Sodium-calcium exchanger

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solute carrier family 8 (sodium/calcium exchanger), member 1
Identifiers
Symbol	SLC8A1 NCX1
HUGO	11068
Entrez	6546
OMIM	182305
RefSeq	NM_021097
UniProt	P32418
Other data
Locus	Chr. 2 p23-p21

solute carrier family 8 (sodium-calcium exchanger), member 2
Identifiers
Symbol	SLC8A2
HUGO	11069
Entrez	6543
OMIM	601901
RefSeq	NM_015063
UniProt	Q9UPR5
Other data
Locus	Chr. 19 q13.2

solute carrier family 8 (sodium-calcium exchanger), member 3
Identifiers
Symbol	SLC8A3
HUGO	11070
Entrez	6547
OMIM	607991
RefSeq	NM_033262
UniProt	P57103
Other data
Locus	Chr. 14 q24.1

The sodium-calcium exchanger (often denoted Na⁺/Ca²⁺ exchanger, NCX, or exchange protein) is an antiporter ion pump membrane protein which removes calcium from cells. It uses the energy that is stored in the electrochemical gradient of sodium (Na⁺) by allowing Na⁺ to flow down its gradient across the plasma membrane in exchange for the countertransport of calcium ions (Ca²⁺). The NCX removes a single calcium ion in exchange for the import of three sodium ions.^[1] using the Na⁺

The Na⁺/Ca²⁺ exchanger does not bind very tightly to Ca²⁺ (has a low affinity), but it can transport the ions rapidly (has a high capacity), transporting up to five thousand Ca2+ ions per second.^[2] Therefore it requires large concentrations of Ca²⁺ to be effective, but is useful for ridding the cell of large amounts of Ca²⁺ in a short time, as is needed in a neuron after an action potential. Thus the exchanger also likely plays an important role in regaining the cell's normal calcium concentrations after an excitotoxic insult. Another, more ubiquitous transmembrane pump that exports calcium from the cell is the Plasma membrane Ca²⁺ ATPase (PMCA), which has a much higher affinity but a much lower capacity. Since the PMCA is capable of effectively binding to Ca²⁺ even when its concentrations are quite low, it is better suited to the task of maintaining the very low concentrations of calcium that are normally within a cell.^[3] Therefore the activities of the NCX and the PMCA complement each other.

1 Reversibility
2 See also
3 References
4 External links

[edit] Reversibility

Since the transport is electrogenic (alters the membrane potential), depolarization of the membrane can reverse the exchanger's direction if the cell is depolarized enough, as may occur in excitotoxicity.^[1] In addition, like other transport proteins, the amount and direction of transport depends on transmembrane substrate gradients.^[1] This fact can be protective because increases in intracellular Ca²⁺ concentration that occur in excitotoxicity may activate the exchanger in the forward direction even in the presence of a lowered extracellular Na⁺ concentration.^[1] However, it also means that when intracellular levels of Na⁺ rise beyond a critical point, the NCX begins importing Ca²⁺^[1]^[4]^[5] The NCX may operate in both forward and reverse directions simultaneously in different areas of the cell, depending on the combined effects of Na⁺ and Ca²⁺ gradients.^[1]

[edit] See also

[edit] References

^ ^a ^b ^c ^d ^e ^f Yu, SP; Choi DW (1997). "Na⁺–Ca²⁺ exchange currents in cortical neurons: concomitant forward and reverse operation and effect of glutamate". European Journal of Neuroscience 9 (6): 1273-1281. PMID 9215711. Retrieved on 2007-01-15.
^ Carafoli, E; Santella L, Branca D, and Brini M. (2001). "Generation, control, and processing of cellular calcium signals". Critical Reviews in Biochemistry and Molecular Biology 36 (2): 107–260. Retrieved on 2007-01-09.
^ Siegel, GJ; Agranoff BW, Albers RW, Fisher SK, Uhler MD, editors (1999). Basic Neurochemistry: Molecular, Cellular, and Medical Aspects. 6th ed. Philadelphia: Lippincott,Williams & Wilkins.
^ Bindokas, VP; Miller RJ (1995). "Excitotoxic degeneration is initiated at non-random sites in cultured rat cerebellar neurons". Journal of Neuroscience 15 (11): 6999-7011. PMID 7472456. Retrieved on 2007-01-15.
^ Wolf, JA; Stys PK, Lusardi T, Meaney D, and Smith DH (2001). "Traumatic Axonal Injury Induces Calcium Influx Modulated by Tetrodotoxin-Sensitive Sodium Channels". Journal of Neuroscience 21 (6): 1923-1930. PMID 11245677. Retrieved on 2007-01-15.