Product Name	phospholamban
Chinese Name	受磷蛋白/心脏磷蛋白抗体
Alias	Cardiac phospholamban; CMD1P; PLB; PLN; PPLA_HUMAN.
Research Area	Tumour  Cardiovascular  immunology  Signal transduction  Channel protein  Mitochondrion  The cell membrane蛋白
Immunogen Species	Rabbit
Clonality	Polyclonal
React Species	(predicted: Human, Mouse, Rat, Pig, Cow, )
Applications	ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 （Paraffin sections need antigen repair） not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
Theoretical molecular weight	5.7kDa
Cellular localization	cytoplasmic The cell membrane Mitochondrion
Form	Liquid
Concentration	1mg/ml
immunogen	KLH conjugated synthetic peptide derived from human phospholamban: 1-35/52
Lsotype	IgG
Purification	affinity purified by Protein A
Buffer Solution	0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
Storage	Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
Attention	This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed	PubMed
Product Detail	The Sarco(endo)plasmic-reticulum (SER) regulatory protein, Phospholamban (PLB), is a small, plasma membrane-associated phospho-protein found in the SER of cardiac, smooth and slow-twitch muscle. Believed to assemble into a pentamer, PLB regulates cardiac contractility and Ca2+ affinity for cardiac SER Ca2+ ATPase (SERCA2a). Non-phosphorylated PLB associates with SERCA2a, and inhibits Ca2+ reuptake into the SER. PLB activation occurs when key Serine/Threonine residues in PLB (Ser-10, Ser-16, Thr-17) are phosphorylated by numerous effectors, which include PKC, PKA, PKG, and CaM kinase. Phosphorylation of PLB causes dissociation from SERCA2a and a subsequent increase in the rate of Ca2+ reuptake into the SER, which accelerates ventricular relaxation. Function: Phospholamban has been postulated to regulate the activity of the calcium pump of cardiac sarcoplasmic reticulum. Subcellular Location: Mitochondrion membrane; Single-pass membrane protein. Sarcoplasmic reticulum. Tissue Specificity: Heart. Post-translational modifications: Phosphorylated at Thr-17 by CaMK2, and in response to beta-adrenergic stimulation. Phosphorylation by DMPK may stimulate sarcoplasmic reticulum calcium uptake in cardiomyocytes. DISEASE: Defects in PLN are the cause of cardiomyopathy dilated type 1P (CMD1P) [MIM:609909]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death. Defects in PLN are the cause of familial hypertrophic cardiomyopathy type 18 (CMH18) [MIM:613874]. CMH18 is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death. Similarity: Belongs to the phospholamban family. SWISS: P26678 Gene ID: 5350 Database links: Entrez Gene: 5350 Human Entrez Gene: 18821 Mouse Entrez Gene: 64672 Rat Omim: 172405 Human SwissProt: A4IFH6 Cow SwissProt: P26678 Human SwissProt: P61014 Mouse SwissProt: P61013 Pig SwissProt: P61015 Rabbit SwissProt: P61016 Rat Unigene: 170839 Human Unigene: 34145 Mouse Unigene: 9740 Rat

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