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Molecular Control of Melanogenesis in Malignant Melanoma: Functional Assessment of Tyrosinase and Lamp Gene Families by UV Exposure and Gene Co‐Transfection, and Cloning of a cDNA Encoding Calnexin, A Possible Melanogenesis “Chaperone”
Author(s) -
Jimbow Kowichi,
Hara Hiroyuki,
Vinayagamoorthy Thuraiayah,
Luo Dong,
Dakour Jamal,
Yamada Koji,
Dixon Walter,
Chen Hua
Publication year - 1994
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/j.1346-8138.1994.tb03309.x
Subject(s) - tyrosinase , calnexin , gene , biology , gene family , transfection , microbiology and biotechnology , complementary dna , genetics , gene expression , calreticulin , biochemistry , endoplasmic reticulum , enzyme
Abstract Melanogenesis is a cascade of events significantly controlled by regulatory genes which are associated with the melanosomal membrane. This report introduces our current research efforts dealing with (a) the gene and protein expressions of tyrosinase and Lamp (lysosome‐associated membrane protein) families by human melanoma cells after repeated exposures to UV light, (b) the coordinated alterations in the expression of the Lamp family gene and its encoding product after transfection of two genes of the tyrosinase family in human melanoma cells and (c) cloning and sequencing of a Ca 2+ ‐binding phosphoprotein, calnexin, which could be a candidate as a chaperone for sorting and maturation of tyrosinase and Lamp family glycoproteins in melanogenesis cascade. Our UV exposure study, as well as gene transfection and antisense hybridization experiments, has clearly indicated a marked and coordinated interaction of the Lamp‐1 gene with the tyrosinase and TRP‐1 genes in this process. We propose that melanogenesis is controlled at least by two major gene family products, i.e. , (a) the tyrosinase family of tyrosinase, TRP‐1 and TRP‐2, and the Lamp family of Lamp‐1, Lamp‐2 and Lamp‐3. These two gene families probably derived from primordial melanogenesis‐associated genes which are common or closely related to each other.