Apoptosis calcium

Cell Cycle Analysis and Kinetics Apoptosis Calcium Flux Chromosome Analysis Micronuclei Analysis Intracellular pH Intracellular Glutathione Oxidative Burst Cell Viability... 

A simple example searching for BDNF, BDNF Gene, and BDNF gene polymorphism against the words antidepressant, antipsychotic, atypical antipsychotic, neuronal atrophy, apoptosis, calcium, lithium, mood stabilizer, and bipolar is shown in the figure as a demonstration. 

PubMatlix antidepressant antipsychotic atypical antipsychotic neuronal atrophy apoptosis calcium lithium mood stabilizer bipolar... 

Lentiviridae HIV gpl20 Chemokine mimic HIV entry, leukocyte chemotaxis, apoptosis, calcium flux... 

ALG-2 is the fust calcium-binding protein of the EF-hand family found to be directly involved in apoptosis. ALG-2 is a 22 kDa protein and like the other members of the penta EF-hand family, contains five EF-hands, with only two of them functional. ALG-2 protein is expressed in the brain and eye and was found to be upregulated in various cancer tissues. Several targets have been found, such as proteins AEP, Alix, preflin, and annexins, suggesting a putative role of ALG-2 in apoptosis. 

The CaR regulates numerous biological processes, including the expression of various genes (e.g., PTH) the secretion of hormones (PTH and calcitonin), cytokines (MCP-1), and calcium (e.g., into breast milk) the activities of channels (potassium channels) and transporters (aquaporin-2) cellular shape, motility (of macrophages), and migration cellular adhesion (of hematopoietic stem cells) and cellular proliferation (of colonocytes), differentiation (of keratinocytes), and apoptosis (of H-500 ley dig cancer cells) [3]. 

Mitochondrial permeability transition involves the opening of a larger channel in the inner mitochondrial membrane leading to free radical generation, release of calcium into the cytosol and caspase activation. These alterations in mitochondrial permeability lead eventually to disruption of the respiratory chain and dqDletion of ATP. This in turn leads to release of soluble intramito-chondrial membrane proteins such as cytochrome C and apoptosis-inducing factor, which results in apoptosis. 

Acute over-activation of NHE1 results in a marked elevation in intracellular sodium concentration with a subsequent increase in intracellular calcium, via the Na +/Ca++ exchanger. This in turn triggers a cascade of injurious events that can culminate in tissue dysfunction and ultimately apoptosis and necrosis. This is commonly seen in organs such as the heart, brain and kidneys as a consequence of ischemia-reperfusion. 

Deiva K, Geeraerts T, Salim H, Leclerc P, Hery C, Hugel B, Freyssinet JM, Tardieu M (2004) Fractalkine reduces N-methyl-d-aspartate-induced calcium flux and apoptosis in human neurons through extracellular signal-regulated kinase activation. Eur J Neurosci 20(12) ... 

Kruman 11, Nath A, Mattson MP (1998) HlV-1 protein Tat induces apoptosis of hippocampal neurons by a mechanism involving caspase activation, calcium overload, and oxidative stress. Exp Neurol 154(2) 276-288... 

Sui Y, Potula R, Dhillon N, Pinson D, Li S, Nath A, Anderson C, Turchan J, Kolson D, Narayan O, Buch S (2004) Neuronal apoptosis is mediated by CXCLIO overexpression in simian human immunodeficiency virus encephalitis. Am J Pathol 164 1557-1566 Sui Y, Stehno-Bittel L, Li S, Loganathan R, DhUlon NK, Pinson D, Nath A, Kolson D, Narayan O, Buch S (2006) CXCLlO-induced cell death in neurons role of calcium dysregulation. Eur J NeuroSci 23 957-964... 

Systematic cell degradation and death, apoptosis, on the other hand, is thought to be necessary to avoid cell damage accumulating so as to cause incorrect differentiation. The process is very complicated involving activation of a number of destructive enzymes where once more increase in cell calcium often initiates the hydrolyses using special internal calcium-dependent enzymes, calpains (see Demaurex in Further Reading). 

The functions of mtNOS in mitochondria have been studied (see Chapter 23). Ghafourifar et al. [177] found that the calcium-induced stimulation of mtNOS caused the release of cytochrome c from mitochondria and induced apoptosis. On the other hand, the same group of authors [178] showed that the production of NO by mtNOS and superoxide in mitochondria resulted in the formation of peroxynitrite and stimulated calcium release, indicating the existence of a feedback loop which prevents calcium overload in mitochondria. 

Fas ligand and interleukin-ip), the neurotransmitter glutamate and thrombin. Like tumor necrosis factor (TNF) receptors, Fas is coupled to downstream death effector proteins that ultimately induce caspase activation (Ch. 22). Fas and TNF receptors recruit proteins called FADD and TRADD respectively FADD and TRADD then activate caspase-8, which, in turn, activates caspase-3 (Fig. 35-4). Calcium ion influx mediates neuronal apoptosis induced by glutamate receptor activation calcium induces mitochondrial membrane permeability transition pore opening, release of cytochrome c and caspase activation. Interestingly, in the absence of neurotrophic factors some neurotrophic factor receptors can activate apoptotic cascades, the low-affinity NGF receptor being one example of such a death receptor mechanism [23],... 

Once apoptosis is triggered, a stereotyped sequence of premitochondrial events occurs that executes the cell death process. In many cases proteins and/or lipid mediators that induce changes in mitochondrial membrane permeability and calcium regulation are produced or activated. For example, the pro-apoptotic Bcl-2 family members Bax, Bad and Bid may associate with the mitochondrial membrane and modify its permeability. Membrane-derived lipid mediators such as ceramide and 4-hydroxynonenal can also induce mitochondrial membrane alterations that are critical for the execution of apoptosis. 

Several different changes in mitochondria occur during apoptosis. These include a change in membrane potential (usually depolarization), increased production of reactive oxygen species, potassium channel activation, calcium ion uptake, increased membrane permeability and release of cytochrome c and apoptosis inducing factor (AIF) [25]. Increased permeability of the mitochondrial membranes is a pivotal event in apoptosis and appears to result from the formation of pores in the membrane the proteins that form such permeability transition pores (PTP) may include a voltage-dependent anion channel (VDAC), the adenine nucleotide translocator, cyclophilin D, the peripheral benzodiazepine receptor, hexokinase and... 

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