Disease Info Card

Albinism, Oculocutaneous

Information about Albinism, Oculocutaneous: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.

Overview of Albinism, Oculocutaneous

Most recent studies have shown that Albinism, Oculocutaneous shares some biological mechanisms with albinism, albinism-ocular, bleeding-tendency, chediak-higashi-syndrome, colitis, fibrosis, hemorrhage, hereditary-diseases, hermanski-pudlak-syndrome, hypopigmentation-disorder, hypoplasia, infective-disorder, malignant-neoplasms, melanoma, nystagmus, oculocutaneous-albinism-type-2, platelet-storage-pool-deficiency, pulmonary-fibrosis, skin-neoplasms, tyrosinase-negative-oculocutaneous-albinism.

Among the many pathways, these few ones have gauged particular interests from scientists studying Albinism, Oculocutaneous, and have been seen in publications frequently: Aging, Chemotaxis, Coagulation, Excretion, Exocytosis, Eye Development, Eye Pigmentation, Glycosylation, Hypersensitivity, Innervation, Localization, Mating, Pathogenesis, Pigment Accumulation, Pigmentation, Platelet Aggregation, Reflex, Secretion, Transport, Vesicle Transport

Quite a number of genes have been found to play important roles in Albinism, Oculocutaneous, such as AP3B1, B3GALNT1, CD63, DCT, GPR143, HPS1, HPS3, HPS4, KAT2B, LYST, MC1R, MITF, OCA2, PMEL, SLC45A2, TYR, TYRP1. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.

In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.