Pink-eyed dilution protein controls the processing of tyrosinase.
暂无分享,去创建一个
[1] B. Westerink,et al. UvA-DARE ( Digital Academic Repository ) Glycosphingolipids are required for sorting melanosomal proteins in the Golgi complex , 2001 .
[2] S. Orlow,et al. Inverse correlation between pink-eyed dilution protein expression and induction of melanogenesis by bafilomycin A1. , 2001, Pigment cell research.
[3] S. Orlow,et al. Mislocalization of melanosomal proteins in melanocytes from mice with oculocutaneous albinism type 2. , 2001, Experimental eye research.
[4] R. Halaban,et al. Proper Folding and Endoplasmic Reticulum to Golgi Transport of Tyrosinase Are Induced by Its Substrates, DOPA and Tyrosine* , 2001, The Journal of Biological Chemistry.
[5] M. Brilliant. The mouse p (pink-eyed dilution) and human P genes, oculocutaneous albinism type 2 (OCA2), and melanosomal pH. , 2001, Pigment cell research.
[6] S. Orlow,et al. Intracellular Distribution and Late Endosomal Effects of the Ocular Albinism Type 1 Gene Product: Consequences of Disease‐Causing Mutations and Implications for Melanosome Biogenesis , 2001, Traffic.
[7] G. Raposo,et al. Distinct Protein Sorting and Localization to Premelanosomes, Melanosomes, and Lysosomes in Pigmented Melanocytic Cells✪ , 2001, The Journal of cell biology.
[8] B. Fuller,et al. Regulation of the catalytic activity of preexisting tyrosinase in black and Caucasian human melanocyte cell cultures. , 2001, Experimental cell research.
[9] R. Spritz,et al. The molecular basis of oculocutaneous albinism type 1 (OCA1): sorting failure and degradation of mutant tyrosinases results in a lack of pigmentation. , 2001, The Biochemical journal.
[10] M. Brilliant,et al. Aberrant pH of melanosomes in pink-eyed dilution (p) mutant melanocytes. , 2000, The Journal of investigative dermatology.
[11] R. Halaban,et al. Endoplasmic reticulum retention is a common defect associated with tyrosinase-negative albinism. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[12] M. Marks,et al. A Common Temperature-sensitive Allelic Form of Human Tyrosinase Is Retained in the Endoplasmic Reticulum at the Nonpermissive Temperature* , 2000, The Journal of Biological Chemistry.
[13] R. Dwek,et al. Mutations at Critical N-Glycosylation Sites Reduce Tyrosinase Activity by Altering Folding and Quality Control* , 2000, The Journal of Biological Chemistry.
[14] R. Dwek,et al. Protein specific N-glycosylation of tyrosinase and tyrosinase-related protein-1 in B16 mouse melanoma cells. , 1999, The Biochemical journal.
[15] R. Dwek,et al. Tyrosinase folding and copper loading in vivo: a crucial role for calnexin and alpha-glucosidase II. , 1999, Biochemical and biophysical research communications.
[16] E. Kominami,et al. Analysis of where and which types of proteinases participate in lysosomal proteinase processing using bafilomycin A1 and Helicobacter pylori Vac A toxin. , 1999, Journal of biochemistry.
[17] M. Brilliant,et al. The pink-eyed dilution locus controls the biogenesis of melanosomes and levels of melanosomal proteins in the eye. , 1999, Experimental eye research.
[18] J. Park,et al. Promotion of tyrosinase folding in COS 7 cells by calnexin. , 1999, Journal of biochemistry.
[19] D. Bennett,et al. Normal tyrosine transport and abnormal tyrosinase routing in pink-eyed dilution melanocytes. , 1998, Experimental cell research.
[20] B. Kwon,et al. Melanosomal defects in melanocytes from mice lacking expression of the pink-eyed dilution gene: correction by culture in the presence of excess tyrosine. , 1998, Experimental cell research.
