ML-SA1 is an activator of TRPML1-3. It induces TRPML-mediated Ca2+ release from lysosomes.
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HazMat fee for 500 gram (Estimated)
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The TRPML channels (TRPML1, TRPML2, and TRPML3), belonging to the mucolipin TRP subfamily, primary localize to a population of membrane-bonded vesicles along the endocytosis, and exocytosis pathways. Human viruses enter host cells by plasma membrane penetration or by receptor-mediated endocytosis. TRPML2 enhances the infectivity of a number of enveloped viruses by promoting virus vesicular trafficking and escape from endosomal compartment. TRPML2 expression is stimulated by interferon and by several toll like receptor (TLR) activators, suggesting a possible role in the activation of the innate immune response[1]. ML-SA1, as a selective TRPML agonist, inhibits Dengue virus 2 (DENV2) and Zika virus (ZIKV) by promoting lysosomal acidification and protease activity. The IC50 value of ML-SA1 against DENV2 RNA and ZIKV RNA is 8.3 μM and 52.99 μM, respectively. ML-SA1 can be used for the research of broad-spectrum antiviral. ML-SA1 (25 μM; 0~14 hours; A549 cells) possibly affects the entry of DENV2 into host cells. ML-SA1 (0~200 μM; A549 cells) shows that there is no cytotoxicity to the cell line observed, even at concentrations up to 200 μM. ML-SA1 (0~50 μM; A549 cells) significantly suppresses DENV2 at the RNA levels and the IC50 is 8.93 μM. ML-SA1 results in a dose-dependent decrease in ZIKV in A549 cells at both the RNA and protein levels, and the IC50 value of ML-SA1 against ZIKV RNA is 52.99 μM. ML-SA1, as an activator of TRPMLs, appears to be a potent inhibitor of DENV2 and ZIKV in vitro. ML-SA1 can induce autophagy in Huh7 cells or A549 cells[2]. ML-SA1 blocked LDL-induced increases in intraneuronal and secreted levels of Aβ as well as Aβ accumulation in endolysosomes, prevented BACE1 accumulation in endolysosomes, and decreased BACE1 activity levels. LDL downregulated TRPML1 protein levels, and TRPML1 knockdown worsens LDL-induced increases in Aβ Liang Hui,et al..
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