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

• Five of the 50 MRAs were considered nondiagnostic and excluded because of poor patient cooperation [4].

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