Ignet

Gene Information

Gene symbol: MAS1

Gene name: MAS1 oncogene

HGNC ID: 6899

Related Genes

#	Gene Symbol	Number of hits
1	ACE	1 hits
2	ACE2	1 hits
3	ADCY7	1 hits
4	AGT	1 hits
5	AGTR1	1 hits
6	AKT1	1 hits
7	CD34	1 hits
8	ITK	1 hits
9	PIK3CA	1 hits
10	REN	1 hits

Related Sentences

#	PMID	Sentence
1	8077356	Activating mutations of codon 201 in the gene encoding the alpha-subunit of Gs, the G-protein that stimulates adenylyl cyclase, have been found in all affected MAS tissues that have been studied.
2	18948167	In this review we will examine the role of the renin-angiotensin system in the physiopathology and treatment of diabetes and highlight the potential benefits of the ACE2/Ang-(1-7)/Mas receptor axis, focusing on recent data about ACE2.
3	20554647	EMT was assessed at 3 days by expression of alpha-smooth muscle actin (alpha-SMA) and E-cadherin and the induction of a myofibroblastic phenotype.
4	20554647	Selective blockade of the AT(1) receptor or the AT(2) receptor failed to inhibit ANG II-induced EMT.
5	20554647	However, blockade of the ANG 1-7 receptor, Mas-1, was able to prevent ANG II-dependent EMT.
6	20554647	To confirm these findings, both ANG 1-7 and the selective Mas receptor agonist, AVE-0991, were able to induce NRK-52E cells in a dose-dependent manner.
7	20554647	EMT was assessed at 3 days by expression of alpha-smooth muscle actin (alpha-SMA) and E-cadherin and the induction of a myofibroblastic phenotype.
8	20554647	Selective blockade of the AT(1) receptor or the AT(2) receptor failed to inhibit ANG II-induced EMT.
9	20554647	However, blockade of the ANG 1-7 receptor, Mas-1, was able to prevent ANG II-dependent EMT.
10	20554647	To confirm these findings, both ANG 1-7 and the selective Mas receptor agonist, AVE-0991, were able to induce NRK-52E cells in a dose-dependent manner.
11	21792177	Despite evidence that hyperactivity of the vasodeleterious axis (ACE/angiotensin II (Ang II)/AT1 receptor) of the renin-angiotensin system (RAS) is associated with the pathogenesis of diabetic retinopathy (DR) use of the inhibitors of this axis has met with limited success in the control of this pathophysiology.
12	21792177	Diabetes was associated with approximately tenfold and greater than threefold increases in the ratios of ACE/ACE2 and AT1R/Mas mRNA levels in the retina respectively.
13	22564510	The role of the renin-angiotensin system in the development of insulin resistance in skeletal muscle.
14	22564510	The canonical renin-angiotensin system (RAS) involves the initial action of renin to cleave angiotensinogen to angiotensin I (ANG I), which is then converted to ANG II by the angiotensin converting enzyme (ACE).
15	22564510	In addition, ANG II, by acting on both endothelial and myocellular AT1 receptors, can induce insulin resistance by increasing cellular oxidative stress, leading to impaired insulin signaling and insulin-stimulated glucose transport activity.
16	22564510	Interventions that target RAS overactivity, including ACE inhibitors, ANG II receptor blockers, and, most recently, renin inhibitors, are effective both in reducing hypertension and in improving whole-body and skeletal muscle insulin action, due at least in part to enhanced Akt-dependent insulin signaling and insulin-dependent glucose transport activity.
17	22564510	ANG-(1-7), which is produced from ANG II by the action of ACE2 and acts via Mas receptors, can counterbalance the deleterious actions of the ACE/ANG II/AT1 receptor axis on the insulin-dependent glucose transport system in skeletal muscle.
18	22564510	This beneficial effect of the ACE2/ANG-(1-7)/Mas receptor axis appears to depend on the activation of Akt.
19	23230080	Activation of the ACE2/angiotensin-(1-7)/Mas receptor axis enhances the reparative function of dysfunctional diabetic endothelial progenitors.
