scholarly journals Mammary Epithelial-Specific Ablation of the Focal Adhesion Kinase Suppresses Mammary Tumorigenesis by Affecting Mammary Cancer Stem/Progenitor Cells

2009 ◽  
Vol 69 (2) ◽  
pp. 466-474 ◽  
Author(s):  
Ming Luo ◽  
Huaping Fan ◽  
Tamas Nagy ◽  
Huijun Wei ◽  
Chenran Wang ◽  
...  
Keyword(s):  
Focal Adhesion Kinase ◽  
Progenitor Cells ◽  
Focal Adhesion ◽  
Mammary Cancer ◽  
Mammary Tumorigenesis ◽  
Mammary Epithelial

scholarly journals Bionic Silk Fibroin Film Promotes Tenogenic Differentiation of Tendon Stem/Progenitor Cells by Activating Focal Adhesion Kinase

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Kang Lu ◽  
Xiaodie Chen ◽  
Hong Tang ◽  
Mei Zhou ◽  
Gang He ◽  
...  
Keyword(s):  
Focal Adhesion Kinase ◽  
Progenitor Cells ◽  
Silk Fibroin ◽  
Focal Adhesion ◽  
Cell Morphology ◽  
Biological Activities ◽  
Biological Effects ◽  
Tendon Injuries ◽  
Regeneration Ability ◽  
Gene And Protein Expression

Background. Tendon injuries are common musculoskeletal disorders in clinic. Due to the limited regeneration ability of tendons, tissue engineering technology is often used as an effective approach to treat tendon injuries. Silk fibroin (SF) films have excellent biological activities and physical properties, which is suitable for tendon regeneration. The present study is aimed at preparing a SF film with a bionic microstructure and investigating its biological effects. Methods. A SF film with a smooth surface or bionic microstructure was prepared. After seeding tendon stem/progenitor cells (TSPCs) on the surface, the cell morphology, the expression level of tenogenic genes and proteins, and the focal adhesion kinase (FAK) activation were measured to evaluate the biological effect of SF films. Results. The TSPCs on SF films with a bionic microstructure exhibited a slender cell morphology, promoted the expression of tenogenic genes and proteins, such as SCX, TNC, TNMD, and COLIA1, and activated FAK. FAK inhibitors blocked the enhanced expression of tenogenic genes and proteins. Conclusion. SF films with a bionic microstructure may serve as a scaffold, provide biophysical cues to alter the cellular adherence arrangement and cell morphology, and enhance the tenogenic gene and protein expression in TSPCs. FAK activation plays a key role during this biological response process.

scholarly journals Mammary epithelial-specific disruption of the focal adhesion kinase blocks mammary tumor progression

2007 ◽  
Vol 104 (51) ◽  
pp. 20302-20307 ◽  
Author(s):  
H. Lahlou ◽  
V. Sanguin-Gendreau ◽  
D. Zuo ◽  
Robert. D. Cardiff ◽  
G. W. McLean ◽  
...  
Keyword(s):  
Tumor Progression ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Mammary Tumor ◽  
Mammary Epithelial ◽  
Mammary Tumor Progression

Early signalling events of autophagy

2013 ◽  
Vol 55 ◽  
pp. 1-15 ◽  
Author(s):  
Laura E. Gallagher ◽  
Edmond Y.W. Chan
Keyword(s):  
Protein Kinase ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Mammalian Cells ◽  
Mammalian Target Of Rapamycin ◽  
Interacting Protein ◽  
The Core ◽  
Autophagy Gene ◽  
Autophagy Induction ◽  
Cellular Pathways

Autophagy is a conserved cellular degradative process important for cellular homoeostasis and survival. An early committal step during the initiation of autophagy requires the actions of a protein kinase called ATG1 (autophagy gene 1). In mammalian cells, ATG1 is represented by ULK1 (uncoordinated-51-like kinase 1), which relies on its essential regulatory cofactors mATG13, FIP200 (focal adhesion kinase family-interacting protein 200 kDa) and ATG101. Much evidence indicates that mTORC1 [mechanistic (also known as mammalian) target of rapamycin complex 1] signals downstream to the ULK1 complex to negatively regulate autophagy. In this chapter, we discuss our understanding on how the mTORC1–ULK1 signalling axis drives the initial steps of autophagy induction. We conclude with a summary of our growing appreciation of the additional cellular pathways that interconnect with the core mTORC1–ULK1 signalling module.

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