P16INK4a Upregulation Mediated by SIX6 Defines Retinal Ganglion Cell Pathogenesis in Glaucoma.
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ABSTRACT:
SUBMITTER: Skowronska-Krawczyk D
PROVIDER: S-EPMC4648709 | biostudies-literature | 2015 Sep
REPOSITORIES: biostudies-literature
Publications
P16INK4a Upregulation Mediated by SIX6 Defines Retinal Ganglion Cell Pathogenesis in Glaucoma.
Skowronska-Krawczyk Dorota D Zhao Ling L Zhu Jie J Weinreb Robert N RN Cao Guiqun G Luo Jing J Flagg Ken K Patel Sherrina S Wen Cindy C Krupa Martin M Luo Hongrong H Ouyang Hong H Lin Danni D Wang Wenqiu W Li Gen G Xu Yanxin Y Li Oulan O Chung Christopher C Yeh Emily E Jafari Maryam M Ai Michael M Zhong Zheng Z Shi William W Zheng Lianghong L Krawczyk Michal M Chen Daniel D Shi Catherine C Zin Carolyn C Zhu Jin J Mellon Pamela L PL Gao Weiwei W Abagyan Ruben R Zhang Liangfang L Sun Xiaodong X Zhong Sheng S Zhuo Yehong Y Rosenfeld Michael G MG Liu Yizhi Y Zhang Kang K
Molecular cell 20150910 6
Glaucoma, a blinding neurodegenerative disease, whose risk factors include elevated intraocular pressure (IOP), age, and genetics, is characterized by accelerated and progressive retinal ganglion cell (RGC) death. Despite decades of research, the mechanism of RGC death in glaucoma is still unknown. Here, we demonstrate that the genetic effect of the SIX6 risk variant (rs33912345, His141Asn) is enhanced by another major POAG risk gene, p16INK4a (cyclin-dependent kinase inhibitor 2A, isoform INK4a ...[more]
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