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MAS1

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Immunopharmacology Ligand target has curated data in GtoImmuPdb

Target id: 150

Nomenclature: MAS1

Family: Class A Orphans

Contents:

Gene and Protein Information Click here for help
class A G protein-coupled receptor
Species TM AA Chromosomal Location Gene Symbol Gene Name Reference
Human 7 325 6q25.3 MAS1 MAS1 proto-oncogene, G protein-coupled receptor 47,49,71
Mouse 7 324 17 8.69 cM Mas1 MAS1 oncogene 12
Rat 7 324 1q11 Mas1 MAS1 proto-oncogene, G protein-coupled receptor 30,70
Gene and Protein Information Comments
Homologs of MAS1 are absent in model organisms like Zebra fish (D. rerio), Fruit fly (D. melanogaster) and C. elegans [19].
Previous and Unofficial Names Click here for help
MAS | angiotensin 1-7 receptor [45] | MAS1 proto-oncogene, G protein-coupled receptor | MAS1 proto-oncogene
Database Links Click here for help
Specialist databases
GPCRdb mas_human (Hs), mas_mouse (Mm), mas_rat (Rn)
Other databases
Alphafold P04201 (Hs), P30554 (Mm), P12526 (Rn)
ChEMBL Target CHEMBL3559701 (Hs)
Ensembl Gene ENSG00000130368 (Hs), ENSMUSG00000068037 (Mm), ENSRNOG00000014971 (Rn)
Entrez Gene 4142 (Hs), 17171 (Mm), 25153 (Rn)
Human Protein Atlas ENSG00000130368 (Hs)
KEGG Gene hsa:4142 (Hs), mmu:17171 (Mm), rno:25153 (Rn)
OMIM 165180 (Hs)
Pharos P04201 (Hs)
RefSeq Nucleotide NM_002377 (Hs), NM_008552 (Mm), NM_012757 (Rn)
RefSeq Protein NP_002368 (Hs), NP_032578 (Mm), NP_036889 (Rn)
UniProtKB P04201 (Hs), P30554 (Mm), P12526 (Rn)
Wikipedia MAS1 (Hs)

Download all structure-activity data for this target as a CSV file go icon to follow link

Agonists
Key to terms and symbols View all chemical structures Click column headers to sort
Ligand Sp. Action Value Parameter Reference
[125I]angiotensin-(1-7) (human, mouse, rat) Peptide Ligand is labelled Ligand is radioactive Mm Full agonist 9.1 pKd 54
⤷ pKd 9.1 (Kd 8.3x10-10 M) [54]
angiotensin-(1-7) {Sp: Human, Mouse, Rat} Peptide Mm Agonist 7.3 pKi 25
⤷ pKi 7.3 (Ki 4.92x10-8 M) [25]
AR234958 Small molecule or natural product Hs Agonist 7.0 pEC50 22
⤷ pEC50 7.0 (EC50 9.6x10-8 M) [22]
neuropeptide FF {Sp: Human, Mouse, Rat} Peptide Mm Full agonist 6.4 pEC50 16
⤷ pEC50 6.4 (EC50 4x10-7 M) [16]
AR234960 Small molecule or natural product Hs Full agonist 6.1 – 6.5 pEC50 72
⤷ pEC50 6.1 – 6.5 (EC50 7.2x10-7 – 3.5x10-7 M) [72]
AR234960 Small molecule or natural product Rn Full agonist 5.8 – 6.8 pEC50 72
⤷ pEC50 5.8 – 6.8 (EC50 1.71x10-6 – 1.7x10-7 M) [72]
CGEN-856 Peptide Hs Full agonist 6.2 pEC50 56,58
⤷ pEC50 6.2 (EC50 5.7x10-7 M) [56,58]
CGEN-857 Peptide Hs Full agonist 6.0 pEC50 56,58
⤷ pEC50 6.0 (EC50 1x10-6 M) [56,58]
MBP7 Peptide Rn Full agonist 4.4 pEC50 5
⤷ pEC50 4.4 (EC50 3.641x10-5 M) [5]
angiotensin-(1-7) {Sp: Human, Mouse, Rat} Peptide Mm Agonist 8.2 pIC50 54
⤷ pIC50 8.2 (IC50 6.9x10-9 M) [54]
AVE 0991 Small molecule or natural product Immunopharmacology Ligand Mm Full agonist 7.3 pIC50 44
⤷ pIC50 7.3 (IC50 4.75x10-8 M) [44]
View species-specific agonist tables
Agonist Comments
Other agonists at this receptor include cyclised angiotensin (1-7) [31], angioprotectin [29], angiotensin III and angiotensin IV [24].