20	23230080	We tested the hypothesis that activation of the protective arm of the renin angiotensin system, the angiotensin-converting enzyme 2 (ACE2)/angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis, corrects the vasoreparative dysfunction typically seen in the CD34(+) cells isolated from diabetic individuals.
21	23230080	The survival and proliferation of CD34(+) cells from diabetic individuals were enhanced by Ang-(1-7) in a Mas/phosphatidylinositol 3-kinase (PI3K)/Akt-dependent manner.
22	23230080	A cohort of patients who remained free of microvascular complications despite having a history of longstanding inadequate glycemic control had higher expression of ACE2/Mas mRNA than patients with diabetes with microvascular complications matched for age, sex, and glycemic control.
23	23230080	Thus, ACE2/Ang-(1-7)Mas pathway activation corrects existing diabetes-induced CD34(+) cell dysfunction and also confers protection from development of this dysfunction.
24	23230080	Activation of the ACE2/angiotensin-(1-7)/Mas receptor axis enhances the reparative function of dysfunctional diabetic endothelial progenitors.
25	23230080	We tested the hypothesis that activation of the protective arm of the renin angiotensin system, the angiotensin-converting enzyme 2 (ACE2)/angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis, corrects the vasoreparative dysfunction typically seen in the CD34(+) cells isolated from diabetic individuals.
26	23230080	The survival and proliferation of CD34(+) cells from diabetic individuals were enhanced by Ang-(1-7) in a Mas/phosphatidylinositol 3-kinase (PI3K)/Akt-dependent manner.
27	23230080	A cohort of patients who remained free of microvascular complications despite having a history of longstanding inadequate glycemic control had higher expression of ACE2/Mas mRNA than patients with diabetes with microvascular complications matched for age, sex, and glycemic control.
28	23230080	Thus, ACE2/Ang-(1-7)Mas pathway activation corrects existing diabetes-induced CD34(+) cell dysfunction and also confers protection from development of this dysfunction.
29	23230080	Activation of the ACE2/angiotensin-(1-7)/Mas receptor axis enhances the reparative function of dysfunctional diabetic endothelial progenitors.
30	23230080	We tested the hypothesis that activation of the protective arm of the renin angiotensin system, the angiotensin-converting enzyme 2 (ACE2)/angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis, corrects the vasoreparative dysfunction typically seen in the CD34(+) cells isolated from diabetic individuals.
31	23230080	The survival and proliferation of CD34(+) cells from diabetic individuals were enhanced by Ang-(1-7) in a Mas/phosphatidylinositol 3-kinase (PI3K)/Akt-dependent manner.
32	23230080	A cohort of patients who remained free of microvascular complications despite having a history of longstanding inadequate glycemic control had higher expression of ACE2/Mas mRNA than patients with diabetes with microvascular complications matched for age, sex, and glycemic control.
33	23230080	Thus, ACE2/Ang-(1-7)Mas pathway activation corrects existing diabetes-induced CD34(+) cell dysfunction and also confers protection from development of this dysfunction.
34	23230080	Activation of the ACE2/angiotensin-(1-7)/Mas receptor axis enhances the reparative function of dysfunctional diabetic endothelial progenitors.
35	23230080	We tested the hypothesis that activation of the protective arm of the renin angiotensin system, the angiotensin-converting enzyme 2 (ACE2)/angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis, corrects the vasoreparative dysfunction typically seen in the CD34(+) cells isolated from diabetic individuals.
36	23230080	The survival and proliferation of CD34(+) cells from diabetic individuals were enhanced by Ang-(1-7) in a Mas/phosphatidylinositol 3-kinase (PI3K)/Akt-dependent manner.
37	23230080	A cohort of patients who remained free of microvascular complications despite having a history of longstanding inadequate glycemic control had higher expression of ACE2/Mas mRNA than patients with diabetes with microvascular complications matched for age, sex, and glycemic control.
