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High MAS1 expression in the endometrium might promote the initiation of endometriosis via migration of proliferative tissue.
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These findings suggest a critical role for MasR in cardiomyocyte survival.
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ANG-(1-7) acts on the receptor MAS to influence a range of mechanisms in the heart, kidney, brain, and other tissues. [review]
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These findings suggest that mitochondrial assembly receptor signaling may be a promising novel target for oral tongue squamous cell carcinoma.
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High levels of MAS is associated with angiogenesis in bladder cancer.
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Here, we review the role and effects of ACE2, ACE2 activators, Ang-(1-7) and synthetic Mas receptor agonists in the control of inflammation and fibrosis in cardiovascular and renal diseases and as counter-regulators of the ACE-Ang II-AT1 axis.
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Downregulation of ACE2/Ang-(1-7)/Mas axis stimulates breast cancer metastasis through the activation of store-operated calcium entry and PAK1/NF-kappaB/Snail1 pathways.
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These results indicated that angiotensin-(1-7)/ACE2/Mas axis may reduce liver lipid accumulation partly by regulating lipid-metabolizing genes through ATP/P2 receptor/CaM signaling pathway.
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Ang-(1-7) downregulated AT1R mRNA, upregulated mRNA levels of Ang II type 2 receptor (AT2R) and Mas receptor (MasR) and p38-MAPK phosphorylation and suppressed H22 cell-endothelial cell communication
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MAS1 might act as an inhibitory regulator of breast cancer.
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Data show that MAS receptor exhibited constitutive activity that was inhibited by the non-peptide inverse agonist.
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Data suggest that angiotensin converting enzyme 2/angiotensin II-(1-7)/MAS1 axis regulates leukocyte recruitment/activation, cell proliferation, and inflammation/fibrosis; main topic here is kidney/inflammatory renal disease. [REVIEW]
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Up-regulation of the ACE2/Ang-(1-7)/Mas axis protected against pulmonary fibrosis by inhibiting the MAPK/NF-kappaB pathway.
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A proximal promoter construct for the MAS gene was repressed by the SOX [SRY (sex-determining region on the Y chromosome) box] proteins SRY, SOX2, SOX3 and SOX14, of which SRY is known to interact with the KRAB domain.
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Mas appears to be a critical component required for NO-mediated vasodilatation induced by renin angiotensin system-dependent and RAS-independent agonists and therefore arises as a key pharmacological target to modulate endothelial function
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Control of adipogenesis by the autocrine interplays between angiotensin 1-7/Mas receptor and angiotensin II/AT1 receptor signaling pathways.
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MasR was significantly upregulated in colon adenocarcinoma compared with non-neoplastic colon mucosa, which showed little or no expression of it. ACE gene expression and enzymatic activity were also increased in the tumors.
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Activation of Mas during myocardial infarction contributes to ischemia-reperfusion injury and suggest that inhibition of Mas-G(q) signaling may provide a new therapeutic strategy directed at cardioprotection.
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Report expression (pro)renin receptors and angiotensin converting enzyme 2/angiotensin-(1-7)/Mas receptor axis in human aortic valve stenosis.
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Angiotensin-(1-7), its receptor Mas, and ACE2 are expressed in the human ovary