Macrophage Stimulating 1 (Hepatocyte Growth Factor-Like) (MST1) Kits ELISA

Human Macrophage Stimulating 1 (Hepatocyte Growth Factor-Like) (MST1) interaction partners

1. Our analysis suggests that MST1 might interact with key susceptibility genes involved in autophagy and bacterial recognition. These findings provide insight into the genetic architecture of Crohn's disease in Chinese and may partially explain the disparity of genetic signals in Crohn's disease susceptibility across different ethnic populations by highlighting the contribution of gene-gene interactions.

2. Mst1 overexpression inhibits mitophagy activity via suppressing the ERK-Mfn2 pathway, ultimately augmenting IL-24-inducd esophageal cancer death via enhanced mitochondrial stress.

3. Legionella pneumophila effector protein LegK7(lpg1924) hijacks the conserved Hippo signaling pathway by molecularly mimicking host Hippo kinase (MST1 in mammals), which is the key regulator of pathway activation.

4. Mst1 has an important role in inhibiting the growth of NSCLC in vitro and in vivo; its antiproliferative effect is associated with induction of apoptosis.

5. These data suggest that MSP is an effective inhibitor of inflammation and lipid accumulation in the stressed liver, thereby indicating that MSP has a key regulatory role in non-alcoholic steatohepatitis.

6. Identify MST1/MSP as a mitogen for tracheal basal cells.

7. MSP appears to promote the migration of fibroblasts, enhances collagen synthesis and remodeling, and effectively improves wound healing.

8. Elevated serum levels of MST1 were found in subjects with excessive alcohol use.

9. These results support the hypothesis that the alpha-chain of MSPalphabeta mediates RON dimerization.

10. functional consequences of the macrophage stimulating protein 689C inflammatory bowel disease risk allele

11. Results suggest that the [AA] genotype of the common MST1 variant rs3197999 enhances genetic risk of sporadic extrahepatic cholangiocarcinoma irrespective of primary sclerosing cholangitis status.

12. MSP may be one of the major determinants that affects the properties of tumor stroma and that produces a permissive microenvironment to promote cancer metastasis

13. The present results refine the known genetic architecture in primary sclerosing cholangitis by confirming MST1 locus association.

14. the missense SNP impairs MSP function by reducing its affinity to RON and perhaps through a secondary effect on in vivo concentration arising from reduced thermodynamic stability, resulting in down-regulation of the MSP/RON signaling pathway.

15. HAT cleaves proMSP at the physiological activation site

16. Studies indicate that the cylindromatosis/turban tumor syndrome gene (CYLD) ranked highest, followed by acylaminoacyl-peptidase (APEH), dystroglycan (DAG1), macrophage-stimulating protein (MST1) and ubiquitin-specific peptidase 4 (USP4).

17. These findings suggest that the MSP/RON signaling pathway may be regulated by hepsin in tissue homeostasis and in disease pathologies, such as in cancer and immune disorders.

18. considerable number of Merkel cell carcinoma cases expressed both RON and MSP, while Merkel cells do not express these molecules

19. MSP-induced RSK2 activation is a critical determinant linking RON signaling to cellular EMT program.

20. the oncogenic effect of BRAF(V600E) is associated with the inhibition of MST1 tumor suppressor pathways, and that the activity of RASSF1A-MST1-FoxO3 pathways determines the phenotypes of BRAF(V600E) tumors.

Mouse (Murine) Macrophage Stimulating 1 (Hepatocyte Growth Factor-Like) (MST1) interaction partners

1. this study confirms that melatonin rescues the impaired mitophagy activity of diabetic cardiomyopathy . The underlying mechanism may be attributed to activation of Parkin translocation via inhibition of Mst

2. our results implicate Mst1 upregulation as a critical step in exacerbating HFD-mediated hepatic injury. Increased Mst1 blocks the AMPK pathway and thus diminishes Parkin expression, repressing mitophagy and consequently activating mitochondrial apoptosis in HFD-treated livers.

3. data revealed that OSM alleviated postinfarction cardiac remodeling and dysfunction by enhancing cardiomyocyte autophagy. OSM holds promise as a therapeutic target in treating HF after MI through Obeta receptor by inhibiting Mst1 phosphorylation.

4. The results identify Mst1 as a malefactor in the development of post-infarction cardiac injury and that it acts through the JNK-Drp1-mitochondrial fission pathway.

5. The results suggest that melatonin alleviates cardiac remodeling and dysfunction in diabetic cardiomyopathy by upregulating autophagy, limiting apoptosis, and modulating mitochondrial integrity and biogenesis. The mechanisms are associated with Mst1/Sirt3 signaling.

6. These data suggest that MSP is an effective inhibitor of inflammation and lipid accumulation in the stressed liver, thereby indicating that MSP has a key regulatory role in non-alcoholic steatohepatitis.

7. kinases, including Slk, Lok and Mst1, are inhibited by BI-D1870 but to a much lesser extent by BIX 02565 and that phosphorylation of some of their substrates is blocked by BI-D1870 in living cells.

8. Nicorandil alleviates post-MI cardiac dysfunction and remodeling. The mechanisms were associated with enhancing autophagy and inhibiting apoptosis through Mst1 inhibition.

9. Using a standard two-thirds partial hepatectomy (PH) model in young and aged mice, the activity of the core kinases MST1 and LATS1 increased during the early hypertrophic phase and returned to steady state levels in the proliferative phase, coinciding with activation of YAP1 target genes and hepatocyte proliferation.

10. The MST1 acts as a molecular brake to maintain immune tolerance by regulating T cell-mediated B cell activation.

11. Mst1 knockout alleviated while Mst1 overexpression aggravated cardiac dysfunction in diabetes.

12. these findings highlight a role for MST1 in vesicle trafficking and extravasation in neutrophils, providing an additional mechanistic explanation for the severe immune defect

13. Results identify L-plastin as a key effector of Mst1 and establish a novel mechanism linking a signaling intermediate to an actin-binding protein critical to T cell migration.

14. MIST1 is a scaling factor necessary and sufficient by itself to induce and maintain secretory cell architecture

15. Mst1 deficiency diminishes atherosclerosis and stabilizes atherosclerotic plaques in ApoE(-/-) mice. Mst1 may participate in atherosclerosis progression through inhibition of macrophage autophagy and promotion of macrophage apoptosis.

16. These results suggest that melatonin alleviates postinfarction cardiac remodeling and dysfunction by upregulating autophagy, decreasing apoptosis, and modulating mitochondrial integrity and biogenesis. The attributed mechanism involved, at least in part, Mst1/Sirt1 signaling

17. TRAF2 functions as a key activator of MST1 in oxidative stress-induced intracellular signaling processes.

18. Mst1 regulates hepatic lipid metabolism by inhibiting Sirt1 ubiquitination in mice.

19. Mst1 enhances Foxp3 expression and Treg function at the post-translational level.

20. our study demonstrates the existence of a direct crosstalk between mTORC2 and MST1 that is critical for cardiac cell survival and growth.