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10.1089/ars.2010.3359 http://scihub22266oqcxt.onion/10.1089/ars.2010.3359 20615073/?report=reader!3122891!20615073     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 284.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 284.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Antioxid+Redox+Signal 2011 ; 14 (7): 1275-88 Nephropedia Template TP {{tp|p=20615073|t=2011. Calcium dysregulation and homeostasis of neural calcium in the molecular mechanisms of neurodegenerative diseases provide multiple targets for neuroprotection |pdf=|usr=}}{{20615073}} gab.com Text Calcium dysregulation and homeostasis of neural calcium in the molecular mechanisms of neurodegenerative diseases provide multiple targets for neuroprotection JO: Antioxid Redox Signal http://www.kidney.de/pget.php?&tw=1&pmid=20615073 #FOAvip The intracellular free calcium concentration subserves complex signaling roles in brain. Calcium cations (Ca(2+)) regulate neuronal plasticity underlying learning and memory and neuronal survival. Homo- and heterocellular control of Ca(2+) homeostasis supports brain physiology maintaining neural integrity. Ca(2+) fluxes across the plasma membrane and between intracellular organelles and compartments integrate diverse cellular functions. A vast array of checkpoints controls Ca(2+), like G protein-coupled receptors, ion channels, Ca(2+) binding proteins, transcriptional networks, and ion exchangers, in both the plasma membrane and the membranes of mitochondria and endoplasmic reticulum. Interactions between Ca(2+) and reactive oxygen species signaling coordinate signaling, which can be either beneficial or detrimental. In neurodegenerative disorders, cellular Ca(2+)-regulating systems are compromised. Oxidative stress, perturbed energy metabolism, and alterations of disease-related proteins result in Ca(2+)-dependent synaptic dysfunction, impaired plasticity, and neuronal demise. We review Ca(2+) control processes relevant for physiological and pathophysiological conditions in brain tissue. Dysregulation of Ca(2+) is decisive for brain cell death and degeneration after ischemic stroke, long-term neurodegeneration in Alzheimer's disease, Parkinson's disease, Huntington's disease, inflammatory processes, such as in multiple sclerosis, epileptic sclerosis, and leucodystrophies. Understanding the underlying molecular processes is of critical importance for the development of novel therapeutic strategies to prevent neurodegeneration and confer neuroprotection. Twit Text FOAVip Calcium dysregulation and homeostasis of neural calcium in the molecular mechanisms of neurodegenerative diseases provide multiple targets for neuroprotection ????Antioxid Redox Signal http://www.kidney.de/pget.php?&tw=1&pmid=20615073 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20615073 #FOAvip English Wikipedia <ref>{{Cite pmid|20615073}}</ref> Calcium dysregulation and homeostasis of neural calcium in the molecular mechanisms of neurodegenerative diseases provide multiple targets for neuroprotection #MMPMID20615073 Zundorf G; Reiser G Antioxid Redox Signal 2011[Apr]; 14 (7): 1275-88 PMID20615073show ga The intracellular free calcium concentration subserves complex signaling roles in brain. Calcium cations (Ca(2+)) regulate neuronal plasticity underlying learning and memory and neuronal survival. Homo- and heterocellular control of Ca(2+) homeostasis supports brain physiology maintaining neural integrity. Ca(2+) fluxes across the plasma membrane and between intracellular organelles and compartments integrate diverse cellular functions. A vast array of checkpoints controls Ca(2+), like G protein-coupled receptors, ion channels, Ca(2+) binding proteins, transcriptional networks, and ion exchangers, in both the plasma membrane and the membranes of mitochondria and endoplasmic reticulum. Interactions between Ca(2+) and reactive oxygen species signaling coordinate signaling, which can be either beneficial or detrimental. In neurodegenerative disorders, cellular Ca(2+)-regulating systems are compromised. Oxidative stress, perturbed energy metabolism, and alterations of disease-related proteins result in Ca(2+)-dependent synaptic dysfunction, impaired plasticity, and neuronal demise. We review Ca(2+) control processes relevant for physiological and pathophysiological conditions in brain tissue. Dysregulation of Ca(2+) is decisive for brain cell death and degeneration after ischemic stroke, long-term neurodegeneration in Alzheimer's disease, Parkinson's disease, Huntington's disease, inflammatory processes, such as in multiple sclerosis, epileptic sclerosis, and leucodystrophies. Understanding the underlying molecular processes is of critical importance for the development of novel therapeutic strategies to prevent neurodegeneration and confer neuroprotection. |*Homeostasis[MESH] |Animals[MESH] |Antiporters/metabolism[MESH] |Brain/metabolism[MESH] |Calcium Channels/metabolism[MESH] |Calcium Signaling[MESH] |Calcium-Transporting ATPases/metabolism[MESH] |Calcium/*metabolism[MESH] |Endoplasmic Reticulum/metabolism[MESH] |Humans[MESH] |Mitochondrial Proteins/metabolism[MESH] |Neurodegenerative Diseases/*metabolism/prevention & control[MESH] |Neurons/*metabolism[MESH] |Neuroprotective Agents/therapeutic use[MESH] |Potassium Channels, Calcium-Activated/metabolism[MESH] |Reactive Oxygen Species/metabolism[MESH] |Receptors, G-Protein-Coupled/metabolism[MESH]Calcium dysregulation and homeostasis of neural calcium in the molecul(epmc).pdf DeepDyve Pubget Overpricing