Purified from rabbit antiserum by affinity chromatography using epitope specific phosphopeptide. The antibody against non-phosphopeptide was removed by chromatography using non-phosphopeptide corresponding to the phosphorylation site.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use at an assay dependent concentration. Predicted molecular weight: 6 kDa. PubMed: 24386101
1/500 - 1/1000.
Reversibly inhibits the activity of ATP2A2 in cardiac sarcoplasmic reticulum by decreasing the apparent affinity of the ATPase for Ca(2+). Modulates the contractility of the heart muscle in response to physiological stimuli via its effects on ATP2A2. Modulates calcium re-uptake during muscle relaxation and plays an important role in calcium homeostasis in the heart muscle. The degree of ATP2A2 inhibition depends on the oligomeric state of PLN. ATP2A2 inhibition is alleviated by PLN phosphorylation.
Phosphorylation by PKA abolishes the inhibition of ATP2A2-mediated calcium uptake. Phosphorylated at Thr-17 by CaMK2, and in response to beta-adrenergic stimulation. Phosphorylation by DMPK may stimulate sarcoplasmic reticulum calcium uptake in cardiomyocytes.
Endoplasmic reticulum membrane. Sarcoplasmic reticulum membrane. Mitochondrion membrane. Membrane. Colocalizes with HAX1 at the endoplasmic reticulum (PubMed:17241641). Colocalizes with DMPK a the sarcoplasmic reticulum (PubMed:15598648).
Immunofluorescence analysis of HuvEc cells, using Phospholamban (phospho S16 + T17) antibody (ab62170) at 1/500 - 1/1000 dilution, in the presence (right panel) and absence (left panel) of immunising phosphopeptide.
References for Anti-Phospholamban (phospho S16 + T17) antibody (ab62170)
This product has been referenced in:
Kim GE et al. LKB1 deletion causes early changes in atrial channel expression and electrophysiology prior to atrial fibrillation. Cardiovasc Res108:197-208 (2015).
Read more (PubMed: 26378152) »
Huang Y et al. Sarcoplasmic phospholamban protein is involved in the mechanisms of postresuscitation myocardial dysfunction and the cardioprotective effect of nitrite during resuscitation. PLoS One8:e82552 (2013).
Read more (PubMed: 24386101) »