[21] R. Halaban,et al. Aberrant retention of tyrosinase in the endoplasmic reticulum mediates accelerated degradation of the enzyme and contributes to the dedifferentiated phenotype of amelanotic melanoma cells. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[22] R. Spritz,et al. Complementation of hypopigmentation in p-mutant (pink-eyed dilution) mouse melanocytes by normal human P cDNA, and defective complementation by OCA2 mutant sequences. , 1997, The Journal of investigative dermatology.
[23] M. Brilliant,et al. Melanosomal tyrosine transport in normal and pink-eyed dilution murine melanocytes. , 1995, Pigment cell research.
[24] A. Houghton,et al. Intracellular sorting and targeting of melanosomal membrane proteins: identification of signals for sorting of the human brown locus protein, gp75 , 1995, The Journal of cell biology.
[25] S. Orlow,et al. Interaction of melanosomal proteins with melanin. , 1995, European journal of biochemistry.
[26] R. Spritz,et al. Organization and sequence of the human P gene and identification of a new family of transport proteins. , 1995, Genomics.
[27] M. Brilliant,et al. Identification of a melanosomal membrane protein encoded by the pink-eyed dilution (type II oculocutaneous albinism) gene. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[28] S. Orlow,et al. Identification of a melanosomal matrix protein encoded by the murine si (silver) locus using "organelle scanning". , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[29] M. Brilliant,et al. African origin of an intragenic deletion of the human P gene in tyrosinase positive oculocutaneous albinism , 1994, Nature Genetics.
[30] R. Spritz,et al. Mutations of the P gene in oculocutaneous albinism, ocular albinism, and Prader-Willi syndrome plus albinism. , 1994, The New England journal of medicine.
[31] F. Solano,et al. Improved tyrosinase activity stains in polyacrylamide electrophoresis gels. , 1993, Pigment cell research.
[32] R. Spritz,et al. A gene for the mouse pink-eyed dilution locus and for human type II oculocutaneous albinism , 1993, Nature.
[33] M. Farrall,et al. The tyrosinase-positive oculocutaneous albinism locus maps to chromosome 15q11.2-q12. , 1992, American journal of human genetics.
[34] V. Hearing,et al. Tyrosinases from two different loci are expressed by normal and by transformed melanocytes. , 1991, The Journal of biological chemistry.
[35] D. Bennett,et al. Cloned mouse melanocyte lines carrying the germline mutations albino and brown: complementation in culture. , 1989, Development.
[36] R. Lewis,et al. Brown Ocuuiocutaneous Albinism: Clinical, Ophthalmological, and Biochemical Characterization , 1985 .
[37] R. Lewis,et al. Brown oculocutaneous albinism. Clinical, ophthalmological, and biochemical characterization. , 1985, Ophthalmology (Rochester, Minn.).
[38] S. Pomerantz. L-Tyrosine-3, 5-3H Assay for Tyrosinase Development in Skin of Newborn Hamsters , 1969, Science.
[39] E. Rittenhouse. Genetic effects on fine structure and development of pigment granules in mouse hair bulb melanocytes: II. Thec andp loci, andddpp interaction , 1968 .
[40] Frank H. Mover. Genetic Variations in the Fine Structure and Ontogeny of Mouse Melanin Granules. , 1966 .
[41] T. Fitzpatrick,et al. SUBCELLULAR LOCALIZATION OF MELANIN BIOSYNTHESIS , 1963, Annals of the New York Academy of Sciences.
[42] E. J. Scott,et al. Tyrosinase Activity in Melanocytes of Human Albinos1 , 1961 .
[43] E. V. Van Scott,et al. Tyrosinase activity in melanocytes of human albinos. , 1961, The Journal of investigative dermatology.
[44] E. Russell. A Quantitative Histological Study of the Pigment Found in the Coat-Color Mutants of the House Mouse. IV. the Nature of the Effects of Genic Substitution in Five Major Allelic Series. , 1949, Genetics.