期刊
NEUROSCIENCE LETTERS
卷 639, 期 -, 页码 88-93出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2016.12.068
关键词
Cadps2; GeneChip; KEGG; Neurotrophin; Secretion; Autism
资金
- Japan Intractable Diseases Research Foundation
- SENSHIN Medical Research Foundation
- Takeda Science Foundation
- Sumitomo Foundation
- Japanese Ministry of Education, Culture, Sports, Science and Technology (MEXT) [23110524]
- Japan Society for the Promotion of Science (JSPS) [25430061]
- Program to Disseminate Tenure Tracking System of MEXT
- Institute of Physical and Chemical Research (RIKEN)
- Grants-in-Aid for Scientific Research [15K08192, 17H03563, 26290026, 15K14356, 25430061, 26250024] Funding Source: KAKEN
In the mouse cerebellum, Ca2+-dependent activator protein for secretion 2 (CADPS2, CAPS2) is involved in regulated secretion from dense-core vesicles (DCVs), which contain neuropeptides including brain derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3). Capds2 knockout (KO) mice show impaired cerebellar development in addition to autistic-like behavioral phenotypes. To understand the molecular impact caused by loss of Capds2, we analyzed gene expression profiles in the Capds2 KO cerebellum using a GeneChip microarray and the KEGG Pathway database. Significant differential expression was observed in 1211 of 22,690 (5.34%) genes represented on the chip. The expression levels of exocytosis-related genes (Stx5a, Syt6), genes encoding secretory (Fgf2, Fgf4, Edn2) and synaptic proteins (Grin2b, Gabbr1), neurotrophin signaling-associated genes (Sos1, Shc1, Traf6, Psen2), and a gene for Rett syndrome (Mecp2) were significantly changed. Taken together, these results suggest that deregulated gene expression caused by loss of Capds2 may cause developmental deficits and/or pathological symptoms, resulting in autistic-like phenotypes. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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