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10.3390/ijms21030765 http://scihub22266oqcxt.onion/10.3390/ijms21030765 31991573!7037201!31991573     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+J+Mol+Sci 2020 ; 21 (3): ä Nephropedia Template TP {{tp|p=31991573|t=2020. The Role of Calmodulin in Tumor Cell Migration, Invasiveness, and Metastasis |pdf=|usr=}}{{31991573}} gab.com Text The Role of Calmodulin in Tumor Cell Migration, Invasiveness, and Metastasis JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=31991573 #FOAvip Calmodulin (CaM) is the principal Ca(2+) sensor protein in all eukaryotic cells, that upon binding to target proteins transduces signals encoded by global or subcellular-specific changes of Ca(2+) concentration within the cell. The Ca(2+)/CaM complex as well as Ca(2+)-free CaM modulate the activity of a vast number of enzymes, channels, signaling, adaptor and structural proteins, and hence the functionality of implicated signaling pathways, which control multiple cellular functions. A basic and important cellular function controlled by CaM in various ways is cell motility. Here we discuss the role of CaM-dependent systems involved in cell migration, tumor cell invasiveness, and metastasis development. Emphasis is given to phosphorylation/dephosphorylation events catalyzed by myosin light-chain kinase, CaM-dependent kinase-II, as well as other CaM-dependent kinases, and the CaM-dependent phosphatase calcineurin. In addition, the role of the CaM-regulated small GTPases Rac1 and Cdc42 (cell division cycle protein 42) as well as CaM-binding adaptor/scaffold proteins such as Grb7 (growth factor receptor bound protein 7), IQGAP (IQ motif containing GTPase activating protein) and AKAP12 (A kinase anchoring protein 12) will be reviewed. CaM-regulated mechanisms in cancer cells responsible for their greater migratory capacity compared to non-malignant cells, invasion of adjacent normal tissues and their systemic dissemination will be discussed, including closely linked processes such as the epithelial-mesenchymal transition and the activation of metalloproteases. This review covers as well the role of CaM in establishing metastatic foci in distant organs. Finally, the use of CaM antagonists and other blocking techniques to downregulate CaM-dependent systems aimed at preventing cancer cell invasiveness and metastasis development will be outlined. Twit Text FOAVip The Role of Calmodulin in Tumor Cell Migration, Invasiveness, and Metastasis ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=31991573 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31991573 #FOAvip English Wikipedia <ref>{{Cite pmid|31991573}}</ref> The Role of Calmodulin in Tumor Cell Migration, Invasiveness, and Metastasis #MMPMID31991573 Villalobo A; Berchtold MW Int J Mol Sci 2020[Jan]; 21 (3): ä PMID31991573show ga Calmodulin (CaM) is the principal Ca(2+) sensor protein in all eukaryotic cells, that upon binding to target proteins transduces signals encoded by global or subcellular-specific changes of Ca(2+) concentration within the cell. The Ca(2+)/CaM complex as well as Ca(2+)-free CaM modulate the activity of a vast number of enzymes, channels, signaling, adaptor and structural proteins, and hence the functionality of implicated signaling pathways, which control multiple cellular functions. A basic and important cellular function controlled by CaM in various ways is cell motility. Here we discuss the role of CaM-dependent systems involved in cell migration, tumor cell invasiveness, and metastasis development. Emphasis is given to phosphorylation/dephosphorylation events catalyzed by myosin light-chain kinase, CaM-dependent kinase-II, as well as other CaM-dependent kinases, and the CaM-dependent phosphatase calcineurin. In addition, the role of the CaM-regulated small GTPases Rac1 and Cdc42 (cell division cycle protein 42) as well as CaM-binding adaptor/scaffold proteins such as Grb7 (growth factor receptor bound protein 7), IQGAP (IQ motif containing GTPase activating protein) and AKAP12 (A kinase anchoring protein 12) will be reviewed. CaM-regulated mechanisms in cancer cells responsible for their greater migratory capacity compared to non-malignant cells, invasion of adjacent normal tissues and their systemic dissemination will be discussed, including closely linked processes such as the epithelial-mesenchymal transition and the activation of metalloproteases. This review covers as well the role of CaM in establishing metastatic foci in distant organs. Finally, the use of CaM antagonists and other blocking techniques to downregulate CaM-dependent systems aimed at preventing cancer cell invasiveness and metastasis development will be outlined. |*Calcium Signaling[MESH] |*Cell Movement[MESH] |Animals[MESH] |Calmodulin/*metabolism[MESH] |Humans[MESH] |Neoplasm Invasiveness[MESH] |Neoplasm Metastasis[MESH] |Neoplasm Proteins/*metabolism[MESH]The Role of Calmodulin in Tumor Cell Migration, Invasiveness, and Meta(epmc).pdf DeepDyve Pubget Overpricing