Jackson et al. reported that angiotensins I and II activated the MAS1 receptor [28]. However, Dong et al. did not detect responses in MAS1-expressing cells exposed to angiotensins I and II [16]. It was then reported that angiotensin-(1-7), which can be generated from angiotensin II by angiotensin-converting enzyme 2(ACE2) and functions as a vasodilator and antiproliferative agent, binds to Mas-transfected cells and elicits arachidonic acid release [54] and nitric oxide [50]. Angiotensin III and IV can also induce a significant but less pronounced arachidonic acid release [24]. Angiotensin-(1-7) was shown to not activate MAS in G protein coupled receptor functional assays measuring calcium, inositol-1-phosphate and cAMP [5,58,72]. There is very poor pharmacological data including radioligand binding studies that suggest a direct interaction between Ang(1-7) and MAS [25,54,66].

Alamandine, a novel component in renin-angiotensin system (RAS), is reported to act through MrgD, a member of Mas related gene family (Mrg) for which MAS is the founding member [34].
Antagonists
Key to terms and symbols View all chemical structures Click column headers to sort
Ligand Sp. Action Value Parameter Reference
[D-Ala7]-angiotensin(1-7) Peptide Mm Antagonist 8.3 pKi 25
⤷ pKi 8.3 (Ki 4.96x10-9 M) [25]
AR291903 Small molecule or natural product Hs Inverse agonist 8.0 pEC50 22
⤷ pEC50 8.0 (EC50 1x10-8 M) [22]
[D-Ala7]-angiotensin(1-7) Peptide Mm Antagonist 9.5 pIC50 54
⤷ pIC50 9.5 (IC50 3x10-10 M) [54]
AR305352 Peptide Hs Inverse agonist 6.8 pIC50 72
⤷ pIC50 6.8 (IC50 1.66x10-7 M) [72]
AR244555 Small molecule or natural product Hs Inverse agonist 6.7 pIC50 72
⤷ pIC50 6.7 (IC50 1.86x10-7 M) [72]
AR305352 Peptide Rn Inverse agonist 6.5 pIC50 72
⤷ pIC50 6.5 (IC50 3.2x10-7 M) [72]
AR244555 Small molecule or natural product Rn Inverse agonist 6.5 pIC50 72
⤷ pIC50 6.5 (IC50 3.48x10-7 M) [72]
View species-specific antagonist tables
Antagonist Comments
[D-Pro7]-angiotensin (1-7) is an antagonist of the mouse MAS1 receptor [53].
Immunopharmacology Comments
Experimental evidence from animal studies suggest a role for MAS1 in the anti-inflammatory pathway mediated by angiotensin-(1-7) [15,17].
Immuno Process Associations
Immuno Process:  Inflammation
Immuno Process:  Immune regulation
Primary Transduction Mechanisms Click here for help
Transducer Effector/Response
Gi/Go family
Gq/G11 family 		Phospholipase C stimulation
Other - See Comments
Comments:  Transducer Gi is linked to the effector cAMP inhibition.

MAS is reported to activate G protein constitutively [9,72]. However, no G protein activation by MAS is observed upon stimulation with angiotensin-(1-7) [5,58,72].

MAS is shown to function as a physiological antagonist of AT1R by altering AngII response in different tissues in mice [32,48,62].

Complex vascular effects of Ang(1-7) involving interactions of MAS with AT1R and AT2R are reported in the hearts of MAS knockout mice [10].

MAS upregulates AT1R by constitutive activation of Gαq/11 and subsequent PKC-dependent phosphorylation of AT1R [9].

Trafficking defective AT1R is rescued by co-expression with MAS in CHO and COS7 cells [51].

MAS transformation of cells is mediated by Rac-dependent signaling in NIH 3T3 cells [73].

