p(HGNC:SRC)

Entity

Name

SRC

Namespace

hgnc

Namespace Version

20180906

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

The projection domain of tau may be involved in cell signaling that occurs through the interaction with Lck, Fgr and cSrc (Src-family kinases), growth factor receptor-bound protein 2 (Grb2), phospholipase C- [70], phosphatidylinositol and phosphatidylinositol bisphosphate [71,72], peptidyl-prolyl cis/trans isomerase Pin 1, and many others (for review see [73]), making them potential therapeutic targets in tauopathies [74]. PubMed:26751493

The projection domain of tau may be involved in cell signaling that occurs through the interaction with Lck, Fgr and cSrc (Src-family kinases), growth factor receptor-bound protein 2 (Grb2), phospholipase C- [70], phosphatidylinositol and phosphatidylinositol bisphosphate [71,72], peptidyl-prolyl cis/trans isomerase Pin 1, and many others (for review see [73]), making them potential therapeutic targets in tauopathies [74]. PubMed:26751493

The mechanism underlying the effect of BDNF and CNTF on NF-κB activation has been attributed to the activation of Src and Lck non-receptor tyrosine kinases which phosphorylate IκBα on Tyr42 resulting in subsequent NF-κB activation PubMed:28745240

Furthermore, inhibitors of SRC, a closely related tyrosine kinase, also prevent nicotinic protection of differentiated PC12 cells against serum-deprivation-induced cell death (Li et al., 1999b), and inhibitors of FYN or Janus kinase-2 (JAK-2) block the neuroprotection against Abeta toxicity of therapeutic AChE inhibitors (Takada-Takatori et al., 2006). PubMed:19293145

The projection domain of tau may be involved in cell signaling that occurs through the interaction with Lck, Fgr and cSrc (Src-family kinases), growth factor receptor-bound protein 2 (Grb2), phospholipase C- [70], phosphatidylinositol and phosphatidylinositol bisphosphate [71,72], peptidyl-prolyl cis/trans isomerase Pin 1, and many others (for review see [73]), making them potential therapeutic targets in tauopathies [74]. PubMed:26751493

The projection domain of tau may be involved in cell signaling that occurs through the interaction with Lck, Fgr and cSrc (Src-family kinases), growth factor receptor-bound protein 2 (Grb2), phospholipase C- [70], phosphatidylinositol and phosphatidylinositol bisphosphate [71,72], peptidyl-prolyl cis/trans isomerase Pin 1, and many others (for review see [73]), making them potential therapeutic targets in tauopathies [74]. PubMed:26751493

PP2A enzymes can also become transiently inactivated following tyrosine phosphorylation of the catalytic subunit at the putative Tyr-307 site,via activation of src kinase, epidermal growth factor receptor or insulin signaling (Chen et al.,1992). PubMed:24653673

Besides Ser/Thr kinases, the protein tyrosine kinase src promotes the phosphorylation of PP2A on Tyr-307, resulting in PP2A inactivation and subsequent tau phosphorylation (Xiong et al.,2013; Arif et al.,2014). PubMed:24653673

PP2A enzymes can also become transiently inactivated following tyrosine phosphorylation of the catalytic subunit at the putative Tyr-307 site,via activation of src kinase, epidermal growth factor receptor or insulin signaling (Chen et al.,1992). PubMed:24653673

Besides Ser/Thr kinases, the protein tyrosine kinase src promotes the phosphorylation of PP2A on Tyr-307, resulting in PP2A inactivation and subsequent tau phosphorylation (Xiong et al.,2013; Arif et al.,2014). PubMed:24653673

The responsible kinases include 1) proline-directed protein kinases (PDPKs) targeting SP or TP motifs [e.g., GSK3b, cyclindependent kinase (CDK)-5, and MAPKs]; 2) non–proline directed protein kinases targeting KXGS-motifs [e.g., PKA, microtubule affinity-regulating kinase and synapses of the amphid defective (SADK)]; 3) protein kinases specific for tyrosines (e.g., Src, Lck, Syk, Fyn, and c-Abl kinase) (91). PubMed:29191965

The mechanism underlying the effect of BDNF and CNTF on NF-κB activation has been attributed to the activation of Src and Lck non-receptor tyrosine kinases which phosphorylate IκBα on Tyr42 resulting in subsequent NF-κB activation PubMed:28745240