Differentiation-defective mutants of mouse embryonal carcinoma cells: response to hexamethylenebisacetamide and retinoic acid.
We have generated by mutagenesis eight differentiation-defective sublines from three murine embryonal carcinoma (EC) cell lines. These mutants grossly resemble parental cells in the absence of inducers of differentiation. Based upon response to retinoic acid (RA) or hexamethylenebisacetamide (HMBA), the mutants can be grouped into three types: (a) RA-selected cells that lack cellular RA binding protein (cRABP) activity and fail to differentiate in response to RA or HMBA; (b) RA- or HMBA-selected cells that possess cRABP but differentiate poorly, if at all, in the presence of RA or HMBA; and (c) cells originally selected for lack of response to HMBA but which retain cRABP and the ability to differentiate in response to RA.
D000081:Acetamides / Q000494:pharmacology*; D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism; D002454:Cell Differentiation / Q000187:drug effects*; D002460:Cell Line; D051379:Mice; D009154:Mutation; D010960:Plasminogen Activators / Q000378:metabolism; D018168:Receptors, Retinoic Acid; D013724:Teratoma / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D014212:Tretinoin / Q000494:pharmacology*
D000081:Acetamides; D002352:Carrier Proteins; D018168:Receptors, Retinoic Acid; D014212:Tretinoin; D010960:Plasminogen Activators; C014026:hexamethylene bisacetamide