International Journal of Pure & Applied Bioscience (IJPAB)
Year : 2016, Volume : 4, Issue : 1
First page : (15) Last page : (23)
Article doi: http://dx.doi.org/10.18782/2320-7051.2189
Myocilin and Glaucoma its Risk Factors
Mahesh Kumar Lohano1,2*, Li Su1, Wang Ruochen1, Buddha Bahdur Basnet1, Hameem Naveed1 Vash Dev Khemani2, and Aijaz Ali Khooharo3
1Key Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology,Wuhan 430074, China
2Liaquat University of Medical and Health Sciences, Jamshoro / Hyderabad
3Sindh Agriculture University Tandojam, Sindh, Pakistan
*Corresponding Author E-mail: mklohana@yahoo.com
Received: 10.01.2016 | Revised: 22.01.2016 | Accepted: 26.01.2016
Abstract
Myocilin (OMIM601652) MYOC gene, first revealed as a protein isolated from cultured human Trabecular Meshwork (TM) cells after prolong dexamethasone treatment. Hence given the name TIGR (Trabecular Meshwork Inducible Glucocorticoid Response Protein). The human myocilin gene, a concealed acidic glycoprotein,contains 504 amino acids, positioned at chromosome 1(1q24.3 – 1q25.2), and filled with olfactomedin domain at its C terminus. Myocilin exists in various tissues throughout the eye and many other organs. Mutant myocilin cause endoplasmic reticulum pressure in eye angle tissues, including the trabecular meshwork, damaging the cells inside the meshwork, ultimately leading to structural changes in the outflow pathway, and high intraocular pressure.TM is vital in controlling pressure and mutations in MYOC.It has been recognized as the cause of juvenile and adult onset of primary open angle glaucoma.
Key words: Myocilin gene, glaucoma, Trabecular Meshwork, mutation.
Full Text : PDF; Journal doi : http://dx.doi.org/10.18782
Cite this article: Lohano, M.K., Su, L., Ruochen, W., Basnet, B.B., Naveed, H., Khemani, V.D., and Khooharo, A.A., Myocilin and Glaucoma its Risk Factors, Int. J. Pure App. Biosci. 4(1): 15-23 (2016). doi: http://dx.doi.org/10.18782/2320-7051.2189