Expression of Leukemia-associated Rho guanine nucleotide exchange factor (LARG) diminished transforming activity of MAS in NIH 3T3 cells [6].
References:  72
Tissue Distribution Click here for help
Heart
Species:  Human
Technique:  RT-PCR, immunohistochemical staining
References:  72
Hippocampus and cerebral cortex
Species:  Human
Technique:  Northern blot
References:  28
Testis, kidney, heart and brain (especially in forebrain and low amounts of MAS1 mRNA in medulla oblongata).
Species:  Mouse
Technique:  RNase protection assay
References:  40
Leydig cells, Sertoli cells, primary spermatocytes
Species:  Mouse
Technique:  in situ hybridisation
References:  2
Platelets
Species:  Mouse
Technique:  Fluorescently labeled angiotensin-(1-7) binding
References:  20
Kidney
Species:  Mouse
Technique:  Autoradiography
References:  54
Forebrain, areas of the hippocampus and cerebral cortex (dentate gyrus, the CA3, CA2, and CAI area of the gyrus hippocampi, olfactory tubercle, piriform cortex, and olfactory bulb), cortical areas. Not detectable in medulla oblongata.
Species:  Mouse
Technique:  in situ hybridisation
References:  40
Knee joint
Species:  Mouse
Technique:  Western blot
References:  15
Myocardium
Species:  Rat
Technique:  Western blot
References:  4
Platelets
Species:  Rat
Technique:  Fluorescently labeled angiotensin-(1-7) binding
References:  20
Hippocampus and cerebral cortex
Species:  Rat
Technique:  Northern blot
References:  70
Strong labelling in the dentate gyrus, the CA3 and CA4 areas of the hippocampus, the olfactory tubercle (medial part), the piriform cortex and the olfactory bulb. Weak to moderate labelling in the neocortex and frontal lobe.
Species:  Rat
Technique:  in situ hybridisation
References:  8
Heart and cardiomyocytes
Species:  Rat
Technique:  RT-PCR and Western blot
References:  59
Smooth muscle bundles and in arteriolar endothelial and smooth muscle cells of the rat corpus cavernosum
Species:  Rat
Technique:  Immunofluorescence
References:  14
In both adult and developing rats, mas transcripts are present in hippocampal pyramidal neurons and dentate granular cells.
Species:  Rat
Technique:  in situ hybridisation
References:  38-39
Cerebral endothelial cells
Species:  Rat
Technique:  Northern blot
References:  33
Heart
Species:  Rat
Technique:  RT-PCR, Immunohistochemical staining
References:  72
Tissue Distribution Comments
The expression of MAS1 was higher in decidual explants from women carrying a female foetus than from women carrying a male foetus [65]. MAS1 mRNAs were not detected in human placenta when examined by quantitative real-time PCR [45].
Expression Datasets Click here for help

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Log average relative transcript abundance in mouse tissues measured by qPCR from Regard, J.B., Sato, I.T., and Coughlin, S.R. (2008). Anatomical profiling of G protein-coupled receptor expression. Cell, 135(3): 561-71. [PMID:18984166] [Raw data: website]

