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Ca < sup > 2 +</ sup > influx to the mitochondrial matrix has recently been implicated as a mechanism to regulate respiratory bioenergetics by allowing the electrochemical potential across the membrane to transiently " pulse " from ΔΨ-dominated to pH-dominated, facilitating a reduction of oxidative stress.
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Ca and <
* Isoforms I, III and VIII are also stimulated by Ca < sup > 2 +</ sup >/ calmodulin.
* Isoforms V and VI are inhibited by Ca < sup > 2 +</ sup > in a calmodulin-independent manner.
In neurons, calcium-sensitive adenylate cyclases are located next to calcium ion channels for faster reaction to Ca < sup > 2 +</ sup > influx ; they are suspected of playing an important role in learning processes.
Calcium ion ( Ca < sup >++</ sup >) antagonists ( Calcium channel blockers ) are used in the treatment of chronic stable angina.
The inorganic composition of bone ( bone mineral ) is formed from carbonated hydroxyapatite ( Ca < sub > 10 </ sub >( PO < sub > 4 </ sub >)< sub > 6 </ sub >( OH )< sub > 2 </ sub >) with lower crystallinity.
Calcium is essential for living organisms, in particular in cell physiology, where movement of the calcium ion Ca < sup > 2 +</ sup > into and out of the cytoplasm functions as a signal for many cellular processes.
Calcium salts are colorless from any contribution of the calcium, and ionic solutions of calcium ( Ca < sup > 2 +</ sup >) are colorless as well.
Calcium has four stable isotopes (< sup > 40 </ sup > Ca, < sup > 42 </ sup > Ca, < sup > 43 </ sup > Ca and < sup > 44 </ sup > Ca ), plus two more isotopes (< sup > 46 </ sup > Ca and < sup > 48 </ sup > Ca ) that have such long half-lives that for all practical purposes they also can be considered stable.
Ca and >
This forms another material known as slaked lime ( Ca ( OH )< sub > 2 </ sub >), which is an inexpensive base material used throughout the chemical industry.
Ca and 2
A similar system exists in the ocean, where seawater < sup > 44 </ sup > Ca /< sup > 40 </ sup > Ca tends to rise when the rate of removal of Ca < sup > 2 +</ sup > from seawater by mineral precipitation exceeds the input of new calcium into the ocean, and fall when calcium input exceeds mineral precipitation.
It follows that rising < sup > 44 </ sup > Ca /< sup > 40 </ sup > Ca corresponds to falling seawater Ca < sup > 2 +</ sup > concentration, and falling < sup > 44 </ sup > Ca /< sup > 40 </ sup > Ca corresponds to rising seawater Ca < sup > 2 +</ sup > concentration.
More recent papers have confirmed this observation, demonstrating that seawater Ca < sup > 2 +</ sup > concentration is not constant, and that the ocean probably never is in “ steady state ” with respect to its calcium input and output.
In the simplest terms, uplift of mountains exposes Ca-bearing rocks to chemical weathering and releases Ca < sup > 2 +</ sup > into surface water.
This Ca < sup > 2 +</ sup > eventually is transported to the ocean where it reacts with dissolved CO < sub > 2 </ sub > to form limestone.
Ca and +</
The result is that each Ca < sup > 2 +</ sup > ion released by chemical weathering ultimately removes one CO < sub > 2 </ sub > molecule from the surficial system ( atmosphere, ocean, soils and living organisms ), storing it in carbonate rocks where it is likely to stay for hundreds of millions of years.
As the weathering of limestone ( CaCO < sub > 3 </ sub >) liberates equimolar amounts of Ca < sup > 2 +</ sup > and CO < sub > 2 </ sub >, it has no net effect on the CO < sub > 2 </ sub > content of the atmosphere and ocean.
Ca and influx
This increase in intracellular sodium makes the actions of the Na / Ca exchange pump unfavorable, thereby decreasing sodium influx and calcium efflux via this pump.
Decreasing this negative charge towards zero, via the influx of the positive cations, Na < sup >+</ sup > and Ca < sup >++</ sup >, is called depolarization, which activates the mechanisms in the cell that cause it to contract.
ABA binds to receptor proteins in the guard cells ' plasma membrane and cytosol, which first raises the pH of the cytosol of the cells and cause the concentration of free Ca < sup > 2 +</ sup > to increase in the cytosol due to influx from outside the cell and release of Ca < sup > 2 +</ sup > from internal stores such as the endoplasmic reticulum and vacuoles.
Since LTP and LTD ( long-term depression ) rely on the influx of Ca < sup > 2 +</ sup > through NMDA channels, metaplasticity may be due to changes in NMDA receptors, altered calcium buffering, altered states of kinases or phosphatases and a priming of protein synthesis machinery.
Change in voltage provides a graded control of postsynaptic Ca < sup > 2 +</ sup > by regulating NMDAR-dependent Ca < sup > 2 +</ sup > influx, which is responsible for initiating LTD.
