Recombinant Human Cardiac phospholamban(PLN)

Code CSB-YP018198HU
Size US$1298
Image
  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
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Product Details

Purity Greater than 90% as determined by SDS-PAGE.
Target Names P26678
Uniprot No. P26678
Research Area Cardiovascular
Alternative Names Cardiac phospholamban; CMD1P; CMH18; PLB; Pln; PPLA_HUMAN
Species Homo sapiens (Human)
Source Yeast
Expression Region 1-52aa
Target Protein Sequence MEKVQYLTRSAIRRASTIEMPQQARQKLQNLFINFCLILICLLLICIIVMLL
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight 33.1kDa
Protein Length Full Length
Tag Info N-terminal GST-tagged
Form Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer Tris-based buffer,50% glycerol
Reconstitution We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting
and FAQs
Protein FAQs
Storage Condition Store at -20°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA Please contact us to get it.

Q&A and Customer Reviews

 Q&A
Q:

I ask if there is a cleavage site between the GST tag and the protein for item CSB-YP018198HU Recombinant Homo sapiens Cardiac phospholamban.

A:
Very nice to receive your inquiry. The product details are as below.
Code: CSB-YP018198HU
Name: Recombinant Human Cardiac phospholamban(P26678)
Lead Time for Regular Size: 22-32 working days.
Expression Region: 1-52aa, full length
Tag Info: N-terminal GST-tag
Target Protein Sequence:

MEKVQYLTRSAIRRASTIEMPQQARQKLQNLFINFCLILICLLLICIIVMLL


The sequence of GST-tag is as below.

MSPILGYWKIKGLVQPTRLLLEYLEEKYEEHLYERDEGDKWRNKKFELGLEFPNLPYYIDGDVKLTQSMAIIRYIADKHNMLGGCPKERAEISMLEGAVLDIRYGVSRIAYSKDFETLKVDFLSKLPEMLKMFEDRLCHKTYLNGDHVTHPDFMLYDALDVVLYMDPMCLDAFPKLVCFKKRIEAIPQIDKYLKSSKYIAWPLQGWQATFGGGDHPPKSDLEVLFQGPLGSPEFRT


The restriction site is LGSPEF. The enzyme is PSP (PreScission Protease).