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Physiological Functions Click here for help
MAS1 has been proposed to be involved in angiotensin-(1-7)-mediated anti-inflammatory pathway in allergic asthma
Species:  Mouse
Tissue:  Lung
References:  17
Activation of the MAS1 receptor, by AVE 0991 or angiotensin-(1-7), reduced the neutrophil accumulation, hypernociception and production of TNF-α, IL-1β, CXCL1 and histopathological changes evoked in antigen-induced arthritis.
Species:  Mouse
Tissue:  Knee joint
References:  15
Angiotensin-(1-7)-MAS1 axis has been proposed to play a role in normal erectile function
Species:  Rat
Tissue:  Penile structures
References:  14
Activation of MAS1 receptor by angiotensin-(1-7) inhibited protein synthesis in cardiac myocytes.
Species:  Rat
Tissue:  Cardiac myocytes
References:  59
Physiological Functions Comments
The physiological role of MAS1 is directly evident in knockout mice studies (see Physiological Consequences of Altering Gene Expression section). The role of MAS1 in several physiological functions is derived indirectly from studies wherein [D-Ala7]-angiotensin(1-7)/A779 or AVE 0991 antagonized the physiological effects of angiotensin-(1-7).
Physiological Consequences of Altering Gene Expression Click here for help
Mice with deletion or blockade of MAS1 receptor show a substantial increase in the coronary perfusion pressure in the baseline and reperfusion periods
Species:  Mouse
Tissue:  Heart
Technique:  Gene knockouts and perfusion with MAS1 antagonist A-779
References:  11
Angiotensin-(1-7)-induced relaxation response of the aorta was abolished in MAS1-deficient mice
Species:  Mouse
Tissue:  Aorta
Technique:  Gene knockouts
References:  54
MAS1-deficient mice showed elevated blood pressure, impaired endothelial function and an imbalance between NO and reactive oxygen species
Species:  Mouse
Tissue:  Not specified
Technique:  Gene knockouts
References:  67
Transfection of neonatal rat myocytes with an antisense oligonucleotide to the MAS1 receptor blocked angiotensin-(1-7)-mediated inhibition of serum-stimulated MAP kinase activation
Species:  Rat
Tissue:  Myocytes
Technique:  Transfection with antisense oligonucleotides
References:  59
Mice with MAS1 receptor knockout showed erectile dysfunction and a marked increase in fibrous tissue in the penile corpus cavernosum
Species:  Mouse
Tissue:  Penile corpus cavernosum
Technique:  Gene knockouts
References:  14
Overexpression of MAS1 in cones of retina induced cell death without the formation of tumours
Species:  Mouse
Tissue:  Retina
Technique:  Gene overexpression
References:  69
Mice with MAS1 receptor knockout showed increased duration of long term potentiation in the dentate gyrus, increased anxiety and alterations in the onset of depotentiation
Species:  Mouse
Tissue:  Dentate gyrus
Technique:  Gene knockouts
References:  63
MAS1-deficient female mice showed a marked reduction of heart rate variability, whereas MAS1-deficient male mice showed a significant increase in blood pressure variability. MAS1-deficient mice of both genders displayed increased sympathetic tone
Species:  Mouse
Tissue:  Not specified
Technique:  Gene knockouts
References:  64
Depletion of MAS1 affects the expression of proteins involved in mitochondrial function and steroidogenesis in the testis
Species:  Mouse
Tissue:  Testis
Technique:  Gene knockouts
References:  68
The binding of angiotensin-(1-7) to mouse kidney was abolished in MAS1-deficient mice
Species:  Mouse
Tissue:  Kidney
Technique:  Gene knockouts
References:  54
MAS1-deficient mice demonstrate selective expression of extracellular matrix proteins like collagen types I, III and IV, fibronectin, MMP-2 and MMP-9 in ventricular myocardium and AV valves
Species:  Mouse
Tissue:  Heart
Technique:  Gene knockouts, RT-PCR, Immunostaining
References:  72
MAS1-deficient mice subjected to antigen-induced arthritis showed greater neutrophil accumulation and cytokine release
Species:  Mouse
Tissue:  Knee joint
Technique:  Gene knockouts
References:  15
