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Conservation of Amino Acids Between Human 12, Mouse G6pc2, Human G6PC1 and Mouse G6pc1.
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posted on 2016-09-09, 17:39 authored by Kayla A. Boortz, Kristen E. Syring, Lynley D. Pound, Yingda Wang, James K. Oeser, Richard M. O’BrienSequence alignment showing the conservation of AAs between human (h) G6PC2, mouse (m) G6pc2, human G6PC1 and mouse G6pc1. Residues highlighted in green represent AAs mutation of which in G6PC1 causes GSD type 1a [40]. Residues highlighted in pink represent AAs that are changed by human G6PC2 SNPs that were identified using the UCSC Genome Browser (https://genome.ucsc.edu/) and HumSAVR (http://omictools.com/humsavar-tool) databases. Residues highlighted in yellow represent conserved AAs in human G6PC2, mouse G6pc2, human G6PC1 and mouse G6pc1 that are changed by a human G6PC2 SNP and where mutation in G6PC1 can cause GSD type 1a. Identities are indicated by filled circles and similarities by vertical bars.
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Glucose -6-Phosphatase ActivityTyr 207Ser rs 374055555Conserved Human G 6PC Amino Acidsmouse G 6pc activitymouse G 6pc enzyme activityG 6PC genes encode glucose -6-phosphatasePro 340Leu SNPsArg 293Trp rs 2232326G 6PC Protein Expression Elevated fasting blood glucoseGly 8Glu rs 138726309cause glycogen storage disease type 1Mouse G 6pc Mutationstype 2 diabetesSer 324Pro SNPsglucose -6-phosphatase activityG 6PC isoformSingle nucleotide polymorphismsG 6PC rs 144254880G 6PC protein expressionFBGG 6PCG 6PC mouse G 6pcArg 79Gln variantSer 324Pro rs 137857125Arg 79Gln rs 149663725177Tyr rs 2232323mouse G 6pc22 non-synonymous G 6PC SNPsG 6PC variantsG 6pc knockout mice
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