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Autophagy Diseases

The mechanism by which duplication of TBK1 causes retinal ganglion cell death and NTG is poorly understood. However, recent data suggests that dysregulation of autophagy, a process by which the intracellular accumulation of proteins, organelles, or pathogens may be eliminated, might be important in the pathogenesis of NTG. Autophagy is activated in experimental animal models of glaucoma including optic nerve transection and ocular ischemia model systems. Moreover, the NTG genes, TBK1 and OPTN, have both been shown to be important regulators of autophagy. For instance, TBK1 encodes a kinase that phosphorylates OPTN, which then recruits the microtubule-associated protein 1 light chain 3 beta (MAP1LC3B, LC3B) that is instrumental in assembling the autophagosome and initiating autophagy. Duplication of TBK1 gene in NTG patients has been shown to cause increased transcription of TBK1, suggesting that this form of glaucoma may be caused by stimulation of autophagy. John H Fingert, Duplication of TBK1 Stimulates Autophagy in iPSC-derived Retinal Cells from a Patient with Normal Tension Glaucoma
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Last date updated on June, 2014

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