MSH receptors and function in amelanotic B16 melanoma cells.

摘要: The possible mechanisms for the reduced melanin content and poor melanogenic response to MSH was investigated in B16-F10DD differentiation deficient melanoma cells. In particular, receptor status associated signal transduction pathway linking tyrosinase activity these cells studied evidence of any defects. F10DD contained high-affinity binding sites alpha-MSH, with KD values similar those previously reported other variants B16 melanoma. SDS-PAGE analysis after radioactive ligand cross-linking showed no gross structural alterations receptor. expressed approximately twice as many receptors F10 parent cell line, suggesting a feedback attempting compensate amelanotic condition. functional integrity confirmed by presence increased levels cAMP stimulation. These results, coupled observation that express mRNA protein, point defect or post-translational control which this enzyme is regulated.