User:Haze2332/sandbox

Calcium Concentration Regulation

[Move picture somewhere later]

The resting concentration of Ca²⁺ in the

Depletion of calcium from the endoplasmic reticulum will lead to Ca²⁺ entry from outside the cell by activation of "Store-Operated Channels" (SOCs). This inflowing calcium current that results after stored calcium reserves have been released is referred to as Ca²⁺-release-activated Ca²⁺ current (ICRAC). The mechanisms through which ICRAC occurs are currently still under investigation, although two candidate molecules, Orai1 and STIM1, have been linked by several studies, and a model of store-operated calcium influx, involving these molecules, has been proposed. Recent studies have cited the phospholipase A2 beta,^[2] nicotinic acid adenine dinucleotide phosphate (NAADP),^[3] and the protein STIM 1^[4] as possible mediators of ICRAC.

Movement of calcium ions from the extracellular compartment to the intracellular compartment alters membrane potential. This is seen in the heart, during the plateau phase of ventricular contraction. In this example, calcium acts to maintain depolarization of the heart. Calcium signaling through ion channels is also important in neuronal

Calcium as a secondary messenger

Important physiological roles for calcium signaling range widely. These include

Many of Ca²⁺-mediated events occur when the released Ca²⁺ binds to and activates the regulatory protein calmodulin. Calmodulin may activate calcium-calmodulin-dependent protein kinases, or may act directly on other effector proteins. Besides calmodulin, there are many other Ca²⁺-binding proteins that mediate the biological effects of Ca²⁺.

In

Calcium ions play an important role in cell signaling, especially with regards to the ER. In the neuron, the ER may serve in a network integrating numerous extracellular and intracellular signals in a binary membrane system with the plasma membrane. Such an association with the plasma membrane creates the relatively new perception of the ER and theme of “a neuron within a neuron.” [Rephrase] The ER’s structural characteristics, ability to act as a Ca²⁺ sink, and specific CCa²⁺ releasing proteins, serve to create a system that may produce regenerative waves of Ca²⁺ release that may communicate both locally and globally in the cell. These Ca²⁺ signals, integrating extracellular and intracellular fluxes, have been implicated to play roles in synaptic plasticity and memory, neurotransmitter release, neuronal excitability and long term changes at the gene transcription level. ER stress is also related to Ca²⁺ signaling and along with the unfolded protein response, can cause ER associated degradation (ERAD) and autophagy.[9]

See also

• Nanodomain

References

Further reading

• Petersen, Ole H (2005). "Ca²⁺ signalling and Ca²⁺-activated ion channels in exocrine acinar cells".
  PMID 16107275. {{cite journal}}: Cite has empty unknown parameters: |laydate=, |laysummary=, and |laysource= (help
  )

Wikimedia Commons has media related to Haze2332/sandbox.

Category:Cell signaling Category:Signal transduction