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It has been shown that the propagation of the TRPV1-induced cytosolic calcium and sodium fluxes into mitochondria is dependent on coordinated activity of NCLX and MCU.
Store-operated Ca(2+) entry activates a mitochondrial redox transient which is dependent on NCLX and is required for preventing Orai1 inactivation through oxidation of a critical cysteine (Cys195) in the third transmembrane helix of Orai1.
NCLX, but not LETM1, mediates Ca(2+) extrusion from mitochondria. By controlling the duration of matrix Ca(2+) elevations, NCLX contributes to the regulation of NAD(P)H production and to the conversion of Ca(2+) signals into redox changes.
NCKX6 is a novel member of the Na+/Ca2+ exchanger superfamily
NCLX catalyzes active Li(+)/Ca(2+) exchange.
Results found that NCLX reduction/inhibition markedly suppressed chemotaxis while increasing the random migration of B lymphocytes. In addition, the contributions of NCLX to motility were observed only in B lymphocytes and not in T lymphocytes.
tamoxifen-induced deletion of Slc8b1 in adult mouse hearts causes sudden death, with less than 13% of affected mice surviving after 14 days; lethality correlated with severe myocardial dysfunction and fulminant heart failure
NCLX mediates the mitochondrial Na(+) influx and is tuned to sense the TTX-sensitive cytosolic Na(+) responses.
NCLX is a novel molecule to regulate automaticity of cardiomyocytes via modulating sarcoplasmic reticulum Ca(2+) handling.
Silencing of NCLX expression significantly reduces Ca2+-dependent processes in astrocytes.
The findings suggest that the mitochondrial Na(+)/Ca(2+) exchanger, NCLX, shapes glucose-dependent mitochondrial and cytosolic Ca(2+) signals thereby regulating the temporal pattern of insulin secretion in beta cells.
data provide evidence for the presence of an electrogenic Na(+)/Ca(2+) exchanger that is capable of regulating [Ca(2+)](i) after release of Ca(2+) from cell stores
Presence of a Na(+)-Ca(2+) exchanger in podocytes and its regulation by PKC.
Ca(2+) entering the myocyte via NCX can cause Ca(2+) sparks which are similar to those elicited by electrical stimulation. However, Ca(2+) influx on NCX is much less efficient in inducing Ca(2+) sparks than Ca(2+) influx via I(Ca,L).
An electrophysiologically distinct subset of arcuate nucleus neurons coexpress orexin receptors and glutamate decarboxylase-67 and are excited by orexin, activating a sodium-calcium exchange current, thereby depolarizing the cell and increasing its firing
SLC24A6 belongs to a family of potassium-dependent sodium/calcium exchangers that maintain cellular calcium homeostasis through the electrogenic countertransport of 4 sodium ions for 1 calcium ion and 1 potassium ion (Cai and Lytton, 2004
solute carrier family 24 (sodium/potassium/calcium exchanger), member 6
, solute carrier family 24 member 6
, sodium/potassium/calcium exchanger 6-like
, Na(+)/K(+)/Ca(2+)-exchange protein 6
, sodium/calcium exchanger protein, mitochondrial
, sodium/potassium/calcium exchanger 6, mitochondrial
, sodium/potassium/calcium exchanger 6
, solute carrier family 24 (sodium/lithium/calcium exchanger), member 6