AXL and MET crosstalk to promote gonadotropin releasing hormone (GnRH) neuronal cell migration and survival

被引：43

作者：

Salian-Mehta, Smita ^{[1
]}

Xu, Mei ^{[1
]}

Wierman, Margaret E. ^{[1
,2
,3
]}

机构：

[1] Univ Colorado, Sch Med, Dept Med, Aurora, CO 80045 USA

[2] Univ Colorado, Sch Med, Aurora, CO 80045 USA

[3] Res Serv VAMC, Denver, CO 80220 USA

来源：

MOLECULAR AND CELLULAR ENDOCRINOLOGY | 2013年 / 374卷 / 1-2期

关键词：

GnRH neurons; AXL; MET; HEPATOCYTE GROWTH-FACTOR; SIGNAL-REGULATED KINASE; RECEPTOR TYROSINE KINASE; FACTOR-SCATTER FACTOR; C-MET; ACTIVATION; EXPRESSION; ERK; INDUCTION; MECHANISM;

D O I：

10.1016/j.mce.2013.04.018

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The membrane tyrosine kinase receptors, AXL and MET, are implicated in GnRH neuron migration and/or survival. We hypothesized that the receptors with their ligands, GAS6 and HGF, respectively may crosstalk in GnRH neuronal function. In NLT GnRH neuronal cells, MET co-immunoprecipitated with AXL, although HGF or GAS6 did not transphosphorylate AXL or MET, respectively. Co-expression of a kinase dead AXL blocked HGF activation of MET and indirectly AKT and p38MAPK Silencing of AXL decreased HGF's ability to phosphorylate MET and activate AXL's downstream effectors, p38MAPK and AKT. HGF/MET signaling modulated neuron migration dependent and independent of AXL co-expression and p38MAPK. Conversely, AXL's control of GnRH neuronal survival was dependent on HGF/MET signaling. Together, these data support that the importance of membrane tyrosine kinase receptor crosstalk to regulate neuronal cell-specific developmental functions. (c) 2013 Elsevier Ireland Ltd. All rights reserved.

引用

页码：92 / 100

页数：9

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