Browse our anti-PPP1R12A (PPP1R12A) Antibodies

Mouse (Murine) Myosin Phosphatase, Target Subunit 1 (PPP1R12A) interaction partners

1. The findings define the PI3K/NUAK1/MYPT1/MLCP axis as a critical pathway to regulate actomyosin contractility in endothelial cells, supporting vascular patterning and expansion through the control of cell rearrangement.

2. Mypt1 E24 splice variants tune arterial reactivity and could be worthy targets for lowering vascular resistance in disease states.

3. revealed the presence of two MYPT1 isoforms, full length and variant 2 in human intestinal (Caco-2) epithelial cells and isolated intestinal epithelial cells from mice

4. phosphorylation of MYPT1 T694, but not T852, mediates force maintenance in bladder smooth muscle.

5. Constitutive phosphorylation of myosin phosphatase targeting subunit-1 in smooth muscle

6. Maturation of mesenteric artery smooth muscle involves TRA2beta mediated Mypt1 exon 24 splicing.

7. The role of MYPT1 in vascular smooth muscle was investigated in adult MYPT1 smooth muscle specific knock-out mice. MYPT1 deletion enhanced phosphorylation of myosin regulatory light chain and contractile force in isolated mesenteric arteries.

8. MYPT1 is not essential for smooth muscle function in mice but regulates the Ca(2+) sensitivity of force development and contributes to intestinal phasic contractile phenotype.

9. Tra2beta, by regulating the splicing of Mypt1 E23, sets the sensitivity of smooth muscle to cGMP-mediated relaxation.

10. Organ-specific mechanisms involving MYPT1, M-RIP, and CPI-17 are critical to regulating basal LC20 phosphorylation in gastrointestinal smooth muscles.

11. Findings define a new conserved pathway in which sexual development and pregnancy mediate smooth and striated muscle adaptations through SMTNL1 and MYPT1.

12. a reduction in the protein level of MYPT1 (LZ+) is involved in nitrate tolerance; this may result in part from a proteasome-dependent degradation of MYPT1 (LZ+)

13. Stable transfection of HEK 293 cells with GFP-MYPT1 was obtained. MYPT1 and its N-terminal mutants bound to retinoblastoma protein (Rb), raising the possibility that Rb is implicated in the effects caused by overexpression of MYPT1.

14. Ca(2+)-independent relaxation by urocortin can be attributed to cAMP-mediated increased activity of SMPP-1M which is partly attributable to decrease in inhibitory phosphorylation of MYPT1.

15. Therefore, our results show that preservation of GLUT4 expression prevents enhanced arterial reactivity in hypertension, possibly via effects on myosin phosphatase activity.

16. both eEF1A and MYPT1 have roles in EGCG signaling for cancer prevention through 67LR

17. MYPT1 and CARM1 are substrates of OGT and function to alter OGT substrate specificity in vitro

Human Myosin Phosphatase, Target Subunit 1 (PPP1R12A) interaction partners

1. MYPT1 knockdown by siRNAs reproduced miR-145 effects suggesting miR-145 as a tumor suppressor through MYPT1 targeting.

2. PP2A dephosphorylates MYPT1(pThr696) and thereby stimulates MP activity inducing dephosphorylation of eNOS(pThr497) and the 20 kDa myosin II light chains.

3. These results indicate shear stress induced vascular smooth muscle cell contraction was mediated by cell surface glycocalyx via a ROCK-MLC phosphatase (MLCP) pathway, providing evidence of the glycocalyx mechanotransduction in myogenic response.

4. he phosphorylation of the MP inhibitory MYPT1(T850) and the regulatory PRMT5(T80) residues as well as the symmetric dimethylation of H2A/4 were elevated in human hepatocellular carcinoma and in other types of cancers.

5. Results indicated that MYPT1 was down-regulated in GC tissues and cells, and is related to clinical stages and overall survival of GC. Functional research demonstrated that overexpression of MYPT1 can inhibit cell proliferation, cell cycle progression, and migration and invasion of GC cells.

6. Thus, Cyclin A/Cdk1 phosphorylation primes MYPT1 for Plk1 binding. These data demonstrate cross-regulation between Cyclin A/Cdk1-dependent and Plk1-dependent phosphorylation of substrates during mitosis to ensure efficient correction of kinetochore microtubule attachment errors necessary for high mitotic fidelity.

7. NO-induced cGMP signaling modulated RhoA/ROCK signaling in platelets, leading to the disinhibition of MLCP to control the phosphorylation of MLC and remodeling of platelet actin cytoskeleton.

8. The authors call the mutual sequestration mechanism through which pCPI-17 and myosin light-chain phosphatase interact inhibition by unfair competition: myosin light-chain phosphatase protects pCPI-17 from other phosphatases, while pCPI-17 blocks other substrates from the active site of myosin light-chain phosphatase.

9. Myosin light chain phosphatase (MLCP) is a master regulator of smooth muscle responsiveness to stimuli. (review)

10. BLT2 ligation facilitates F-actin assembly with the upregulated phosphorylation of MYPT1.

11. Lipolysis-stimulated lipoprotein receptors (LSRs) localized to bicellular junctions in association with myosin regulatory light chain 2 (MRLC2) at low cell densities and to tricellular contacts when myosin phosphatase target subunit 1 (MYPT1) localized to the bicellular regions.

12. miR-30d and/or its target gene MYPT1 may serve as novel prognostic markers of PCa. miR-30d promotes tumor angiogenesis of PCa through MYPT1/c-JUN/VEGFA pathway.

13. Study revealed the presence of two MYPT1 isoforms, full length and variant 2 in human intestinal (Caco-2) epithelial cells and isolated intestinal epithelial cells from mice.

14. These results indicate that PPP1R12A indeed plays a role in skeletal muscle insulin signaling

15. the relative expression of LZ+/LZ- MYPT1 isoforms, in part, defines the vascular response to NO and NO based vasodilators, and therefore, plays a role in the regulation of vascular tone in both health and disease

16. Expression of NUAK1 is controlled by cyclin-dependent kinase, PLK1, and the SCFbetaTrCP (Skp, Cullin and F-boxbetaTrCP) E3 ubiquitin ligase complex.

17. distinct roles of two inhibitory phosphorylation sites of MYPT1

18. in apoptotic cells, the myosin-binding domain of myosin phosphatase targeting subunit 1 is cleaved by caspase-3, and the cleaved MYPT1 is strongly phosphorylated at Thr-696 and Thr-853, phosphorylation of which is known to inhibit myosin II binding

19. results suggested that during atherosclerosis progression oxidative stress mediates the downregulation of MYPT1, which may inhibit smooth muscle cell migration and contribute to the aberrant contractility

20. Calcineurin may modulate the phosphorylation level of MLC20 by influencing the phosphorylation state of MYPT1 to regulate endothelial barrier function.