| 1988 |
MAS1 (yeast) encodes the smaller 48 kDa subunit of the mitochondrial processing protease (MPP), a metalloprotease localized in the mitochondrial matrix that cleaves amino-terminal targeting sequences from imported mitochondrial precursor proteins. The MAS1 protein participates in its own cleavage during import into mitochondria. |
Genetic cloning and sequencing of MAS1, temperature-sensitive mutant analysis, in vitro protease activity assay, mitochondrial fractionation |
The EMBO journal |
High |
2905264 3044780
|
| 1988 |
The mitochondrial processing protease consists of two non-identical, loosely associated subunits encoded by MAS1 (48 kDa) and MAS2 (51 kDa); attempts to separate the subunits caused loss of enzymatic activity, indicating both subunits are required for catalytic function. |
Protein purification of the MPP complex, subunit identification by SDS-PAGE, activity assay after fractionation |
The EMBO journal |
High |
2905264 3061808
|
| 2017 |
In Candida albicans, Mas1 (ortholog of yeast MAS1) interacts physically with the Hsp40 chaperone Ydj1; loss of MAS1 or YDJ1 perturbs mitochondrial morphology and function, and deletion of YDJ1 impairs import of Su9, a protein cleaved to its mature form by Mas1/Mas2, placing Mas1 downstream of Ydj1 in the mitochondrial protein import pathway. |
Co-immunoprecipitation/mass spectrometry protein interaction mapping, deletion mutant analysis, mitochondrial import assay with Su9 substrate, microscopy of mitochondrial morphology |
Microbial cell (Graz, Austria) |
Medium |
29082232
|
| 2012 |
Angiotensin-(1-7) acting through the MAS1 receptor (mammalian) attenuates allergic airway inflammation by suppressing phosphorylation of ERK1/2 and IκB-α; these effects were reversed by the selective MAS1 antagonist A779, establishing MAS1 as a required mediator of Ang-(1-7) anti-inflammatory signaling. |
Murine ovalbumin asthma model, pharmacological MAS1 antagonism with A779, Western blot for pERK1/2 and pIκB-α, bronchoalveolar lavage cell counts, histology |
British journal of pharmacology |
Medium |
22339213
|
| 2017 |
MAS1 receptor (mammalian) internalization after agonist stimulation occurs through both clathrin-coated pits and caveolae in a dynamin-dependent manner; internalized receptor traffics to Rab11-positive slow recycling endosomes rather than lysosomes. ERK1/2 activation by Ang-(1-7) requires β-arrestin2 and proceeds from early endosomes, whereas Akt activation from endosomes is β-arrestin2-independent. |
Live-cell imaging of MAS1R-YFP, ligand-binding internalization assay, dominant-negative constructs for Eps15, dynamin, shRNA knockdown of caveolin-1 and β-arrestin2, co-localization with Rab4, Rab11, LysoTracker, Western blot for pERK1/2 and pAkt |
Hypertension |
High |
28874464
|
| 2017 |
Low-dose Ang-(1-7) acting through the MAS1 receptor promotes angiogenesis and vasodilation in rat microvascular endothelial cells; downstream signaling components identified include Rho GTPases, PI3K, protein kinase D1, MAPK, and ERK1/2. Pharmacological inhibition of ERK1/2 and p38 MAPK blocked both endothelial tube formation and vasodilation. |
In vitro endothelial tube formation assay, pharmacological inhibition of ERK1/2/p38, proteomics and genomics downstream pathway mapping, MAS1 receptor antagonism |
Arteriosclerosis, thrombosis, and vascular biology |
Medium |
28082260
|
| 2018 |
Small molecule MAS1 agonists activate multiple G protein-dependent (Gq, Gi, GTPγS binding) and independent (β-arrestin recruitment, ERK1/2 phosphorylation, Akt phosphorylation, arachidonic acid release, receptor internalization) signaling pathways through recombinant MAS1. In contrast, Ang-(1-7) failed to induce or block signaling in any of these platforms at recombinant MAS1, and radiolabeled Ang-(1-7) showed no specific binding to recombinant MAS1 (negative result). Ang-(1-7) potently inhibited both phases of AT1R-mediated Ang II signaling in rat aortic endothelial cells. |
Recombinant MAS1 overexpression in HEK cells, GTPγS binding assay, β-arrestin recruitment assay, Erk1/2 and Akt phosphorylation assay, arachidonic acid release assay, dynamic mass redistribution (DMR) pathway-agnostic assay, radioligand binding assay |
Cellular signalling |
High |
29928987
|
| 2019 |
The Ang-(1-7)/MAS1 receptor axis mediates anti-inflammatory effects in allergic asthma at least in part by inhibiting Src kinase-dependent transactivation of EGFR and downstream ERK1/2 phosphorylation; Ang-(1-7) also directly inhibited neutrophil and eosinophil chemotaxis ex vivo, and all effects were reversed by A779 MAS1 antagonism. |