Thus, the influx of Ca < sup > 2 +</ sup > in the postsynaptic cell is reduced.
On the other hand, influx of cations, e. g. Na < sup >+</ sup > through Na < sup >+</ sup > channels or Ca < sup > 2 +</ sup > through Ca < sup > 2 +</ sup > channels, inhibits hyperpolarization.
Depolarization is often caused by influx of cations, e. g. Na < sup >+</ sup > through Na < sup >+</ sup > channels, or Ca < sup > 2 +</ sup > through Ca < sup > 2 +</ sup > channels.
The resulting influx of Ca < sup > 2 +</ sup > ions lead to the initiation of excitation-contraction coupling and thus contraction of the myocyte.
This influx of calcium causes calcium-induced calcium release from the sarcoplasmic reticulum, and free Ca < sup > 2 +</ sup > causes muscle contraction.
# This influx of Ca < sup > 2 +</ sup > causes neurotransmitter-containing vesicles to dock and fuse to the presynaptic neuron's cell membrane through SNARE proteins.
Excitotoxins like NMDA and kainic acid which bind to these receptors, as well as pathologically high levels of glutamate, can cause excitotoxicity by allowing high levels of calcium ions < ref name =" Manev "> Manev H, Favaron M, Guidotti A, and Costa E. Delayed increase of Ca < sup > 2 +</ sup > influx elicited by glutamate: role in neuronal death.
Ca < sup > 2 +</ sup > influx into cells activates a number of enzymes, including phospholipases, endonucleases, and proteases such as calpain.
An influx of Ca < sup > 2 +</ sup > produces increased intracellular cAMP levels and thus, an increase in motility.
# The Ca < sup > 2 +</ sup > influx causes vesicles containing the neurotransmitter acetylcholine to fuse with the plasma membrane, releasing acetylcholine out into the extracellular space between the motor neuron terminal and the neuromuscular junction of the skeletal muscle fiber.
MK-801 binds inside the ion channel of the receptor at several of PCP's binding sites thus preventing the flow of ions, including an influx of calcium ( Ca < sup > 2 +</ sup >), through the channel.
In non-excitable cells such as blood cells, capacitative calcium entry appears to be the major means of regulated influx of Ca < sup > 2 +</ sup > and signal transduction.
By binding to the NMDA receptor with a higher affinity than Mg < sup > 2 +</ sup > ions, memantine is able to inhibit the prolonged influx of Ca < sup > 2 +</ sup > ions, particularly from extrasynaptic receptors, which forms the basis of neuronal excitotoxicity.
Calcium channels are activated and cause the influx of Ca < sup > 2 +</ sup > ions over the membrane and to the release of calcium from the endoplasmic reticulum.
Ca and mitochondrial
A critical role for the ER in calcium signaling was acknowledged before such a role for the mitochondria was widely accepted, in part because the low affinity of Ca < sup > 2 +</ sup > channels localized to the outer mitochondrial membrane seemed to fly in the face of this organelle ’ s purported responsiveness to changes in intracellular Ca < sup > 2 +</ sup > flux.
SERCA is likewise affected by mitochondrial feedback: uptake of Ca < sup > 2 +</ sup > by the MAM stimulates ATP production, thus providing energy that enables SERCA to reload the ER with Ca < sup > 2 +</ sup > for continued Ca < sup > 2 +</ sup > efflux at the MAM.
However, once Ca < sup > 2 +</ sup > signaling in the mitochondria passes a certain threshold, it stimulates the intrinsic pathway of apoptosis in part by collapsing the mitochondrial membrane potential required for metabolism.
Studies examining the role of pro-and anti-apoptotic factors support this model ; for example, the anti-apoptotic factor Bcl-2 has been shown to interact with IP3Rs to reduce Ca < sup > 2 +</ sup > filling of the ER, leading to reduced efflux at the MAM and preventing collapse of the mitochondrial membrane potential post-apoptotic stimuli.
Given the need for such fine regulation of Ca < sup > 2 +</ sup > signaling, it is perhaps unsurprising that dysregulated mitochondrial Ca < sup > 2 +</ sup > has been implicated in several neurodegenerative diseases, while the catalogue of tumor suppressors includes a few that are enriched at the MAM.
In addition to the matrix pool of grp75, a portion serves as a chaperone that physically links the mitochondrial and ER Ca < sup > 2 +</ sup > channels VDAC and IP3R for efficient Ca < sup > 2 +</ sup > transmission at the MAM.
The release of Ca < sup > 2 +</ sup > from the ER causes an increase in the cytosolic and mitochondrial concentrations of Ca < sup > 2 +</ sup >.
In ALS, a disorder in the glutamate receptor channels leads to high calcium conductivity, resulting in high Ca < sup > 2 +</ sup > loads and increased risk for mitochondrial damage.
As Ca < sup > 2 +</ sup > accumulates in the neuron, the buffering levels of mitochondrial Ca < sup > 2 +</ sup > sequestration are exceeded, which has major consequences for the neuron.
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