| Literature DB >> 24333914 |
Yushi Hayashi1, Norio Yamamoto2, Takayuki Nakagawa3, Juichi Ito4.
Abstract
We previously reported that insulin-like growth factor 1 (IGF-1) protects cochlear hair cells against aminoglycosides through activation of the PI3K/Akt and MEK/ERK pathways in supporting cells. In this study, we found that IGF-1 up-regulated the expression levels of Gap43 and Ntn1 as measured using cDNA microarray analysis and qRT-PCR. Using inhibitors of the PI3K/Akt and MEK/ERK pathways, we reveal that both pathways are involved in the up-regulation of Gap43 and Ntn1 expression. Moreover the time window of Gap43 and Ntn1 transcription was limited to within 12h after IGF-1 treatment, indicating that downstream gene expression was tightly controlled by IGF-1.Entities:
Keywords: Adcy7; Cochlea; ERK; Gap43; Growth associated protein 43 (Gap43); IGF-1; Ier5; Insulin-like growth factor 1 (IGF-1); Kitl; MAPK/ERK kinase; MEK; Microarray; Netrin 1 (Ntn1); Ntn1; PI3K; adenylate cyclase 7; extracellular signal-regulated kinase; growth associated protein 43; immediate early response 5; insulin-like growth factor 1; kit ligand; netrin 1; phosphatidylinositol 3-kinase; qRT-PCR; quantitative reverse transcriptase polymerase chain reaction
Mesh：
Substances：
Year: 2013 PMID： 24333914 DOI： 10.1016/j.neulet.2013.11.062
Source DB: PubMed Journal: Neurosci Lett ISSN： 0304-3940 Impact factor: 3.046