras3 [5].
  • Ectopic expression of either R-Ras3 or GRP in PC12 cells induced efficient neuronal differentiation [6].
  • R-Ras3/M-Ras is a novel member of the Ras subfamily of GTP-binding proteins which has a unique expression pattern highly restricted to the mammalian central nervous system [6].
  • One of the isolated genes encodes for the newly described M-Ras or R-Ras3, which is part of the Ras gene superfamily [7].
  • Interleukin-9-induced expression of M-Ras/R-Ras3 oncogene in T-helper clones [7].
 

Biological context of MRAS

  • This novel human ras-related gene, R-ras3, encodes for a protein of 209 amino acids, and shows approximately 60-75% sequence identity in the N-terminal catalytic domain with members of the Ras subfamily of GTP-binding proteins [8].
  • Identification and characterization of R-ras3: a novel member of the RAS gene family with a non-ubiquitous pattern of tissue distribution [8].
  • The predicted amino acid sequences and the sizes of the three MRAS proteins exhibit a high degree of similarity with other ras proteins, including that encoded by H-ras, which have been implicated in regulation of proliferation and development in eucaryotic cells by mediating signal transduction pathways [9].
  • The unique patterns of MRAS transcript accumulation suggest that individual MRAS genes and proteins may play distinct roles in cell growth or development [9].
  • Thus, R-Ras3 represents a novel G-protein which may play a role in cell survival of neural-derived cells [2].
 

Anatomical context of MRAS

  • The feasibility of the method was demonstrated in studies on a Lucite stenosis phantom, on MRAs of carotid arteries using three bolus injections, and on MRAs of renal arteries using a single contrast injection [10].
  • Coronary MRAs of the left anterior descending artery and the right coronary artery were obtained using a fat-suppressed 3D MRA sequence before and 0 to 5, 10 to 15, 20 to 25, and 30 to 35 minutes after administration of Gd-DTPA-BMA [11].
  • RATIONALE AND OBJECTIVES: The purpose of this study was to identify the cross-sectional location of collateral vessels in patients with peripheral vascular disease on three-dimensional magnetic resonance angiograms (3D MRAs) to suggest sites for intravascular or transcutaneous angiogenesis gene delivery in the lower extremity [12].
  • Steady bidimensional numerical simulations of MRAs of an anatomically realistic severely stenotic carotid artery bifurcation are presented, for both time-of-flight and contrast-enhanced imaging modalities [13].
  • However, subsequent MRAs were suspicious for vertebral artery dissection, which was confirmed by TFA [14].
 

Associations of MRAS with chemical compounds

  • The MRAS proteins show conservation of functional domains proposed for ras proteins, including guanine nucleotide interaction domains, an effector domain, a binding epitope for neutralizing antibody Y13-259, and the COOH-terminal CAAX box, which is a site of thiocylation and membrane attachment [9].
  • As expected, this biological activity of R-Ras3 was also abrogated by the addition of LY294002 [2].
  • Conclusions MRAs provide refined information on allergen activity, either confirming the results of IgE-inhibition assay, or indicating differences requiring further investigation, and represent a highly sensitive novel tool in allergen standardization [15].
  • Of 13 patients with normalized velocities on transfusion, 10 had normal MRAs, and transfusion therapy was stopped and HU begun [16].
  • METHODS: 3D phase-contrast MRAs were obtained from the foramen magnum to C3 in 4 normal volunteers in neutral and rotated (45 degrees) positions [17].
 

Other interactions of MRAS

  • Regulatory proteins of R-Ras, TC21/R-Ras2, and M-Ras/R-Ras3 [18].
  • Some genes whose expression was increased by overexpressed STAT3, but not by activated STAT3 dimers, encode well-known oncoproteins (e.g., MRAS and MET) [19].
  • Most of the identified genes/proteins have not been linked to cellular zinc status before (e.g. PEC-60, R-ras3) [20].
 

Analytical, diagnostic and therapeutic context of MRAS

  • Interestingly, Northern blot analysis of total RNA isolated from various tissues revealed that the 3.8 kilobasepair (kb) transcript of R-ras3 is highly restricted to the brain and heart [8].
  • In situ hybridization using an R-Ras3 cRNA probe revealed high levels of R-Ras3 transcripts in the hippocampal region of the mouse brain as well as a pattern of expression in the cerebellum that was distinct from that of H-Ras [6].
  • Twenty-five MRAs and 47 NMAs as the control group were enrolled in our study [3].
  • The results of intraoperative completion arteriography and preoperative MRAs were identical for all but two patients who had minor discrepancies [21].
  • MRAs falsely suggested reduced or absent ICA flow in 11 of 22 patients, nine of whom with stents [22].