MAS1 knockout mice have impaired heart function - Lower systolic tension, higher coronary vessel resistance; decreased fractional shortening, posterior wall thickness in systole and left ventricle end-diastolic dimension; higher left ventricle end-systolic dimension; lower global ventricular function as evident by higher myocardial performance index; higher delayed time to peak calcium current; profibrotic profile change in collagen expression.
Species:  Mouse
Tissue:  Heart
Technique:  Gene knockouts
References:  52
MAS1 knockout mice have reduced infarct size after ischemia-reperfusion injury. Treatment of rat hearts with inverse agonist AR244555 improved coronary blood flow, reduced arrhythmias and provided cardioprotection from ischemia-reperfusion injury.
Species:  Mouse
Tissue:  Heart
Technique:  Gene knockouts in mouse and perfusion with inverse agonist AR244555 in rat hearts
References:  72
MAS1-deficient mice have higher ratio of circulating angiotensin-II/angioteinsin-(1-7) and increased ACE2 in left ventricle.
Species:  Mouse
Tissue:  Heart
Technique:  Gene knockouts, RT-PCR , Immunostaining
References:  26
MAS1-deficient mice have endothelium dysfunction as shown by loss of response to endothelium-dependent vasorelaxant bradykinin and acetylcholine
Species:  Mouse
Tissue:  Mesenteric arteries
Technique:  Gene knockouts
References:  42
MAS1-deficient mice have endothelium dysfunction as shown by acute blood pressure effect of endothelium-dependent vasorelaxant acetylcholine. Changes in blood pressure in MAS1-deficient mice are strain dependent.
Species:  Mouse
Tissue:  Not specified
Technique:  Gene knockouts
References:  46
MAS1-deficient mice were protected from salt induced hypertension as evident by the absence of any change in basal hemodynamic properties. However, urinary electrolytes and osmolality were significantly higher suggesting possible mode of protection from salt induced hypertension.
Species:  Mouse
Tissue:  Not specified
Technique:  Gene knockouts
References:  27
MAS1 deficient mice show reduction in urine volume and fractional sodium excretion, reduced renal blood flow (renal dysfunction) and microalbuminuria. Fibrogenic changes in the kidneys if knockout mice are also evident.
Species:  Mouse
Tissue:  Kidney
Technique:  Gene knockouts
References:  43
MAS1 deficient mice were protected from renal damage in models of renal sufficiency as unilateral ureteral obstruction and ischemia/reperfusion injury
Species:  Mouse
Tissue:  Kidney
Technique:  Gene knockouts
References:  18
MAS1-deficient mice have normal body weight but have dyslipidemia, increased levels of insulin, increased leptin and abdominal fat mass, increased muscle triglycerides, reduced insulin sensitivity and glucose intolerance.
Species:  Mouse
Tissue:  Not specified
Technique:  Gene knockouts
References:  55
Decreased bleeding time in MAS1 deficient mice.
Species:  Mouse
Tissue:  Platelets
Technique:  Gene knockouts
References:  20
The antidiuretic action of angiotensin-(1-7) after an acute water load was absent in MAS1 deficient mice
Species:  Mouse
Tissue:  Not specified
Technique:  Gene knockouts
References:  54
In C57Bl/6 genetic background MAS1-deficient mice were normotensive; however major difference were evident in hemodynamic measurements like decrease in stroke volume; decrease in cardiac index; increase in vascular resistance; decrease in blood flow in the kidney, lung, adrenal gland, mesentry, spleen and brown fat tissue.
Species:  Mouse
Tissue:  Not specified
Technique:  Gene knockouts
References:  7
In MAS1-deficient mice there in decreased gene expression of peroxisome proliferator-activated receptor gamma (PPARγ), acetyl-CoA carboxylase and amount of fatty acid synthase. There was increase in in serum nonesterified fatty acids and no change in basal and isoproterenol stimulated lipolysis and lipolytic index.
Species:  Mouse
Tissue:  Adipocytes
Technique:  Gene knockouts
References:  37
Physiological Consequences of Altering Gene Expression Comments
Early Mas1 knockout mice were in a mixed genetic background (129xC57BL/6) [63]. Later these mice were backcrossed to generate knockout mice with pure C57Bl/6 [68] and FVB/N [55] genetic backgrounds to study strain-specific effects of MAS deficiency.
Phenotypes, Alleles and Disease Models Click here for help Mouse data from MGI

