|Calculated MW||131100 Da|
|Homology||Mouse - 13/14 amino acid residues identical; human - 10/14 amino acid residues identical.|
|Other Names||Potassium channel subfamily T member 2, Sequence like an intermediate conductance potassium channel subunit, Sodium and chloride-activated ATP-sensitive potassium channel Slo21, Kcnt2, Slick|
|Related products for control experiments||Control peptide antigen (supplied with the antibody free of charge).|
|Target/Specificity||Peptide (C)KDVKDPGHHRSIHR, corresponding to amino acid residues 991-1004 of rat KCa4.2 (Accession Q6UVM4). Intracellular, C-terminus.|
|Peptide Confirmation||Confirmed by amino acid analysis.|
|Format||Affinity purified antibody, lyophilized powder|
|Reconstitution||50 µl or 0.2 ml deionized water, depending on the sample size.|
|Antibody Concentration After Reconstitution||0.8 mg/ml.|
|Buffer After Reconstitution||Phosphate buffered saline (PBS), pH 7.4, 1% BSA, 0.025% NaN3.|
|Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Storage After Reconstitution||The reconstituted solution can be stored at 4ºC for up to 2 weeks. For longer periods, small aliquots should be stored at -20ºC or below. Avoid multiple freezing and thawing. The further dilutions should be made using a carrier protein such as BSA (1%). Centrifuge all antibody preparations before use (10000 × g 5 min).|
|Control Antigen Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Control Antigen Reconstitution||100 µl water.|
|Control Antigen Storage After Reconstitution||-20ºC.|
|Preadsorption Control||1 µg peptide per 1 µg antibody.|
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Provided below are standard protocols that you may find useful for product applications.
KCa4.1 (Slack, Na+ activated K+ channel, Slo2.2, KCNT1) was originally cloned and named so due to its high similarity to the Slo genes1. Shortly after its discovery, KCa4.2 (Slick, Slo2.1, KCNT2), its sister channel was also cloned2. Although KCa4.2 (like KCa4.1) is functionally a Na+-activated K+ channel (KNa), it is termed KCa by the IUPHAR nomenclature, due to its sequence homology to other KCa channels. Both channels are activated by high intracellular concentrations of Na+. Like Slack, Slick contains six transmembrane spanning domains, a P-region between transmembrane regions 5 and 6 and intracellular N- and C-termini. However, the N-terminal domain of Slick is significantly shorter than that of Slack. In addition, contrary to Slack, Slick is regulated by ATP as it has an ATP binding site in its C-terminal domain2. ATP binding reduces the activity of the channel and mutations of this site abolish the inhibitory effect2. Both channels are regulated by intracellular Cl- ions, but Slick displays higher sensitivity3. Also, the overall electrical characteristics of Slick channels are different from those of Slack; Slick is rapidly activated in response to depolarization, and also has a basal level of activity in the absence of Na+. Both channels are highly expressed in the brain with overlapping expression. Slick is found in the midbrain, brainstem, and hippocampus and throughout the neocortex. This KNa channel is also detected in the auditory neurons in the brainstem. Detection of Slick was also found in the heart, although at much lower levels2. Many different functions have been attributed to KNa channels including action potential repolarization, slow after-hyperpolarization, burst firing and adaptation after repetitive firing3. These channels also contribute to the response of neurons to hypoxia. Abgent is pleased to offer a highly specific antibody directed against an epitope located at the intracellular C-terminal domain of the rat KCa4.2 channel. Anti-KCa4.2 (Slick) antibody (#AG1088) can be used in western blot applications, and was designed to recognize KCa4.2 from rat and mouse samples.
References 1. Yuan, A. et al. (2003) Neuron 37, 765. 2. Bhattacharjee, A. et al. (2003) J. Neurosci. 23, 11681. 3. Bhattacharjee, A. and Kaczmarek, L.K. (2005) Trends Neurosci. 28, 422.
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