38	23230080	Thus, ACE2/Ang-(1-7)Mas pathway activation corrects existing diabetes-induced CD34(+) cell dysfunction and also confers protection from development of this dysfunction.
39	23381810	Blockade of RAS is advocated at multiple levels by direct renin inhibitor, angiotensin-converting enzyme inhibitor and/or angiotensin II type 1 receptor blocker, or aldosterone inhibitor (spironolactone), and has now become part of the standard of care to control hypertension and related metabolic diseases including diabetes.
40	23381810	In this context, it is highly pertinent that components of RAS are evolutionarily conserved, and novel physiological/adaptive/protective roles for renin and angiotensin-converting enzyme are currently emerging.
41	23381810	Additionally, angiotensin-converting enzyme 2 and the angiotensin II metabolite Ang-(1-7) that acts through the Mas proto-oncogene constitute the cardiovascular and renal protective branch of RAS.
42	23463883	ACE2, angiotensin-(1–7), and Mas: the other side of the coin.
43	23463883	The renin–angiotensin system (RAS) has recently been extended by the addition of a novel axis consisting of the angiotensin-converting enzyme 2 (ACE2), the heptapeptide angiotensin (1–7) (Ang-(1–7)), and the G protein-coupled receptor Mas.
44	23463883	ACE2 converts the vasoconstrictive and pro-oxidative peptide angiotensin II (Ang II) into Ang-(1–7) which exerts vasodilatory and antioxidative effects via its receptor Mas.
45	23463883	Thereby, ACE2 regulates the local actions of the RAS in cardiovascular tissues and the ACE2/Ang-(1–7)/Mas axis exerts protective actions in hypertension, diabetes, and other cardiovascular disorders.
46	23463883	ACE2, angiotensin-(1–7), and Mas: the other side of the coin.
47	23463883	The renin–angiotensin system (RAS) has recently been extended by the addition of a novel axis consisting of the angiotensin-converting enzyme 2 (ACE2), the heptapeptide angiotensin (1–7) (Ang-(1–7)), and the G protein-coupled receptor Mas.
48	23463883	ACE2 converts the vasoconstrictive and pro-oxidative peptide angiotensin II (Ang II) into Ang-(1–7) which exerts vasodilatory and antioxidative effects via its receptor Mas.
49	23463883	Thereby, ACE2 regulates the local actions of the RAS in cardiovascular tissues and the ACE2/Ang-(1–7)/Mas axis exerts protective actions in hypertension, diabetes, and other cardiovascular disorders.
50	23463883	ACE2, angiotensin-(1–7), and Mas: the other side of the coin.
51	23463883	The renin–angiotensin system (RAS) has recently been extended by the addition of a novel axis consisting of the angiotensin-converting enzyme 2 (ACE2), the heptapeptide angiotensin (1–7) (Ang-(1–7)), and the G protein-coupled receptor Mas.
52	23463883	ACE2 converts the vasoconstrictive and pro-oxidative peptide angiotensin II (Ang II) into Ang-(1–7) which exerts vasodilatory and antioxidative effects via its receptor Mas.
53	23463883	Thereby, ACE2 regulates the local actions of the RAS in cardiovascular tissues and the ACE2/Ang-(1–7)/Mas axis exerts protective actions in hypertension, diabetes, and other cardiovascular disorders.
54	23463883	ACE2, angiotensin-(1–7), and Mas: the other side of the coin.
55	23463883	The renin–angiotensin system (RAS) has recently been extended by the addition of a novel axis consisting of the angiotensin-converting enzyme 2 (ACE2), the heptapeptide angiotensin (1–7) (Ang-(1–7)), and the G protein-coupled receptor Mas.
56	23463883	ACE2 converts the vasoconstrictive and pro-oxidative peptide angiotensin II (Ang II) into Ang-(1–7) which exerts vasodilatory and antioxidative effects via its receptor Mas.
57	23463883	Thereby, ACE2 regulates the local actions of the RAS in cardiovascular tissues and the ACE2/Ang-(1–7)/Mas axis exerts protective actions in hypertension, diabetes, and other cardiovascular disorders.