EXOC3L2
Exocyst complex component 3-like 2 is a protein that in humans is encoded by the EXOC3L2 gene.[1][2][3][4]
The EXOC3L2 protein has been shown to interact with EXOC4[1] that is a component of the exocyst complex[5][6] involved exocytosis and more specifically in the targeting of exocytic vesicles to the cell membrane.
The exocyst complex is important for several biological processes, such as the establishment of cell polarity and regulation of cell migration.[5][7] The structure and functions of the exocyst complex are conserved from yeast to higher eukaryotes.[5][6] Endothelial cells in blood vessels express high levels of EXOC3L2 that is required for proper VEGFR-2[1] signaling so that the endothelial cells can migrate towards the growth factor VEGF-A.[8]
Model organisms
Model organisms have been used in the study of EXOC3L2 function. A conditional knockout mouse line called Exoc3l2tm1b(KOMP)Wtsi was generated at the Wellcome Trust Sanger Institute.[9] Male and female animals underwent a standardized phenotypic screen[10] to determine the effects of deletion.[11][12][13][14] Additional screens performed: - In-depth immunological phenotyping[15]
| Characteristic | Phenotype |
|---|---|
| All data available at.[10][15] | |
| Insulin | Normal |
| Homozygous viability at P14 | Abnormal |
| Recessive lethal study | Normal |
| Body weight | Normal |
| Neurological assessment | Normal |
| Grip strength | Normal |
| Dysmorphology | Normal |
| Indirect calorimetry | Normal |
| Glucose tolerance test | Normal |
| Auditory brainstem response | Normal |
| DEXA | Normal |
| Radiography | Normal |
| Eye morphology | Normal |
| Clinical chemistry | Normal |
| Haematology 16 Weeks | Normal |
| Peripheral blood leukocytes 16 Weeks | Normal |
| Salmonella infection | Normal |
References
- ^ a b c Barkefors, I; Fuchs, PF; Heldin, J; Bergström, T; Forsberg-Nilsson, K; Kreuger, J (2011). "Exocyst complex component 3-like 2 (EXOC3L2) associates with the exocyst complex and mediates directional migration of endothelial cells". The Journal of Biological Chemistry. 286 (27): 24189–99. doi:10.1074/jbc.M110.212209. PMC 3129200. PMID 21566143.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ EntrezGene 90332
- ^ Olgiati, P; Politis, AM; Papadimitriou, GN; De Ronchi, D; Serretti, A (2011). "Genetics of late-onset Alzheimer's disease: Update from the alzgene database and analysis of shared pathways". International Journal of Alzheimer's Disease. 2011: 832379. doi:10.4061/2011/832379. PMC 3235576. PMID 22191060.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ Belbin, O; Carrasquillo, MM; Crump, M; Culley, OJ; Hunter, TA; Ma, L; Bisceglio, G; Zou, F; Allen, M (2011). "Investigation of 15 of the top candidate genes for late-onset Alzheimer's disease". Human Genetics. 129 (3): 273–82. doi:10.1007/s00439-010-0924-2. PMC 3036835. PMID 21132329.
- ^ a b c Liu, J; Guo, W (2011). "The exocyst complex in exocytosis and cell migration". Protoplasma. 249 (3): 587–597. doi:10.1007/s00709-011-0330-1. PMID 21997494. S2CID 11946932.
- ^ a b Munson, M; Novick, P (2006). "The exocyst defrocked, a framework of rods revealed". Nature Structural & Molecular Biology. 13 (7): 577–81. doi:10.1038/nsmb1097. PMID 16826234. S2CID 26645238.
- ^ Thapa, N; Sun, Y; Schramp, M; Choi, S; Ling, K; Anderson, RA (2012). "Phosphoinositide signaling regulates the exocyst complex and polarized integrin trafficking in directionally migrating cells". Developmental Cell. 22 (1): 116–30. doi:10.1016/j.devcel.2011.10.030. PMC 3266520. PMID 22264730.
- ^ Carmeliet, P; Jain, RK (2011). "Molecular mechanisms and clinical applications of angiogenesis". Nature. 473 (7347): 298–307. Bibcode:2011Natur.473..298C. doi:10.1038/nature10144. PMC 4049445. PMID 21593862.
- ^ 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. S2CID 85911512.
- ^ a b "International Mouse Phenotyping Consortium".
- ^ 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.
- ^ Dolgin E (Jun 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
- ^ 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. S2CID 18872015.
- ^ White JK, Gerdin AK, Karp NA, Ryder E, Buljan M, Bussell JN, Salisbury J, Clare S, Ingham NJ, Podrini C, Houghton R, Estabel J, Bottomley JR, Melvin DG, Sunter D, Adams NC, Sanger Institute Mouse Genetics Project, Tannahill D, Logan DW, Macarthur DG, Flint J, Mahajan VB, Tsang SH, Smyth I, Watt FM, Skarnes WC, Dougan G, Adams DJ, Ramirez-Solis R, Bradley A, Steel KP (2013). "Genome-wide generation and systematic phenotyping of knockout mice reveals new roles for many genes". Cell. 154 (2): 452–64. doi:10.1016/j.cell.2013.06.022. PMC 3717207. PMID 23870131.
- ^ a b "Infection and Immunity Immunophenotyping (3i) Consortium".