Open Access Articles- Top Results for SLC38A10


SymbolsSLC38A10 ; FLJ35718; FLJ46399; MGC15523
External IDsHomoloGene41556 IUPHAR: 1178 GeneCards: SLC38A10 Gene
RefSeq (mRNA)NM_001037984NM_001164798
RefSeq (protein)NP_001033073NP_001158270
Location (UCSC)Chr 17:
79.22 – 79.27 Mb
Chr 11:
120.1 – 120.15 Mb
PubMed search[1][2]

Sodium-coupled neutral amino acid transporter 10 also known as solute carrier family 38, member 10 is a protein that in humans is encoded by the SLC38A10 gene.[1]

Model organisms

Model organisms have been used in the study of SLC38A10 function. A conditional knockout mouse line, called Slc38a10tm1a(EUCOMM)Wtsi[10][11] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.[12][13][14]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[8][15] Twenty four tests were carried out on mutant mice and four significant abnormalities were observed.[8] Homozygous animals of both sex had decreased body weights, and DEXA analysis showed that this correlated with decreased bone mineral content and decreased body length. Indirect calorimetry analysis showed that males displayed increased oxygen consumption and energy expenditure, while clinical chemistry tests found that females had decreased circulating amylase levels and males had hypoalbuminemia and increased circulating creatinine levels.[8]


  1. ^ "Entrez Gene: solute carrier family 38, member 10". Retrieved 2011-08-30. 
  2. ^ "Body weight data for Slc38a10". Wellcome Trust Sanger Institute. 
  3. ^ "Indirect calorimetry data for Slc38a10". Wellcome Trust Sanger Institute. 
  4. ^ "DEXA data for Slc38a10". Wellcome Trust Sanger Institute. 
  5. ^ "Clinical chemistry data for Slc38a10". Wellcome Trust Sanger Institute. 
  6. ^ "Salmonella infection data for Slc38a10". Wellcome Trust Sanger Institute. 
  7. ^ "Citrobacter infection data for Slc38a10". Wellcome Trust Sanger Institute. 
  8. ^ a b c d Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica 88: 925–7. doi:10.1111/j.1755-3768.2010.4142.x. 
  9. ^ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  10. ^ "International Knockout Mouse Consortium". 
  11. ^ "Mouse Genome Informatics". 
  12. ^ Skarnes, W. C.; Rosen, B.; West, A. P.; Koutsourakis, M.; Bushell, W.; Iyer, V.; Mujica, A. O.; Thomas, M.; Harrow, J.; Cox, T.; Jackson, D.; Severin, J.; Biggs, P.; Fu, J.; Nefedov, M.; De Jong, P. J.; Stewart, A. F.; Bradley, A. (2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature 474 (7351): 337–342. PMC 3572410. PMID 21677750. doi:10.1038/nature10163.  edit
  13. ^ Dolgin E (2011). "Mouse library set to be knockout". Nature 474 (7351): 262–3. PMID 21677718. doi:10.1038/474262a. 
  14. ^ Collins FS, Rossant J, Wurst W (2007). "A Mouse for All Reasons". Cell 128 (1): 9–13. PMID 17218247. doi:10.1016/j.cell.2006.12.018. 
  15. ^ van der Weyden L, White JK, Adams DJ, Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism.". Genome Biol 12 (6): 224. PMC 3218837. PMID 21722353. doi:10.1186/gb-2011-12-6-224. 

Further reading