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Appears in Networks 6

In-Edges 4

p(HBP:"projection domain") association p(HGNC:LCK) View Subject | View Object

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

a(HBP:"projection domain") association p(HGNC:LCK) View Subject | View Object

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

Appears in Networks:

a(PUBCHEM:4878) association p(HGNC:LCK) View Subject | View Object

Tab. 1A-B: Summary of the Tau aggregation modulators (inhibitors = 18 (A), stimulators = 10 (B)) which show decrease / increase in the amount of ThS + cells without affecting the expression level of TauRD∆K compared to the compound untreated control. PubMed:30640040

p(HGNC:CNTF) increases act(p(HGNC:LCK)) View Subject | View Object

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

Out-Edges 6

p(HGNC:LCK) association p(HBP:"projection domain") View Subject | View Object

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

p(HGNC:LCK) association a(HBP:"projection domain") View Subject | View Object

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

Appears in Networks:

p(HGNC:LCK) association a(PUBCHEM:4878) View Subject | View Object

Tab. 1A-B: Summary of the Tau aggregation modulators (inhibitors = 18 (A), stimulators = 10 (B)) which show decrease / increase in the amount of ThS + cells without affecting the expression level of TauRD∆K compared to the compound untreated control. PubMed:30640040

p(HGNC:LCK) directlyIncreases p(HGNC:MAPT, pmod(Ph, Tyr)) View Subject | View Object

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

p(HGNC:LCK) directlyIncreases p(HGNC:MAPT, pmod(Ph, Tyr, 18)) View Subject | View Object

In addition, tau can be phosphorylated by tyrosine kinases such as the SRC family members LCK, SYK and FYN at Tyr18, and the ABL family members ARG and ABL1 at Tyr394 (REF. 45). PubMed:26631930

act(p(HGNC:LCK)) increases p(HGNC:NFKBIA, pmod(Ph, Tyr, 42)) View Subject | View Object

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

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.