PTK6 调节 RTKs 及其效应器 AKT1 和 DOK1
中文名称
通路描述
PTK6 通过抑制 EGFR 的下调来增强 EGFR 信号传导（Kang et al. 2010, Li et al. 2012, Kang and Lee 2013）。PTK6 还可能通过其他受体酪氨酸激酶（RTKs），如 IGF1R（Fan et al. 2013）和 ERBB3（Kamalati et al. 2000）来增强信号传导。PTK6 影响 AKT1 的激活（Zhang et al. 2005, Zheng et al. 2010），并靶向 RTKs 的负调控因子 DOK1 进行降解（Miah et al. 2014）。
英文描述
RHOT1 GTPase cycle This pathway catalogues guanine nucleotide exchange factors (GEFs) and effectors of RHOT1 (also known as MIRO-1). RHOT1 possesses a high intrinsic GTP-ase activity and does not require a GTPase activator protein (GAP) (Peters et al. 2018). No GDP dissociation inhibitors (GDIs) have been reported to interact with RHOT1. RHOT1 is a mitochondrial RHO GTPase. Like related RHOT2 (MIRO-2), RHOT1 localizes to the outer mitochondrial membrane. RHOT1 is implicated in mitochondrial movement inside the cells (Schwarz 2013), including the axonal transport of mitochondria in neurons (Saxton and Hollenbeck 2012; Birsa et al. 2013; Devine et al. 2016), as well as mitochondrial fission and fusion (Saxton and Hollenbeck 2012). RHOT1/RHOT2-mediated mitochondrial turnover is affected in neurodegenerative diseases (Birsa et al. 2013; Devine et al. 2016). RHOT1 can localize to peroxisomes and regulate peroxisome motility and fission (Castro et al. 2018, Okumoto et al. 2018, Covill-Cooke et al. 2020). RHOT1 is also involved in the regulation of ER-mitochondria membrane contact sites (Grossmann et al. 2019, Modi et al. 2019).
Upregulation of RHOT1 has a neuroprotective effect in ischemic stroke (Wei et al. 2019).
Upregulation of RHOT1 has a neuroprotective effect in ischemic stroke (Wei et al. 2019).
所含基因
5 个基因