References

  1. Nutrition, acid-base status and growth in early childhood. Kalhoff, H., Manz, F. European journal of nutrition. (2001) [Pubmed]
  2. R-Ras3, a brain-specific Ras-related protein, activates Akt and promotes cell survival in PC12 cells. Kimmelman, A.C., Osada, M., Chan, A.M. Oncogene (2000) [Pubmed]
  3. Telomerase assay for differentiating between malignancy-related and nonmalignant ascites. Tangkijvanich, P., Tresukosol, D., Sampatanukul, P., Sakdikul, S., Voravud, N., Mahachai, V., Mutirangura, A. Clin. Cancer Res. (1999) [Pubmed]
  4. Intracranial acute arterial ischemia of the anterior circulation: evaluation with three-dimensional time-of-flight magnetic resonance angiography. Lai, P.H., Yang, C.F., Pan, H.B., Chen, C., Lo, Y.K., Hung, K.H. Zhonghua Yi Xue Za Zhi (Taipei) (1999) [Pubmed]
  5. Switch-of-function mutants based on morphology classification of Ras superfamily small GTPases. Heo, W.D., Meyer, T. Cell (2003) [Pubmed]
  6. R-Ras3/M-Ras induces neuronal differentiation of PC12 cells through cell-type-specific activation of the mitogen-activated protein kinase cascade. Kimmelman, A.C., Nuñez Rodriguez, N., Chan, A.M. Mol. Cell. Biol. (2002) [Pubmed]
  7. Interleukin-9-induced expression of M-Ras/R-Ras3 oncogene in T-helper clones. Louahed, J., Grasso, L., De Smet, C., Van Roost, E., Wildmann, C., Nicolaides, N.C., Levitt, R.C., Renauld, J.C. Blood (1999) [Pubmed]
  8. Identification and characterization of R-ras3: a novel member of the RAS gene family with a non-ubiquitous pattern of tissue distribution. Kimmelman, A., Tolkacheva, T., Lorenzi, M.V., Osada, M., Chan, A.M. Oncogene (1997) [Pubmed]
  9. Expression of a gene family in the dimorphic fungus Mucor racemosus which exhibits striking similarity to human ras genes. Casale, W.L., Mcconnell, D.G., Wang, S.Y., Lee, Y.J., Linz, J.E. Mol. Cell. Biol. (1990) [Pubmed]
  10. Local reconstruction of stenosed sections of artery using multiple MRA acquisitions. Herment, A., Roullot, E., Bloch, I., Jolivet, O., De Cesare, A., Frouin, F., Bittoun, J., Mousseaux, E. Magnetic resonance in medicine : official journal of the Society of Magnetic Resonance in Medicine / Society of Magnetic Resonance in Medicine. (2003) [Pubmed]
  11. Three-dimensional coronary magnetic resonance angiography with injection of extracellular contrast medium. Sakuma, H., Goto, M., Nomura, Y., Kato, N., Takeda, K., Higgins, C.B. Investigative radiology. (1999) [Pubmed]
  12. Cross-sectional pattern of collateral vessels in patients with superficial femoral artery occlusion. Wecksell, M.B., Winchester, P.A., Bush, H.L., Kent, K.C., Prince, M.R., Wang, Y. Investigative radiology. (2001) [Pubmed]
  13. Numerical simulation of magnetic resonance angiographies of an anatomically realistic stenotic carotid bifurcation. Lorthois, S., Stroud-Rossman, J., Berger, S., Jou, L.D., Saloner, D. Annals of biomedical engineering. (2005) [Pubmed]
  14. Vertebral artery dissection: issues in diagnosis and management. Khurana, D.S., Bonnemann, C.G., Dooling, E.C., Ouellette, E.M., Buonanno, F. Pediatric neurology. (1996) [Pubmed]
  15. Mediator release assays based on human or murine immunoglobulin E in allergen standardization. Kaul, S., L??ttkopf, D., Kastner, B., Vogel, L., H??ltz, G., Vieths, S., Hoffmann, A. Clin. Exp. Allergy (2007) [Pubmed]
  16. Long-term follow-up of pediatric sickle cell disease patients with abnormal high velocities on transcranial Doppler. Bernaudin, F., Verlhac, S., Coïc, L., Lesprit, E., Brugières, P., Reinert, P. Pediatric radiology. (2005) [Pubmed]
  17. Rotational changes in the morphology of the vertebral artery at a common site of artery dissection. Sheth, T.N., Winslow, J.L., Mikulis, D.J. Canadian Association of Radiologists journal = Journal l'Association canadienne des radiologistes. (2001) [Pubmed]
  18. Regulatory proteins of R-Ras, TC21/R-Ras2, and M-Ras/R-Ras3. Ohba, Y., Mochizuki, N., Yamashita, S., Chan, A.M., Schrader, J.W., Hattori, S., Nagashima, K., Matsuda, M. J. Biol. Chem. (2000) [Pubmed]
  19. Novel roles of unphosphorylated STAT3 in oncogenesis and transcriptional regulation. Yang, J., Chatterjee-Kishore, M., Staugaitis, S.M., Nguyen, H., Schlessinger, K., Levy, D.E., Stark, G.R. Cancer Res. (2005) [Pubmed]
  20. Effects of increased cellular zinc levels on gene and protein expression in HT-29 cells. Kindermann, B., Döring, F., Fuchs, D., Pfaffl, M.W., Daniel, H. Biometals (2005) [Pubmed]
  21. Peripheral vascular surgery with magnetic resonance angiography as the sole preoperative imaging modality. Carpenter, J.P., Baum, R.A., Holland, G.A., Barker, C.F. J. Vasc. Surg. (1994) [Pubmed]
  22. CT and MR imaging findings and their implications in the follow-up of patients with intracranial aneurysms treated with endosaccular occlusion with onyx. Saatci, I., Cekirge, H.S., Ciceri, E.F., Mawad, M.E., Pamuk, A.G., Besim, A. AJNR. American journal of neuroradiology. (2003) [Pubmed]
 
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