{"references": ["Sun W , Shen Y , Shan S , Han L , Li Y , Zhou Z , Zhong Z , Chen J Identification of TYR mutations in patients with oculocutaneous albinism. Mol Med Rep. 2018 Jun;17(6):8409-8413. doi: 10.3892/mmr.2018.8881. Epub 2018 Apr 13.", "Markus N. Preising,1, 2 Hedwig Forster,1 Miriam Gonser,1 Birgit Lorenz1,2; Molecular Vision 2011; 17:939-948 http://www.molvis.org/molvis/v17/a104 Received 17 December 2011 | Accepted 5 April 2011 | Published 15 April 2011.", "KAZUTOMO TOYOFUKU, IKUO WADA,* JULIO C. VALENCIA,\u2020 TSUNETO KUSHIMOTO,VICTOR J. FERRANS,\u2020 AND VINCENT J. HEARING1,Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda,Maryland 20892, USA; *Department of Biochemistry, Sapporo Medical University, Sapporo, Japan;and \u2020Pathology Section, National,Oculocutaneous albinism types 1 and 3 are ERretention diseases: mutation of tyrosinase or Tyrp1can affect the processing of both mutant and wildtypeproteins, 0892-6638/01/0015-2149 \u00a9 FASEBVol. 15 October 2001.", "Karen Gr\u00f8nskov, JakobEk and Karen Brondum-Nielsen*Address: Kennedy Center. National Research Center for Genetics, visual Impairment and Mental Retardation, Gl. Landevej 7, 2600 Glostrup, Denmark. Review Open Access Oculocutaneous albinism* Corresponding author Published: 2 November 2007Orphanet Journal of Rare Diseases 2007, 2:43 doi:10.1186/1750-1172-2-43.", "Kazutomo TOYOFUKU*, Ikuo WADA., Richard A. SPRITZ. and Vincent J. HEARING*1*Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health,Building 37, Room 1B25, Bethesda, MD 20892, U.S.A., .Department of Biochemistry, Sapporo Medical University, Chu-ou-ku, Minami 1, Nishi 17, Sapporo, Hokkaido 060-8556, Japan, and .Human Medical Genetics Program, University of Colorado Health Sciences Center, Denver, CO 80262, U.S.A. The molecular basis of oculocutaneous albinism type 1 (OCA1): sortingfailure and degradation of mutant tyrosinases results in a lack of pigmentation, Biochem. J. (2001) 355, 259\u00b1269", "Ray K ,Chaki M, Sengupta M. Tyrosinase and ocular diseases: some novel,thoughts on the molecular basis of oculocutaneous albinism type 1. ProgRetin Eye Res. 2007 Jul;26(4):323-58. Epub 2007 Jan 17.", "Richard Alan Lewis, MD, MS Departments of Ophthalmology, Medicine, Pediatrics, and Molecular and Human Genetics /Huffington Center on Aging Cullen Eye Institute Baylor College of Medicine Houston, Texas. Ocular Albinism, X-LinkedSynonyms: Nettleship-Falls Ocular Albinism, OA1, Ocular Albinism Type 1, XLOA. Initial Posting: March 12, 2004; Last Update: April 5, 2011.", "Tamio Suzuki, MD, PhD and Masahiro Hayashi, MD, PhD.Oculocutaneous Albinism Type 4. Synonym: OCA4,Initial Posting: November 17, 2005; Last Revision: September 15, 2011.", "Richard Alan Lewis, MD, MS,Cullen Eye Institute, Baylor College of Medicine, Houston, Texas. Oculocutaneous Albinism Type 2 Synonym: OCA2. Includes: Brown OCA. Initial Posting: July 17, 2003; Last Update: August 16, 2012."]}

The aims of the research were to identify the genes responsible for Albinism. The genes have been identified and analyzed using BLAST.The genes responsible for causing albinism are OCA and OA.Albinism is caused by a mutation in one of several genes. Four forms of OCA are now recognized – OCA1, OCA2, OCA3 and OCA4; some are further divided into subtypes.Each of these genes provides instructions for making one of several proteins involved in the production of melanin. Melanin is produced by cells called melanocytes, which are found in the skin and eyes. A mutation may result in no melanin at all or a significant decline in the amount of melanin thus resulting in albinism. The phylogenetic relation of the genes responsible albinism has been established using various bioinformatics tools like Clustal Omega, MUSCLE, PHYLM, MEGA X and BioEdit. This phylogenetic study has helped us analysis how these genes have evolved with time and what level similarity exists between these sequences. This study paves path for the future analysis of the genes and drug designing foralbinism.