NKIRAS2

NF-κB inhibitor interacting Ras-like 2 is a protein that in humans is encoded by the NKIRAS2 gene.[5]

NKIRAS2
Identifiers
Aliases	NKIRAS2, KBRAS2, kappaB-Ras2, NFKB inhibitor interacting Ras like 2
External IDs	OMIM: 604497 MGI: 1919216 HomoloGene: 9738 GeneCards: NKIRAS2
Gene location (Human) Chr. Chromosome 17 (human)[1] Band 17q21.2 Start 42,011,382 bp[1] End 42,025,644 bp[1]
Gene location (Mouse) Chr. Chromosome 11 (mouse)[2] Band 11|11 D Start 100,619,244 bp[2] End 100,627,607 bp[2]
Gene ontology Molecular function • nucleotide binding • GTP binding • GTPase activity Cellular component • cytoplasm • membrane • cellular component Biological process • I-kappaB kinase/NF-kappaB signaling • signal transduction Sources:Amigo / QuickGO
Orthologs
Species	Human	Mouse
Entrez	28511	71966
Ensembl	ENSG00000168256	ENSMUSG00000017837
UniProt	Q9NYR9	Q9CR56
RefSeq (mRNA)	NM_001001349 NM_001144927 NM_001144928 NM_001144929 NM_017595	NM_028024
RefSeq (protein)	NP_001001349 NP_001138399 NP_001138400 NP_001138401 NP_060065 NP_001001349.1 NP_001138399.1 NP_060065.2	NP_082300
Location (UCSC)	Chr 17: 42.01 – 42.03 Mb	Chr 11: 100.62 – 100.63 Mb
PubMed search	[3]	[4]
Wikidata
View/Edit Human View/Edit Mouse

Model organisms

Nkiras2 knockout mouse phenotype

Characteristic	Phenotype
Homozygote viability	Normal
Fertility	Normal
Body weight	Normal
Anxiety	Normal
Neurological assessment	Normal
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
Haematology	Normal
Peripheral blood lymphocytes	Normal
Micronucleus test	Normal
Heart weight	Normal
Salmonella infection	Normal[6]
All tests and analysis from[7]

Model organisms have been used in the study of NKIRAS2 function. A conditional knockout mouse line, called Nkiras2^{tm1a(EUCOMM)Wtsi}[8][9] 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.[10][11][12]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[7][13] Twenty one tests were carried out, but no significant abnormalities were observed.[7]

References

1. GRCh38: Ensembl release 89: ENSG00000168256 - Ensembl, May 2017
2. GRCm38: Ensembl release 89: ENSMUSG00000017837 - Ensembl, May 2017
3. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
4. "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
5. "Entrez Gene: NFKB inhibitor interacting Ras-like 2". Retrieved 2011-08-30.
6. "Salmonella infection data for Nkiras2". Wellcome Trust Sanger Institute.
7. 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.
8. "International Knockout Mouse Consortium".
9. "Mouse Genome Informatics".
10. 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 (Jun 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.
11. Dolgin E (Jun 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
12. Collins FS, Rossant J, Wurst W (Jan 2007). "A mouse for all reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247.
13. van der Weyden L, White JK, Adams DJ, Logan DW (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.

Further reading

• Tago K, Funakoshi-Tago M, Sakinawa M, Mizuno N, Itoh H (Oct 2010). "KappaB-Ras is a nuclear-cytoplasmic small GTPase that inhibits NF-kappaB activation through the suppression of transcriptional activation of p65/RelA". The Journal of Biological Chemistry. 285 (40): 30622–33. doi:10.1074/jbc.M110.117028. PMC 2945557. PMID 20639196.
• Fenwick C, Na SY, Voll RE, Zhong H, Im SY, Lee JW, Ghosh S (Feb 2000). "A subclass of Ras proteins that regulate the degradation of IkappaB". Science. 287 (5454): 869–73. doi:10.1126/science.287.5454.869. PMID 10657303.
• Dieguez-Gonzalez R, Akar S, Calaza M, Perez-Pampin E, Costas J, Torres M, Vicario JL, Velloso ML, Navarro F, Narvaez J, Joven B, Herrero-Beaumont G, Gonzalez-Alvaro I, Fernandez-Gutierrez B, de la Serna AR, Carreño L, Lopez-Longo J, Caliz R, Collado-Escobar MD, Blanco FJ, Fernandez-Lopez C, Balsa A, Pascual-Salcedo D, Gomez-Reino JJ, Gonzalez A (Apr 2009). "Genetic variation in the nuclear factor kappaB pathway in relation to susceptibility to rheumatoid arthritis". Annals of the Rheumatic Diseases. 68 (4): 579–83. doi:10.1136/ard.2007.087304. PMID 18434448.