Mammalian uncoordinated-18-3 (Munc-18-3) (also known as Munc-18c, syntaxin-binding protein 3, STXBP3) is ubiquitously expressed.
Immunogen
synthetic peptide corresponding to amino acids 578-592 located at the C-terminus of mouse Munc-18-3, conjugated to KLH. This sequence is highly conserved (~90% identity) in human and rat Munc-18-3.
Application
Anti-Munc-18-3 antibody produced in rabbit has been used in immunohistochemistry and western blotting[1]
Biochem/physiol Actions
Mammalian uncoordinated-18-3 (Munc-18-3) expressed in 3T3-L1 adipocytes has been shown to interact with syntaxin 2 and 4 and to inhibit the binding of syntaxin-4 to vesicle associated membrane protein 2 (VAMP2). Munc-18c has been suggested to play a role in the docking/fusion of glucose transporter type 4 (GLUT4)-containing vesicles with the cell membrane of 3T3-L1 adipocytes. Heterozygous knock-out of the Munc-18c gene in mice impairs insulin-stimulated GLUT4 translocation in skeletal muscle and increases the susceptibility for severe glucose intolerance.
Munc-18-3 has a role in glucose metabolism and is involved in controlling the translocation of glucose transporter type 4 (GLUT4) in adipocytes.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
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Protein expression of PKCZ (Protein Kinase C Zeta), Munc18c, and Syntaxin-4 in the insulin pathway in endometria of patients with polycystic ovary syndrome (PCOS
<BIG>Rivero R, et al</BIG>
Reproductive Biology and Endocrinology, 10, 17-17 (2012)
Munc18c is associated with glucose metabolism and could play a relevant role in obesity. However, little is known about the regulation of Munc18c expression. We analyzed Munc18c gene expression in human visceral (VAT) and subcutaneous (SAT) adipose tissue and its
Munc18c heterozygous knockout mice display increased susceptibility for severe glucose intolerance
Reproductive biology and endocrinology : RB&E, 10, 17-17 (2012-03-07)
Polycystic Ovary Syndrome (PCOS) is an endocrine-metabolic disorder commonly associated with insulin resistance (IR). Previous studies indicate about the expression of molecules involved in the insulin pathway in endometria of women with PCOS-IR. Therefore, the aim of the present study
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