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From Proteopedia
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There are two chains that compose the GLUT3 protein. These chains are named the <scene name='77/777640/A_chain/3'>A chain</scene> and the <scene name='77/777640/B_chain/2'>B Chain</scene>. | There are two chains that compose the GLUT3 protein. These chains are named the <scene name='77/777640/A_chain/3'>A chain</scene> and the <scene name='77/777640/B_chain/2'>B Chain</scene>. | ||
== Disease == | == Disease == | ||
- | + | Deficiency of GLUT3 protein has associated with the severity of Alzheimer's disease (AD) and expression of AD symptoms. <ref>doi: 10.1016/j.jalz.2017.09.011</ref> Although there is no proven causal relation between GLUT3 deficiency and AD, the relationship between the two suggests that the two are correlated. | |
== Relevance == | == Relevance == | ||
The GLUT3 protein has been found to be the only glucose transport protein that works in bovine (cow) and humans lenses. Glucose transport into eye lenses is important because the metabolism of glucose is necessary to create energy to maintain the transparency of lenses <ref>doi: 10.1016/j.exer.2017.06.012</ref> | The GLUT3 protein has been found to be the only glucose transport protein that works in bovine (cow) and humans lenses. Glucose transport into eye lenses is important because the metabolism of glucose is necessary to create energy to maintain the transparency of lenses <ref>doi: 10.1016/j.exer.2017.06.012</ref> |
Current revision
GLUT3
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References
- ↑ An Y, Varma VR, Varma S, Casanova R, Dammer E, Pletnikova O, Chia CW, Egan JM, Ferrucci L, Troncoso J, Levey AI, Lah J, Seyfried NT, Legido-Quigley C, O'Brien R, Thambisetty M. Evidence for brain glucose dysregulation in Alzheimer's disease. Alzheimers Dement. 2017 Oct 19. pii: S1552-5260(17)33765-2. doi:, 10.1016/j.jalz.2017.09.011. PMID:29055815 doi:http://dx.doi.org/10.1016/j.jalz.2017.09.011
- ↑ Lim JC, Perwick RD, Li B, Donaldson PJ. Comparison of the expression and spatial localization of glucose transporters in the rat, bovine and human lens. Exp Eye Res. 2017 Aug;161:193-204. doi: 10.1016/j.exer.2017.06.012. Epub 2017 Jun, 15. PMID:28625822 doi:http://dx.doi.org/10.1016/j.exer.2017.06.012