Gap junctions and ACTH sensitivity in Y-1 adrenal tumor cells.
Initial studies of adrenocorticotropin-sensitivity (ACTH-sensitive) and ACTH-insensitive Y-1 adrenal cortical tumor cell lines suggest a relationship between responsiveness to ACTH and the presence of gap junctions. An ACTH-sensitive clone of Y-1 cells possesses gap junctions and these junctions appear to enlarge with ACTH treatment. GAP junctions have not been observed, however, in an ACTH-insensitive clone of Y-1 tumor cells even when stimulated to produce cyclic adenosine monophosphate and steroids with cholera toxin.
D000310:Adrenal Gland Neoplasms; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D002460:Cell Line; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology; D002772:Cholera Toxin / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism; D005614:Freeze Fracturing; D007365:Intercellular Junctions / Q000502:physiology*; D007700:Kinetics; D051379:Mice; D008855:Microscopy, Electron, Scanning
D000324:Adrenocorticotropic Hormone; D002772:Cholera Toxin; D000242:Cyclic AMP