Role of the PKCα-c-Src tyrosine kinase pathway in the mediation of p120-catenin degradation in ventilator-induced lung injury

Respirology ◽  
2016 ◽  
Vol 21 (8) ◽  
pp. 1404-1410 ◽  
Author(s):  
Tao Zhao ◽  
Hongwei Zhao ◽  
Gang Li ◽  
Shengfa Zheng ◽  
Mengjie Liu ◽  
...  
Keyword(s):  
Lung Injury ◽  
Tyrosine Kinase ◽  
Src Tyrosine Kinase ◽  
P120 Catenin ◽  
Ventilator Induced Lung Injury ◽  
Kinase Pathway

scholarly journals Protective role of p120‐catenin on mitochondria by inhibiting NLRP3 in ventilator‐induced lung injury

2019 ◽  
Vol 23 (11) ◽  
pp. 7360-7371 ◽  
Author(s):  
Ge Liu ◽  
Changping Gu ◽  
Mengjie Liu ◽  
Huan Liu ◽  
Dong Wang ◽  
...  
Keyword(s):  
Lung Injury ◽  
Protective Role ◽  
P120 Catenin ◽  
Ventilator Induced Lung Injury

scholarly journals Role of Glutamine in the Mediation of E-cadherin, p120-catenin and Inflammation in Ventilator-induced Lung Injury

2018 ◽  
Vol 131 (7) ◽  
pp. 804-812
Author(s):  
Jian-Lei Qiu ◽  
Bai-Ling Song ◽  
Yu-Juan Wang ◽  
Fu-Tao Zhang ◽  
Yue-Lan Wang
Keyword(s):  
Lung Injury ◽  
P120 Catenin ◽  
Ventilator Induced Lung Injury ◽  
E Cadherin

scholarly journals Sphingolipids in Ventilator Induced Lung Injury: Role of Sphingosine-1-Phosphate Lyase

2018 ◽  
Vol 19 (1) ◽  
pp. 114 ◽  
Author(s):  
Vidyani Suryadevara ◽  
Panfeng Fu ◽  
David Ebenezer ◽  
Evgeny Berdyshev ◽  
Irina Bronova ◽  
...  
Keyword(s):  
Lung Injury ◽  
Ventilator Induced Lung Injury ◽  
Sphingosine 1 Phosphate

scholarly journals The Role of Hypoxia and SRC Tyrosine Kinase in Glioblastoma Invasiveness and Radioresistance

Cancers ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 2860 ◽  
Author(s):  
Filippo Torrisi ◽  
Nunzio Vicario ◽  
Federica M. Spitale ◽  
Francesco P. Cammarata ◽  
Luigi Minafra ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Poor Prognosis ◽  
High Rate ◽  
Crucial Importance ◽  
Src Tyrosine Kinase ◽  
Complete Surgical Resection ◽  
Radiation Induced ◽  
Proliferation And Invasion

Advances in functional imaging are supporting neurosurgery and radiotherapy for glioblastoma, which still remains the most aggressive brain tumor with poor prognosis. The typical infiltration pattern of glioblastoma, which impedes a complete surgical resection, is coupled with a high rate of invasiveness and radioresistance, thus further limiting efficient therapy, leading to inevitable and fatal recurrences. Hypoxia is of crucial importance in gliomagenesis and, besides reducing radiotherapy efficacy, also induces cellular and molecular mediators that foster proliferation and invasion. In this review, we aimed at analyzing the biological mechanism of glioblastoma invasiveness and radioresistance in hypoxic niches of glioblastoma. We also discussed the link between hypoxia and radiation-induced radioresistance with activation of SRC proto-oncogene non-receptor tyrosine kinase, prospecting potential strategies to overcome the current limitation in glioblastoma treatment.

The Role Of Mesenchymal Stem Cells During Repair From Ventilator Induced Lung Injury

2011 ◽  
Author(s):  
Gerard F. Curley ◽  
Mairead Hayes ◽  
Maya Contreras ◽  
Brendan D. Higgins ◽  
Daniel P. O'Toole ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Lung Injury ◽  
Ventilator Induced Lung Injury

scholarly journals p130Cas mediates the transforming properties of the anaplastic lymphoma kinase

Blood ◽  
2005 ◽  
Vol 106 (12) ◽  
pp. 3907-3916 ◽  
Author(s):  
Chiara Ambrogio ◽  
Claudia Voena ◽  
Andrea D. Manazza ◽  
Roberto Piva ◽  
Ludovica Riera ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Anaplastic Lymphoma Kinase ◽  
Kinase Activity ◽  
Adaptor Protein ◽  
Dominant Negative ◽  
Lymphoid Cells ◽  
Src Tyrosine Kinase ◽  
Anaplastic Lymphoma ◽  
Proteomic Approach

Translocations of the anaplastic lymphoma kinase (ALK) gene have been described in anaplastic large-cell lymphomas (ALCLs) and in stromal tumors. The most frequent translocation, t(2;5), generates the fusion protein nucleophosmin (NPM)–ALK with intrinsic tyrosine kinase activity. Along with transformation, NPM-ALK induces morphologic changes in fibroblasts and lymphoid cells, suggesting a direct role of ALK in cell shaping. In this study, we used a mass-spectrometry–based proteomic approach to search for proteins involved in cytoskeleton remodeling and identified p130Cas (p130 Crk-associated substrate) as a novel interactor of NPM-ALK. In 293 cells and in fibroblasts as well as in human ALK-positive lymphoma cell lines, NPM-ALK was able to bind p130Cas and to induce its phosphorylation. Both of the effects were dependent on ALK kinase activity and on the adaptor protein growth factor receptor–bound protein 2 (Grb2), since no binding or phosphorylation was found with the kinase-dead mutant NPM-ALKK210R or in the presence of a Grb2 dominant-negative protein. Phosphorylation of p130Cas by NPM-ALK was partially independent from Src (tyrosine kinase pp60c-src) kinase activity, as it was still detectable in Syf-/- cells. Finally, p130Cas-/- (also known as Bcar1-/-) fibroblasts expressing NPM-ALK showed impaired actin filament depolymerization and were no longer transformed compared with wild-type cells, indicating an essential role of p130Cas activation in ALK-mediated transformation.

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