3T3-L1-adipocytes produce the adipocyte complement related protein of 30 kD (Acrp30), which is also designated as AdipoQ. In order to study the expression and secretion of the human homologue of this protein, apM1 (adipose Most abundant gene transcript 1, also named gelatin-binding protein of 28 kD [GBP28] or adiponectin), a polyclonal antibody was produced. Both expression and secretion can be detected beginning with day 4 after induction of differentiation. The amount of expressed apM1 correlates with the specific activity of the differentiation marker glycerol-3-phosphate dehydrogenase. Secretion of apM1 is increased by the addition of ionomycin. Both the nonhydrolysable dibutyryl-cycloAMP and tumour necrosis factor alpha reduce the expression and secretion of apM1.
Background-Surgical resection is the only curative treatment for patients with pheochromocytomas, paragangliomas, and other catecholamine-producing tumors. Activation of glycogen synthase kinase 3β (GSK3β) is thought to promote tumor growth and neuroendocrine (NE) peptide secretion in NE tumors. Thus, we hypothesized that inhibition of this signaling pathway with lithium chloride (LiCl), a well-known GSK3β inhibitor, could be a potential therapeutic strategy to control tumor growth and hormone production.
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