Gene interactions and pathways from curated databases and text-mining

◀ Back to CDH1

CDH1 — SRC

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Menke et al., Cancer Res 2001 (Pancreatic Neoplasms) : Our data demonstrate that specific collagens are able to promote metastatic behavior by down-regulation of E-cadherin gene expression in a Src-kinase dependent manner
Kawai et al., Gastroenterology 2002 (Neoplasm Invasiveness) : Activation of Src by TNF-alpha led to reduced E-cadherin levels and enhanced invasion of src transfectants
Weis et al., J Clin Invest 2004 (Edema...) : Src blockade stabilizes a Flk/cadherin complex, reducing edema and tissue injury following myocardial infarction
Wallez et al., Oncogene 2007 : Finally, we found that in a VEGF induced wound healing assay, cadherin adhesive activity was impaired by Src kinase inhibitors
McLachlan et al., Mol Biol Cell 2007 : Finally, our data implicate PI3-kinase signaling as a target for cadherin activated c-Src signaling that contributes to its positive impact on cadherin function ... We conclude that E-cadherin signaling is an important activator of c-Src at cell-cell contacts, providing a key input into a signaling pathway where quantitative changes in signal strength may result in qualitative differences in functional outcome
Shen et al., J Biol Chem 2008 : Silencing Cdc42 blocks activation of EGFR and Src induced by Ca2+ depletion, resulting in a reduction in E-cadherin degradation
Bonazzi et al., Cell Microbiol 2008 : Here we show that InlA triggers two successive E-cadherin post-translational modifications, i.e. the Src mediated tyrosine phosphorylation of E-cadherin followed by its ubiquitination by the ubiquitin-ligase Hakai
Tsygankova et al., Mol Cell Biol 2010 (Colorectal Neoplasms) : Inhibition of Src impaired spreading and restored E-cadherin at cell/cell contacts
McLachlan et al., Cytoskeleton (Hoboken, N.J.) 2011 : Protein tyrosine phosphatase activity is necessary for E-cadherin activated Src signaling ... Firstly, we report that upstream protein tyrosine phosphatase (PTP) activity is required to stimulate E-cadherin activated Src signaling at junctions ... Moreover, E-cadherin homophilic ligation could not stimulate Src signaling in vanadate treated cells ... Additionally, vanadate treatment phenocopied the effects of Src inhibition on the actin cytoskeleton, suggesting that PTP activity is required for the dynamic regulation of the actin cytoskeleton by cadherin activated Src signaling
Deep et al., Cancer prevention research (Philadelphia, Pa.) 2011 (Neoplasm Invasiveness...) : Selective Src inhibition by dasatinib also showed increased E-cadherin expression in PC3 cells suggesting a possible involvement of Src inhibition in silibinin caused increase in E-cadherin level
Alt-Holland et al., J Invest Dermatol 2011 (Carcinoma, Squamous Cell...) : We found that E-cadherin suppression triggered elevated mRNA and protein expression levels of focal adhesion kinase ( FAK ), and increased FAK and Src activities above the level seen in Ras expressing E-cadherin-competent keratinocytes ... The short hairpin RNA ( shRNA ) -mediated depletion of FAK and Src restored E-cadherin expression levels by increasing its stability in the membrane, and blocked tumor cell invasion in tissues ... These findings suggest that the tumor promoting effect of E-cadherin suppression, a common event in SCC development, is exacerbated by enhanced E-cadherin degradation induced by elevated FAK and Src activities
Serrels et al., Cell Adh Migr 2011 (Neoplasms) : Src/FAK mediated regulation of E-cadherin as a mechanism for controlling collective cell movement : insights from in vivo imaging
Nagathihalli et al., Frontiers in bioscience (Landmark edition) 2012 (Carcinoma, Pancreatic Ductal...) : Src mediated regulation of E-cadherin and EMT in pancreatic cancer ... Recent studies have focused on Src dependent regulation of E-cadherin and other tumor progression related events such as EMT with the development of metastasis ... Although the molecular events associated with Src dependent regulation of E-cadherin are becoming better defined, the cellular processes that trigger the onset of EMT remain unclear
Yan et al., Stroke 2013 (Subarachnoid Hemorrhage) : Downstream to PAR-1, c-Src dependent activation of p21 activated kinase-1 led to an increased serine/threonine phosphorylation of vascular endothelial-cadherin ; immunoprecipitation results revealed an enhanced binding of phosphorylated vascular endothelial-cadherin with endocytosis orchestrator ß-arrestin-2