Murine OVA asthma model, Western blot for phospho-Src, phospho-EGFR, phospho-ERK1/2, A779 MAS1 antagonist, ex vivo chemotaxis assay |
PloS one |
Medium |
31675376
|
| 2020 |
AT1R (AT1RA) physically interacts with MAS1 receptor and is required for the pro-angiogenic signaling of Ang-(1-7) through MAS1; AT1RA knockout in Dahl salt-sensitive rats impaired Ang-(1-7)-mediated skeletal muscle angiogenesis, endothelial tube formation, and altered the protein complex formed upon Ang-(1-7) binding to Mas1 as shown by tandem mass spectrometry proteomics. |
AT1RA knockout rat model, hindlimb angiogenesis assay, in vitro endothelial tube formation, tandem mass spectrometry proteomics of Mas1-associated protein complex |
PloS one |
Medium |
32324784
|
| 2022 |
MAS1 overexpression in cardiomyocytes (H9C2 cells and MI rat model) decreased PTEN expression and enhanced phosphorylation of PI3K and AKT; the cardioprotective effect of MAS1 was reversed by PTEN overexpression or PI3K inhibitor LY294002, placing MAS1 upstream of the PTEN/PI3K/AKT pathway in cardiomyocyte survival signaling. |
MAS1 overexpression in H9C2 cells and rat MI model, Western blot for PTEN, p-PI3K, p-AKT, pharmacological inhibition with LY294002, PTEN overexpression rescue experiment, cardiomyocyte apoptosis assay |
International journal of biological macromolecules |
Medium |
35247425
|
| 2022 |
In pancreatic β-cells (RINm5F), Ang-(1-7) activation of MAS-1 induces intracellular cAMP increase and CREB activation, upregulates CFTR expression, and potentiates glucose-stimulated insulin secretion; MAS-1 inhibition or CFTR RNAi knockdown abolished these effects, placing MAS1 upstream of cAMP/CREB/CFTR in β-cell insulin secretion. |
RINm5F cell pharmacology with selective MAS-1 inhibitor, RNAi knockdown of CFTR and MAS-1, cAMP measurement, Western blot for CREB activation, insulin ELISA |
Endocrine connections |
Medium |
34825893
|
| 2025 |
In a pulmonary arterial hypertension (PAH) mouse model, ACE2 therapeutic effect is blocked in Mas1 knockout mice, establishing Mas1 as necessary for ACE2 action. The small-molecule Mas1 agonist AR234960 reproduces the ACE2 effect (sufficient). However, stabilized Ang-(1-7) failed to reproduce ACE2 effectiveness, indicating Ang-(1-7) alone does not activate Mas1 in this context. RNA-seq identified rescue of cytoskeletal and microtubule gene defects as key downstream mechanisms. |
Mas1 knockout mouse, PAH animal model, pharmacological Mas1 agonist AR234960, stabilized Ang-(1-7) treatment, RNA-seq downstream pathway analysis |
Pulmonary circulation |
Medium |
40248213
|
| 2026 |
Cryo-EM structures of MAS1 (class A GPCR) bound to neuropeptide FF (NPFF) and small-molecule agonist AR234958 in complex with inhibitory G proteins reveal a conserved orthosteric binding pocket. MAS1 uses a non-canonical activation mechanism driven by ligand-induced hydrophobic compression involving residues Y248(6.55), L87(2.60), I84(2.57), and L266(7.39), transmitting mechanical tension to displace TM6 for G protein coupling rather than the canonical W6.48 toggle switch. Functional mutagenesis identified M244(6.51) and F237(6.44) on TM6 as critical molecular switches. |
Cryo-EM structure determination, functional mutagenesis of active-site residues, G protein coupling assay, comparative structural analysis with MRGPRX1-X4 |
The EMBO journal |
High |
41912627
|
| 2025 |
Human CXCL17 activates MAS1 (among 10 human MRGPRs tested) at micromolar concentrations as measured by β-arrestin recruitment and chemotaxis of MAS1-transfected HEK293T cells; removal of the C-terminal fragment of CXCL17 did not affect MAS1 activation, indicating a mechanism distinct from GPR25 activation. |
NanoBiT-based β-arrestin recruitment assay in transfected HEK293T cells, chemotaxis assay, C-terminal deletion mutant of CXCL17 |
bioRxivpreprint |
Low |
|
| 2024 |
Overexpression of Mas1 in mammary epithelial cells (EpH4 EV) reversed LPS-induced activation of NF-κB/MAPK signaling pathways and suppressed pro-inflammatory mediators; conversely, siRNA silencing of Mas1 enhanced LPS-induced inflammatory responses. Mas1 overexpression also reversed LPS-induced downregulation of tight junction proteins ZO-1, Occludin, and Claudin-3. |
Gene overexpression and siRNA knockdown in EpH4 EV cells, Western blot for NF-κB/MAPK pathway components and tight junction proteins, ELISA for inflammatory mediators |
Frontiers in veterinary science |
Medium |
39071779
|