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m Further reading: Task 7c: repair/replace et al. in cs1 author/editor parameters;
m Further reading: replace et al. in author/editor parameters with |display-authors=etal or |display-editors=etal; using AWB
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*{{cite journal |vauthors=Gerhard DS, Wagner L, Feingold EA, etal |title=The Status, Quality, and Expansion of the NIH Full-Length cDNA Project: The Mammalian Gene Collection (MGC) |journal=Genome Res. |volume=14 |issue= 10B |pages= 2121–7 |year= 2004 |pmid= 15489334 |doi= 10.1101/gr.2596504 | pmc=528928 }}
*{{cite journal |vauthors=Gerhard DS, Wagner L, Feingold EA, etal |title=The Status, Quality, and Expansion of the NIH Full-Length cDNA Project: The Mammalian Gene Collection (MGC) |journal=Genome Res. |volume=14 |issue= 10B |pages= 2121–7 |year= 2004 |pmid= 15489334 |doi= 10.1101/gr.2596504 | pmc=528928 }}
*{{cite journal |vauthors=Zaidi SH, Peltekova V, Meyer S, etal |title=A family exhibiting arterial tortuosity syndrome displays homozygosity for markers in the arterial tortuosity locus at chromosome 20q13 |journal=Clin. Genet. |volume=67 |issue= 2 |pages= 183–8 |year= 2005 |pmid= 15679832 |doi= 10.1111/j.1399-0004.2004.00391.x }}
*{{cite journal |vauthors=Zaidi SH, Peltekova V, Meyer S, etal |title=A family exhibiting arterial tortuosity syndrome displays homozygosity for markers in the arterial tortuosity locus at chromosome 20q13 |journal=Clin. Genet. |volume=67 |issue= 2 |pages= 183–8 |year= 2005 |pmid= 15679832 |doi= 10.1111/j.1399-0004.2004.00391.x }}
*{{cite journal | author=[[Karen Mohlke|Mohlke KL]], Skol AD, Scott LJ, ''et al.'' |title=Evaluation of SLC2A10 (GLUT10) as a candidate gene for type 2 diabetes and related traits in Finns |journal=Mol. Genet. Metab. |volume=85 |issue= 4 |pages= 323–7 |year= 2005 |pmid= 15936967 |doi= 10.1016/j.ymgme.2005.04.011 }}
*{{cite journal | author=[[Karen Mohlke|Mohlke KL]], Skol AD, Scott LJ |title=Evaluation of SLC2A10 (GLUT10) as a candidate gene for type 2 diabetes and related traits in Finns |journal=Mol. Genet. Metab. |volume=85 |issue= 4 |pages= 323–7 |year= 2005 |pmid= 15936967 |doi= 10.1016/j.ymgme.2005.04.011 |display-authors=etal}}
*{{cite journal | author=Segade F, Allred DC, Bowden DW |title=Functional characterization of the promoter of the human glucose transporter 10 gene |journal=Biochim. Biophys. Acta |volume=1730 |issue= 2 |pages= 147–58 |year= 2005 |pmid= 16051383 |doi= 10.1016/j.bbaexp.2005.06.012 }}
*{{cite journal | author=Segade F, Allred DC, Bowden DW |title=Functional characterization of the promoter of the human glucose transporter 10 gene |journal=Biochim. Biophys. Acta |volume=1730 |issue= 2 |pages= 147–58 |year= 2005 |pmid= 16051383 |doi= 10.1016/j.bbaexp.2005.06.012 }}
*{{cite journal |vauthors=Coucke PJ, Willaert A, Wessels MW, etal |title=Mutations in the facilitative glucose transporter GLUT10 alter angiogenesis and cause arterial tortuosity syndrome |journal=Nat. Genet. |volume=38 |issue= 4 |pages= 452–7 |year= 2006 |pmid= 16550171 |doi= 10.1038/ng1764 }}
*{{cite journal |vauthors=Coucke PJ, Willaert A, Wessels MW, etal |title=Mutations in the facilitative glucose transporter GLUT10 alter angiogenesis and cause arterial tortuosity syndrome |journal=Nat. Genet. |volume=38 |issue= 4 |pages= 452–7 |year= 2006 |pmid= 16550171 |doi= 10.1038/ng1764 }}

Revision as of 13:20, 26 December 2015

Template:PBB Solute carrier family 2, facilitated glucose transporter member 10 is a protein that in humans is encoded by the SLC2A10 gene.[1][2]

Template:PBB Summary

See also

References

  1. ^ McVie-Wylie AJ, Lamson DR, Chen YT (Mar 2001). "Molecular cloning of a novel member of the GLUT family of transporters, SLC2a10 (GLUT10), localized on chromosome 20q13.1: a candidate gene for NIDDM susceptibility". Genomics. 72 (1): 113–7. doi:10.1006/geno.2000.6457. PMID 11247674.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  2. ^ "Entrez Gene: SLC2A10 solute carrier family 2 (facilitated glucose transporter), member 10".

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.