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10.1016/j.biomaterials.2016.01.028 http://scihub22266oqcxt.onion/10.1016/j.biomaterials.2016.01.028 C4755854!4755854!26826790     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biomaterials 2016 ; 84 (ä): 119-29 Nephropedia Template TP {{tp|p=26826790|t=2016. Matrix Rigidity Differentially Regulates Invadopodia Activity Through ROCK1 and ROCK2 |pdf=|usr=}}{{26826790}} gab.com Text Matrix Rigidity Differentially Regulates Invadopodia Activity Through ROCK1 and ROCK2 JO: Biomaterials http://www.kidney.de/pget.php?&tw=1&pmid=26826790 #FOAvip ROCK activity increases due to ECM rigidity in the tumor microenvironment and promotes a malignant phenotype via actomyosin contractility. Invasive migration is facilitated by actin-rich adhesive protrusions known as invadopodia that degrade the ECM. Invadopodia activity is dependent on matrix rigidity and contractile forces suggesting that mechanical factors may regulate these subcellular structures through ROCK-dependent actomyosin contractility. However, emerging evidence indicates that the ROCK1 and ROCK2 isoforms perform different functions in cells suggesting that alternative mechanisms may potentially regulate rigidity-dependent invadopodia activity. In this study, we found that matrix rigidity drives ROCK signaling in cancer cells but that ROCK1 and ROCK2 differentially regulate invadopodia activity through separate signaling pathways via contractile (NM II) and non-contractile (LIMK) mechanisms. These data suggest that the mechanical rigidity of the tumor microenvironment may drive ROCK signaling through distinct pathways to enhance the invasive migration required for cancer progression and metastasis. Twit Text FOAVip Matrix Rigidity Differentially Regulates Invadopodia Activity Through ROCK1 and ROCK2 ????Biomaterials http://www.kidney.de/pget.php?&tw=1&pmid=26826790 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26826790 #FOAvip English Wikipedia <ref>{{Cite pmid|26826790}}</ref> Matrix Rigidity Differentially Regulates Invadopodia Activity Through ROCK1 and ROCK2 #MMPMID26826790 Jerrell RJ; Parekh A Biomaterials 2016[Apr]; 84 (ä): 119-29 PMID26826790show ga ROCK activity increases due to ECM rigidity in the tumor microenvironment and promotes a malignant phenotype via actomyosin contractility. Invasive migration is facilitated by actin-rich adhesive protrusions known as invadopodia that degrade the ECM. Invadopodia activity is dependent on matrix rigidity and contractile forces suggesting that mechanical factors may regulate these subcellular structures through ROCK-dependent actomyosin contractility. However, emerging evidence indicates that the ROCK1 and ROCK2 isoforms perform different functions in cells suggesting that alternative mechanisms may potentially regulate rigidity-dependent invadopodia activity. In this study, we found that matrix rigidity drives ROCK signaling in cancer cells but that ROCK1 and ROCK2 differentially regulate invadopodia activity through separate signaling pathways via contractile (NM II) and non-contractile (LIMK) mechanisms. These data suggest that the mechanical rigidity of the tumor microenvironment may drive ROCK signaling through distinct pathways to enhance the invasive migration required for cancer progression and metastasis. äMatrix Rigidity Differentially Regulates Invadopodia Activity Through (epmc).pdf DeepDyve Pubget Overpricing