Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.1 (adenylate cyclase)
 19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several studies suggest that beta-carotene reduces the risk of some cancers. Except for its function as an antioxidant, the effect of this vitamin on mammalian cells remains poorly defined. This study was performed to show whether beta-carotene treatment of murine B-16 melanoma cells in culture induces differentiation and alters the adenylate cyclase (AC) system. The AC system mediates the action of agents which regulate cell differentiation and transformation. Results showed that beta-carotene treatment for a period of 24 hours or more caused morphological differentiation without changing the level of melanin, and reduced basal and melanocyte-stimulated hormone (MSH)-, sodium fluoride (NaF)-, and forskolin-stimulated AC activity in vitro. Retinol, a metabolite of beta-carotene, inhibited growth without morphological differentiation and reduced basal and MSH- and NaF-stimulated AC activity. However, butylated hydroxyanisole, a lipid-soluble antioxidant, also reduced growth without morphological differentiation, but it failed to alter basal or MSH-stimulated AC activity. The present and previous studies show that the AC system represents a common site where some antitumor-promoting vitamins (beta-carotene, retinol, retinoic acid, and alpha-tocopheryl succinate) act.
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PMID:Beta-carotene induces morphological differentiation and decreases adenylate cyclase activity in melanoma cells in culture. 233 63

Retinol binding protein (RBP) is the primary circulating transport molecule for retinol, facilitating its transport to target tissues and influencing target cell uptake. Specific signals and molecular mechanisms that regulate RBP gene expression are poorly understood. Using the mouse hepatoma cell line (Hepa 1-6), we examined the role of cAMP in the molecular regulation of RBP. Dibutyryl cAMP (dbcAMP) or the adenylate cyclase activator, forskolin, increased RBP mRNA levels >6-fold at 24 h. Increases in RBP mRNA were dose dependent over the range of 10 microM-1 mM for dbcAMP and 0.5-10 microM for forskolin. 8-Bromo cAMP, a nonhydrolyzable analog, over the range of 0.01-0.5 mM, increased RBP mRNA levels 9.2-fold at 24 h. Induction of RBP transcripts by analogs also resulted in a comparable increase in intracellular RBP protein. Cycloheximide (10 microgram/ml) did not prevent cAMP-mediated induction of RBP mRNA, indicating that de novo protein synthesis is not required for cAMP-mediated induction of RBP transcription. These studies demonstrate that cAMP, or agents which elevate intracellular cAMP, increase RBP transcript levels. The time course and extent of RBP mRNA induction and the resultant increase in RBP protein support the concept that cAMP regulation of RBP gene expression may be physiologically relevent. Given the ubiquitous nature of cAMP as a second messenger, and the several mechanisms by which cAMP regulates gene expression, studies are in progress to define molecular mechanisms by which cAMP regulates RBP gene expression.
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PMID:Induction of mouse retinol binding protein gene expression by cyclic AMP in Hepa 1-6 cells. 972 Nov 91