LRRC16A
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Leucine rich repeat containing 16A is a protein that in humans is encoded by the LRRC16A gene.[3] The gene is also known as LRRC16, CARMIL, CARMIL1 or CARMIL1a.[3]
Model organisms
| 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 |
| Micronucleus test | Normal |
| Heart weight | Normal |
| Brain histopathology | Normal |
| Salmonella infection | Normal[4] |
| Citrobacter infection | Normal[5] |
| All tests and analysis from[6][7] |
Model organisms have been used in the study of LRRC16A function. A conditional knockout mouse line, called Lrrc16atm1a(KOMP)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 — at the Wellcome Trust Sanger Institute.[10][11][12]
Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[6][13] Twenty two tests were carried out on mutant mice but no significant abnormalities were observed.[6]
References
- ↑ "Human PubMed Reference:".
- ↑ "Mouse PubMed Reference:".
- 1 2 "leucine rich repeat containing 16A". Retrieved 2011-12-04.
- ↑ "Salmonella infection data for Lrrc16a". Wellcome Trust Sanger Institute.
- ↑ "Citrobacter infection data for Lrrc16a". Wellcome Trust Sanger Institute.
- 1 2 3 Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica. 88 (S248). doi:10.1111/j.1755-3768.2010.4142.x.
- ↑ Mouse Resources Portal, Wellcome Trust Sanger Institute.
- ↑ "International Knockout Mouse Consortium".
- ↑ "Mouse Genome Informatics".
- ↑ 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. 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 (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
- Yang, C.; Pring, M.; Wear, M. A.; Huang, M.; Cooper, J. A.; Svitkina, T. M.; Zigmond, S. H. (2005). "Mammalian CARMIL Inhibits Actin Filament Capping by Capping Protein". Developmental Cell. 9 (2): 209–221. doi:10.1016/j.devcel.2005.06.008. PMC 2628720. PMID 16054028.
- Liang, Y.; Niederstrasser, H.; Edwards, M.; Jackson, C. E.; Cooper, J. A. (2009). "Distinct Roles for CARMIL Isoforms in Cell Migration". Molecular Biology of the Cell. 20 (24): 5290–5305. doi:10.1091/mbc.E08-10-1071. PMC 2793302. PMID 19846667.
- Gunjaca, G.; Boban, M.; Pehlić, M.; Zemunik, T.; Budimir, D.; Kolcić, I.; Lauc, G.; Rudan, I.; Polasek, O. (2010). "Predictive Value of 8 Genetic Loci for Serum Uric Acid Concentration". Croatian medical journal. 51 (1): 23–31. doi:10.3325/cmj.2010.51.23. PMC 2829178. PMID 20162742.
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