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Allele Composition & genetic background Accession Phenotype Id Phenotype Reference
Mas1tm1Bdr Mas1tm1Bdr/Mas1tm1Bdr
involves: 129P2/OlaHsd		 MGI:96918  MP:0003008 enhanced long term potentiation PMID: 9565612 
Mas1tm1Bdr Mas1tm1Bdr/Mas1tm1Bdr
involves: 129P2/OlaHsd		 MGI:96918  MP:0001363 increased anxiety-related response PMID: 9565612 
Gene Expression and Pathophysiology Comments
A recurring translocation site in chromosome 6q that contains MAS1 has been found to be associated with human malignant melanoma [60].
General Comments
MAS1 is a human cellular oncogene [71]. MAS1 is maternally imprinted in foetal mice [61], but not in adult mice [57] and humans [49]. MAS1 is not imprinted in mice [1,36].

Information on miRNAs predicted to target MAS1 3'UTR can be found at TargetScan [21,35].

In humans, the MAS1 receptor is located on chromosome locus 6q24-27, which is also a protooncogene [PMID 3708691]. MAS1 was initially thought to be the GPCR for AngII, but was not accepted on grounds of pharmacology and pattern of tissue expression [3,28,41]. In 2003, Santos et al., proposed that MAS1 is a functional receptor for Ang(1-7) based on the observations that binding sites and in vivo physiological responses to Ang (1-7) is absent in mice harbouring Mas1 deletion [54]. At present, pharmacological support for direct interaction between Ang(1-7) and MAS1 including radioligand binding and/or conventional G protein mediated second messenger generation is weak [5,58,72]. Similar to Ang(1-7), its analogs like A-779, cyclized derivative and non-peptide mimetics (AVE 0991) do not affect MAS1-mediated G protein signaling [31,66]. Conventional G protein signaling by MAS1 was reported upon stimulation with Neuropeptide FF [16] and in response to other peptide and non-peptide ligands, but not by Ang(1-7) [5,58,72]. MAS1 has also been reported to activate G protein signaling and the small GTPase Rac1 signaling constitutively. At cellular level, Ang(1-7) treatment of human messangial cells or MAS1 transfected CHO and COS cells was shown to cause concentration-dependent release of arachidonic acid (AA) by stimulating mitogen activated protein kinase p38.

Deletion of Mas1 gene in mice suggest functional involvement of MAS1 in behavioral processes and in cardiovascular, renal and several metabolic physiologies [11,13,23,27,43,55,64] the MAS1-null mice have increased anxiety, altered heart rate and blood pressure variability. MAS1 knockout mice exhibited impairment in cardiac function associated with profibrotic changes in the expression of extracellular matrix proteins in the hearts. Renal dysfunction and fibrogenic changes in the kidneys were also reported in MAS1 deficient. MAS1 deficient mice were also shown to have increased abdominal fat mass, dyslipidemia, increased levels of insulin and leptin and altered response of adipocytes to insulin. MAS1 deficiency was shown to offer protection from salt induced hypertension and from ischemia/reperfusion injury in both kidney and heart. Endothelial dysfunction resulting in imbalances in nitric oxide (NO) and reactive oxygen species was reported to be a common mechanism behind the MAS1 deficient mice exhibiting alterations in blood pressure and heart rate, and an increase in vascular resistance and decrease in blood flow in the kidney, lung, adrenal gland, mesentry, spleen and brown fat tissues. MAS1 and AT1R may heterooligomerize and result in the altered function and trafficking of AT1R [32,51,62]. Thus, MAS1 may interact with the components of the renin angiotensin receptor implying a role for MAS1 in physiology.

The interaction between Ang(1-7) and MAS1 is perhaps indirect and complex, may involve cross-talk between different proteins or differential expression of genes. However, it is too early to qualify MAS1 as a member of the angiotensin receptor family.

References

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1. Alenina N, Bader M, Walther T. (2002) Imprinting of the murine MAS protooncogene is restricted to its antisense RNA. Biochem Biophys Res Commun, 290 (3): 1072-8. [PMID:11798184]

2. Alenina N, Baranova T, Smirnow E, Bader M, Lippoldt A, Patkin E, Walther T. (2002) Cell type-specific expression of the Mas proto-oncogene in testis. J Histochem Cytochem, 50 (5): 691-6. [PMID:11967280]

3. Ambroz C, Clark AJ, Catt KJ. (1991) The mas oncogene enhances angiotensin-induced [Ca2+]i responses in cells with pre-existing angiotensin II receptors. Biochim Biophys Acta, 1133 (1): 107-11. [PMID:1721543]

4. Arumugam S, Thandavarayan RA, Palaniyandi SS, Giridharan VV, Arozal W, Sari FR, Soetikno V, Harima M, Suzuki K, Kodama M et al.. (2012) Candesartan cilexetil protects from cardiac myosin induced cardiotoxicity via reduction of endoplasmic reticulum stress and apoptosis in rats: involvement of ACE2-Ang (1-7)-mas axis. Toxicology, 291 (1-3): 139-45. [PMID:22120037]

5. Bikkavilli RK, Tsang SY, Tang WM, Sun JX, Ngai SM, Lee SS, Ko WH, Wise H, Cheung WT. (2006) Identification and characterization of surrogate peptide ligand for orphan G protein-coupled receptor mas using phage-displayed peptide library. Biochem Pharmacol, 71 (3): 319-37. [PMID:16336942]

6. Booden MA, Siderovski DP, Der CJ. (2002) Leukemia-associated Rho guanine nucleotide exchange factor promotes G alpha q-coupled activation of RhoA. Mol Cell Biol, 22 (12): 4053-61. [PMID:12024019]

7. Botelho-Santos GA, Bader M, Alenina N, Santos RA. (2012) Altered regional blood flow distribution in Mas-deficient mice. Ther Adv Cardiovasc Dis, 6 (5): 201-11. [PMID:23045193]

