ALK 信号通路中的 MDK 和 PTN
中文名称
通路描述
多效素 (PTN) 和 Midikine (MDK) 最初被提议作为 ALK 的配体。PTN 或 MDK 与 ALK 的结合在体外或完整细胞中显示出通过 IRS、SHC、PLC 和 PI3K 刺激信号转导，并支持突触生长、生长和生存。然而，PTN 和 MDK 对 ALK 受体的激活效应并不总是可重复的，尽管它们诱导的下游信号与抗 ALK 单克隆抗体类似。最近，ALKAL1 和 ALKAL2 已被确定为生理上相关的 ALK 配体。
英文描述
MDK and PTN in ALK signaling The cytokines pleiotrophin (PTN) and midikine (MDK) were initially proposed to act as ligands for ALK (Stoica et al, 2001; Stoica et al, 2002; reviewed in Wellstein et al, 2012; Winkler et al, 2014; Herradon and Perez-Garcia, 2014). Binding of PTN or MDK to ALK either in cell-free assays or in intact cells was shown to stimulate signaling through IRS, SHC, PLC and PI3K and to support neurite outgrowth, growth and survival (Stoica et al, 2001; Stoica et al, 2002; reviewed in Wellstein et al, 2012; Winkler et al, 2014; Herradon and Perez-Garcia, 2014). The activating effects of PTN and MDK on the ALK receptor were not universally reproducible, however, despite eliciting similar downstream signaling to those with anti-ALK monoclonal antibodies (Mathivet et al, 2007; Moog-Lutz et al, 2005; Motegi et al, 2004; Dirks et al, 2002; Miyake et al, 2002). More recently, ALKAL1 and ALKAL2 have been identified as the physiologically relevant ALK ligands (Zhang et al, 2014; Guan et al, 2015; Reshetnyak et al, 2015; Reshetnyak et al, 2018).
所含基因
4 个基因