SLC38A10
| Solute carrier family 38, member 10 | ||||||
|---|---|---|---|---|---|---|
| Identifiers | ||||||
| Symbols | SLC38A10; FLJ35718; FLJ46399; MGC15523 | |||||
| External IDs | HomoloGene: 41556 GeneCards: SLC38A10 Gene | |||||
|
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| Orthologs | ||||||
| Species | Human | Mouse | ||||
| Entrez | 124565 | 72055 | ||||
| Ensembl | ENSG00000157637 | ENSMUSG00000061306 | ||||
| UniProt | Q9HBR0 | Q5I012 | ||||
| RefSeq (mRNA) | NM_001037984 | NM_001164798 | ||||
| RefSeq (protein) | NP_001033073 | NP_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[edit]
| Characteristic | Phenotype |
|---|---|
| Homozygote viability | Normal |
| Body weight | Abnormal[2] |
| Anxiety | Normal |
| Neurological assessment | Normal |
| Grip strength | Normal |
| Hot plate | Normal |
| Dysmorphology | Normal |
| Indirect calorimetry | Abnormal[3] |
| Glucose tolerance test | Normal |
| Auditory brainstem response | Normal |
| DEXA | Abnormal[4] |
| Radiography | Normal |
| Body temperature | Normal |
| Eye morphology | Normal |
| Clinical chemistry | Abnormal[5] |
| Plasma immunoglobulins | Normal |
| Haematology | Normal |
| Peripheral blood lymphocytes | Normal |
| Micronucleus test | Normal |
| Heart weight | Normal |
| Tail epidermis wholemount | Normal |
| Brain histopathology | Normal |
| Salmonella infection | Normal[6] |
| Citrobacter infection | Normal[7] |
| All tests and analysis from[8][9] |
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]
References[edit]
- ^ "Entrez Gene: solute carrier family 38, member 10". Retrieved 2011-08-30.
- ^ "Body weight data for Slc38a10". Wellcome Trust Sanger Institute.
- ^ "Indirect calorimetry data for Slc38a10". Wellcome Trust Sanger Institute.
- ^ "DEXA data for Slc38a10". Wellcome Trust Sanger Institute.
- ^ "Clinical chemistry data for Slc38a10". Wellcome Trust Sanger Institute.
- ^ "Salmonella infection data for Slc38a10". Wellcome Trust Sanger Institute.
- ^ "Citrobacter infection data for Slc38a10". Wellcome Trust Sanger Institute.
- ^ 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.
- ^ Mouse Resources Portal, Wellcome Trust Sanger Institute.
- ^ "International Knockout Mouse Consortium".
- ^ "Mouse Genome Informatics".
- ^ Skarnes Wc, R. B.; Rosen, B.; West, A. P.; Koutsourakis, M.; Bushell, W.; Iyer, V.; Mujica, A. O.; Thomas, M. et al. (2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature 474 (7351): 337–342. doi:10.1038/nature10163. PMID 21677750.
- ^ Dolgin E (2011). "Mouse library set to be knockout". Nature 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
- ^ Collins FS, Rossant J, Wurst W (2007). "A Mouse for All Reasons". Cell 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247.
- ^ van der Weyden L, White JK, Adams DJ, Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism.". Genome Biol 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.
Further reading[edit]
- Yashin AI, Wu D, Arbeev KG, Ukraintseva SV (2010). "Joint influence of small-effect genetic variants on human longevity.". Aging (Albany NY) 2 (9): 612–20. PMC 2984609. PMID 20834067.
- Strausberg RL, Feingold EA, Grouse LH, et al. (2002). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMC 139241. PMID 12477932.
- Ota T, Suzuki Y, Nishikawa T, et al. (2004). "Complete sequencing and characterization of 21,243 full-length human cDNAs.". Nat. Genet. 36 (1): 40–5. doi:10.1038/ng1285. PMID 14702039.
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