8. Bunnemann B, Fuxe K, Metzger R, Mullins J, Jackson TR, Hanley MR, Ganten D. (1990) Autoradiographic localization of mas proto-oncogene mRNA in adult rat brain using in situ hybridization. Neurosci Lett, 114 (2): 147-53. [PMID:2203997]

9. Canals M, Jenkins L, Kellett E, Milligan G. (2006) Up-regulation of the angiotensin II type 1 receptor by the MAS proto-oncogene is due to constitutive activation of Gq/G11 by MAS. J Biol Chem, 281 (24): 16757-67. [PMID:16611642]

10. Castro CH, Santos RA, Ferreira AJ, Bader M, Alenina N, Almeida AP. (2005) Evidence for a functional interaction of the angiotensin-(1-7) receptor Mas with AT1 and AT2 receptors in the mouse heart. Hypertension, 46 (4): 937-42. [PMID:16157793]

11. Castro CH, Santos RA, Ferreira AJ, Bader M, Alenina N, Almeida AP. (2006) Effects of genetic deletion of angiotensin-(1-7) receptor Mas on cardiac function during ischemia/reperfusion in the isolated perfused mouse heart. Life Sci, 80 (3): 264-8. [PMID:17055538]

12. Cebra-Thomas JA, Tsai JY, Pilder SH, Copeland NG, Jenkins NA, Silver LM. (1992) Localization of the Mas proto-oncogene to a densely marked region of mouse chromosome 17 associated with genomic imprinting. Genomics, 13 (2): 444-6. [PMID:1612602]

13. Crouch E, Persson A, Chang D, Parghi D. (1991) Surfactant protein D. Increased accumulation in silica-induced pulmonary lipoproteinosis. Am J Pathol, 139 (4): 765-76. [PMID:1656758]

14. da Costa Gonçalves AC, Leite R, Fraga-Silva RA, Pinheiro SV, Reis AB, Reis FM, Touyz RM, Webb RC, Alenina N, Bader M et al.. (2007) Evidence that the vasodilator angiotensin-(1-7)-Mas axis plays an important role in erectile function. Am J Physiol Heart Circ Physiol, 293 (4): H2588-96. [PMID:17616753]

15. da Silveira KD, Coelho FM, Vieira AT, Sachs D, Barroso LC, Costa VV, Bretas TL, Bader M, de Sousa LP, da Silva TA et al.. (2010) Anti-inflammatory effects of the activation of the angiotensin-(1-7) receptor, MAS, in experimental models of arthritis. J Immunol, 185 (9): 5569-76. [PMID:20935211]

16. Dong X, Han S, Zylka MJ, Simon MI, Anderson DJ. (2001) A diverse family of GPCRs expressed in specific subsets of nociceptive sensory neurons. Cell, 106 (5): 619-32. [PMID:11551509]

17. El-Hashim AZ, Renno WM, Raghupathy R, Abduo HT, Akhtar S, Benter IF. (2012) Angiotensin-(1-7) inhibits allergic inflammation, via the MAS1 receptor, through suppression of ERK1/2- and NF-κB-dependent pathways. Br J Pharmacol, 166 (6): 1964-76. [PMID:22339213]

18. Esteban V, Heringer-Walther S, Sterner-Kock A, de Bruin R, van den Engel S, Wang Y, Mezzano S, Egido J, Schultheiss HP, Ruiz-Ortega M et al.. (2009) Angiotensin-(1-7) and the g protein-coupled receptor MAS are key players in renal inflammation. PLoS ONE, 4 (4): e5406. [PMID:19404405]

19. Fournier D, Luft FC, Bader M, Ganten D, Andrade-Navarro MA. (2012) Emergence and evolution of the renin-angiotensin-aldosterone system. J Mol Med, 90 (5): 495-508. [PMID:22527880]

20. Fraga-Silva RA, Pinheiro SV, Gonçalves AC, Alenina N, Bader M, Santos RA. (2008) The antithrombotic effect of angiotensin-(1-7) involves mas-mediated NO release from platelets. Mol Med, 14 (1-2): 28-35. [PMID:18026570]

21. Friedman RC, Farh KK, Burge CB, Bartel DP. (2009) Most mammalian mRNAs are conserved targets of microRNAs. Genome Res, 19 (1): 92-105. [PMID:18955434]

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