SLC41A3

SLC41A3
Identifiers
Aliases	SLC41A3, SLC41A1-L2, solute carrier family 41 member 3
External IDs	MGI: 1918949 HomoloGene: 23052 GeneCards: SLC41A3
Gene location (Human)
Chr.	Chromosome 3 (human)[1]
End	126,101,561 bp[1]
Gene location (Mouse)
Chr.	Chromosome 6 (mouse)[2]
End	90,646,412 bp[2]
Gene ontology
Molecular function	• cation transmembrane transporter activity; • protein binding;
Cellular component	• integral component of membrane; • membrane; • plasma membrane;
Biological process	• cation transport; • cation transmembrane transport; • transmembrane transport;
	Sources:Amigo / QuickGO
Orthologs
	54946
	71699
	ENSG00000114544
	ENSMUSG00000030089
	Q96GZ6
	Q921R8
	NM_001008485; NM_001008486; NM_001008487; NM_001164475; NM_017836
	NM_001037493; NM_027868
NP_001008485; NP_001008486; NP_001008487; NP_001157947; NP_060306;
	NP_001008486.1
	NP_001032570; NP_082144
	Wikidata
View/Edit Human	View/Edit Mouse

Solute carrier family 41, member 3 is a protein that in humans is encoded by the SLC41A3 gene.^[5]

Model organisms

*Slc41a3* knockout mouse phenotype
Characteristic	Phenotype
Homozygote viability	Normal
Fertility	Normal
Body weight	Normal
Anxiety	Normal
Neurological assessment	Abnormal
Grip strength	Normal
Hot plate	Normal
Dysmorphology	Normal
Indirect calorimetry	Normal
Glucose tolerance test	Normal
Auditory brainstem response	Normal
DEXA	Normal
Radiography	Normal
Body temperature	Normal
Eye morphology	Normal
Clinical chemistry	Normal
Plasma immunoglobulins	Normal
Haematology	Normal
Micronucleus test	Normal
Heart weight	Normal
Tail epidermis wholemount	Normal
Skin Histopathology	Normal
Brain histopathology	Normal
Eye 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 SLC41A3 function. A conditional knockout mouse line, called Slc41a3^{tm1a(KOMP)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 six tests were carried out on mutant mice and one significant abnormality was observed: homozygous mutants displayed abnormal locomotor coordination.^[8]

References

1 2 3 GRCh38: Ensembl release 89: ENSG00000114544 - Ensembl, May 2017
1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000030089 - Ensembl, May 2017
↑ "Human PubMed Reference:".
↑ "Mouse PubMed Reference:".
↑ "Entrez Gene: Solute carrier family 41, member 3". Retrieved 2011-09-28.
↑ "Salmonella infection data for Slc41a3". Wellcome Trust Sanger Institute.
↑ "Citrobacter infection data for Slc41a3". Wellcome Trust Sanger Institute.
1 2 3 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, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (June 2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
↑ Dolgin E (June 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
↑ Collins FS, Rossant J, Wurst W (January 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 (June 2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biology. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.

SLC41A3

Model organisms

References

Further reading