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国际皮肤性病学杂志 2005 31 (1): 50-52 ISSN: 2096-5540 CN: 32-1880/R |
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黑素细胞内酪氨酸酶翻译后加工运输障碍与某些色素病的关系 |
孙秀坤, 许爱娥 |
杭州市第三人民医院皮肤科 310009 |
收稿日期 2004-03-12 修回日期 null 网络版发布日期 null |
参考文献 [1] Trombetta ES, Parodi AJ. Quality control and protein folding in the secretory pathway. Annu Rev Cell Dev Biol, 2003, 19:649-676. [2] Halaban R, Cheng E, Zhang Y,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. Proc Natl Acad Sci U S A, 1997, 94:6210-6215. [3] Halaban R, Cheng E, Svedine S,et al. Proper folding and endoplasmic reticulum to golgi transport of tyrosinase are induced by its substrates, DOPA and tyrosine. J Biol Chem, 2001, 276:11933. [4] Halaban R, Patton RS, Cheng E, et al. Abnormal acidification of melanoma cells induces tyrosinase retention in the early secretory pathway. J Biol Chem, 2002, 277:14821-14828. [5] Berson JF, Frank DW, Calvo PA, et al. A common temperature-sensitive allelic form of human tyrosinase is retained in the endoplasmic reticulum at the nonpermissive temperature. J Biol Chem, 2000,275:12281-12289. [6] Toyofuku K, Wada I, Valencia JC, et al. Oculocutaneous albinism types 1 and 3 are ER retention diseases:mutation of tyrosinase or Tyrpl can affect the processing of both mutant and wild-type proteins.FASEB J, 2001, 15:2149-2161. [7] Raposo G, Tenza D, Murphy DM, et al. Distinct protein sorting and localization to premelanosomes, melanosomes, and lysosomes in pigmented melanocytic cells. J Cell Biol, 2001, 152:809-824. [8] Kushimoto T, Valencia JC, Costin GE, et al. Tbe Seiji memorial lecture:the melanosome:an ideal model to study cellular differentiation.Pigment Cell Res, 2003, 16:237-244. [9] Huizing M, Sarangarajan R, Strovel E,et al. AP-3 mediates tyrosinase but not TRP-1 trafficking in human melanocytes. Mol Biol Cell, 2001, 12:2075-2085. [10] Chiang PW, Oiso N, Gautam R, et al. The Hermansky-Pudlak syndrome 1 (HPS1) and HPS4 proteins are components of two complexes, BLOC-3 and BLOC-4, involved in the biogenesis of lysosomerelated organelles. J Biol Chem, 2003, 278:20332-20337. [11] Li W, Zhang Q, Oiso N, et al. Hermansky-Pudlak syndrome type 7 (HPS-7) results from mutant dysbindin, a member of the biogenesis of lysosome-related organelles complex 1 (BLOC-1). Nat Genet,2003,35:84-89. [12] Shiflett SL, Kaplan J, Ward DM. Chediak-Higashi Syndrome:a rare disorder of lysosomes and lysosome related organelles. Pigment Cell Res, 2002, 15:251-257. [13] Raposo G, Marks MS. The dark side of lysosome-related organelles:specialization of the endocytic pathway for melanosome biogenesis.Traffic, 2002, 3:237-248. [14] Simons K, Zerial M. Rab proteins and the road maps for intracellular transport. Neuron, 1993, 11:789-799. [15] Hirosaki K, Yamashita T, Wada I, et al. Tyrosinase and tyrosinaserelated protein 1 require Rab7 for their intracellular transport. J Invest Dermatol, 2002, 119:475-480. [16] Seabra MC, Mules EH, Hume AN. Rab GTPases, intracellular traffic and disease. Trends Mol Med, 2002, 8:23-30. [17] Boissy RE, Liu YY, Medrano EE, et al. Structural aberration of the rough endoplasmic reticulum and melanosome compartmentalization in long-term cultures of melanocytes from vitiligo patients. J Invest Dermatol, 1991,97:395-404. [18] Le Poole IC, Boissy RE, Sarangarajan R, et al. PIG3V, an immortalized human vitiligo melanocyte cell line, expresses dilated endoplasmic reticulum. In Vitro Cell Dev Biol Anim, 2000, 36:309-319. |
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