Target Data

Function 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.
Gene References into Functions
  1. 2 lethal PLN mutations, R9C and R25C, which lead to dilated cardiomyopathy, were studied by biomolecular NMR. R25C enhances phospholmaban dynamics and shifts the conformational equilibrium toward the R state. R9C drives the amphipathic cytoplasmic domain toward the membrane-associate state, enriching the T state. PMID: 29501609
  2. Structure-Function Relationship of the SERCA Pump and Its Regulation by Phospholamban and Sarcolipin. PMID: 29594859
  3. The co-transfection of VHL and PLN in HEK293 cells decreased PLN expression under oxidative stress, whereas knockdown of VHL increased PLN expression both under normal and oxidative stress conditions. PMID: 29068413
  4. Hearts from patients with a p. Arg14del PLN mutation have a pattern of Right Ventricle Fibrofatty Replacement and Left Ventricular Fibrosis with fatty changes mostly in the posterolateral wall, independently of clinical presentation. PMID: 28365402
  5. LMOD1, SYNPO2, PDLIM7, PLN, and SYNM down-regulation reflect the altered phenotype of smooth muscle cells in vascular disease and could be early sensitive markers of SMC dedifferentiation. PMID: 27470516
  6. microRNAs (miRNAs) 1 and 21 bind PLN strongly and relieve PLN inhibition of SERCA to a greater extent than a similar length random sequence RNA mixture. PMID: 27531746
  7. Data suggest phospholamban (PLN) gene is a rare cause of cardiomyopathy in African patients. PMID: 26917049
  8. Phospholamban and sarcolipin are membrane proteins that differentially regulate SERCA function. (Review) PMID: 26743715
  9. PLN may be a key molecular player in rigid substrate-induced cellular hypertrophy in eosinophilic esophagitis. PMID: 26542032
  10. These data suggest that PLN is, at least partially, oligo-ubiquitinated at Lys(3) and degraded through Ser(16)-phosphorylation-mediated poly-ubiquitination during heart failure. PMID: 26966065
  11. hereditary mutants of phospholamban are associated with heart failure [review] PMID: 25563649
  12. PLN pentamers reduce phosphorylation of monomers at baseline and delay monomer phosphorylation upon PKA stimulation leading to increased interaction of PLN monomers with SERCA2a. PMID: 25562800
  13. Phospholamban R14del mutation carriers are at high risk for malignant ventricular arrhythmias and end-stage heart failure, with left ventricular ejection fraction <45% and sustained or nonsustained ventricular tachycardia as independent risk factors. PMID: 24909667
  14. Although SLN and PLB binding to SERCA have different functional outcomes on the coupling efficiency of SERCA, both proteins decrease the apparent Ca(2+) affinity of the pump, suggesting that SLN and PLB inhibit SERCA by using a similar mechanism. PMID: 25983321
  15. Phospholamban, and its interacting partners, regulates excitation contraction coupling and myocardial contraction. [Review] PMID: 25451386
  16. PLN mutations rarely cause cardiomyopathy PMID: 25928149
  17. analysis of how the conformational dynamics of protein kinase A induced by a lethal mutant of phospholamban hinder phosphorylation PMID: 25775607
  18. Aim of the present study is to determine the exact pattern of fibrosis and fatty replacement in PLN p.Arg14del mutation positive patients. PMID: 24732829
  19. Engineered upregulation of PLB expression in hESC/iPSC-vCMs restores a positive inotropic response to beta-adrenergic stimulation. PMID: 25504561
  20. a previously unrecognized mechanism for ESM cell contraction that depends on TGF-beta1, its receptors, and PLN. PMID: 24835503
  21. We conclude that PLB C-terminal residues are critical for localization, oligomerization, and regulatory function. In particular, the PLB C terminus is an important determinant of the quaternary structure of the SERCA regulatory complex. PMID: 25074938
  22. SLN and PLN are co-expressed in most fibers, which suggests that super-inhibition of SERCAs may be physiologically important in the regulation of intracellular Ca2+ in human skeletal muscle. PMID: 24358354
  23. Report PLN mutations in dilated cardiomyopathy. PMID: 24037902
  24. A PLN founder mutation and LMNA mutations were most prevalent and often demonstrated a specific phenotype in dilated cardiomyopathy patients PMID: 23349452
  25. PLN mutation carriers have ARVD/C characteristics, including important right ventricular involvement, and additionally more often low-voltage electrocardiograms, inverted T waves in the left precordial leads, and left ventricular involvement. PMID: 23871674
  26. In the context of data on PLN/SERCA interaction and on Ca(2+) accumulation in the sarcoplasmic reticulum the present results are consistent with the view that PLN channel activity could participate in the balancing of charge during Ca(2+) uptake. PMID: 23308118
  27. The researchers found evidence of an association between the phospholamban R14del and the presence of dilated or arrhythmogenic cardiomyopathies in a group of patients. PMID: 22820313
  28. 1,014 patients with heart failure screened for mutations in PLN gene; identified 4 unrelated patients with PLN mutations, 3 in same amino acid residue (R9); conclude mutations in PLN gene are rare cause of heart failure, present almost exclusively in patients with dilated cardiomyopathy etiology; Arg9 and Leu39 residues are leading location of mutations described to date PMID: 22137083
  29. human PLN-R14Del is misrouted to the sarcolemma, in the absence of endogenous PLN, and alters NKA activity, leading to cardiac remodeling. PMID: 22155237
  30. Hydrophobic imbalance in the cytoplasmic domain of phospholamban is a determinant for lethal dilated cardiomyopathy. PMID: 22427649
  31. TOAC spin labels placed on the WT-PLB transmembrane domain showed highly restricted motion with more than 100ns rotational correlation time (tau(c)); whereas the loop, and the cytoplasmic regions each consists of two distinct motional dynamics PMID: 22172806
  32. Characterizing phospholamban to sarco(endo)plasmic reticulum Ca2+-ATPase 2a (SERCA2a) protein binding interactions in human cardiac sarcoplasmic reticulum vesicles using chemical cross-linking. PMID: 22247554
  33. PLN generates canonical ion channel fluctuations with two conductance levels and a moderate cation selectivity PMID: 21687864
  34. both topology and function of PLN are shaped by the interactions with lipids, which fine-tune the regulation of SERCA PMID: 21576492
  35. PLN gene mutations were not found to be associated with HCM in the study group. PMID: 21332051
  36. Lethal Arg9Cys phospholamban mutation hinders Ca2+-ATPase regulation and phosphorylation by protein kinase A. PMID: 21282613
  37. Mutations in PLN are rare in frequency, yet the small size of the genetic locus may make it amenable to inclusion on HCM gene test panels. PMID: 21167350
  38. In this study, they investigated the effects of PLB phosphorylation and mutation on the interaction between a PLB oligomer and SERCA in the context of 2D crystals. PMID: 21108950
  39. Study conclude that PLN is enriched in the ER due to COP I-mediated transport that is dependent on its intact di-arginine motif and that the N-terminal di-arginine motif may act as a general ER retrieval sequence. PMID: 20634894
  40. sarcolipin binds to phospholamban and inhibits polymerization PMID: 12032137
  41. phosphorylation of phospholamban does not affect its structure and gives it more loose helical packing than if not phosphorylated PMID: 12080135
  42. Modeling of the inhibitory interaction of phospholamban with the Ca2+ ATPase. PMID: 12525698
  43. report that an inherited human dilated cardiomyopathy with refractory congestive heart failure is caused by a dominant Arg --> Cys missense mutation at residue 9 (R9C) in phospholamban PMID: 12610310
  44. role in regulating sarco(endo)plasmic reticulum Ca2+-ATPase by binding to transmembrane helices in conjunction with sarcolipin PMID: 12692302
  45. Mutation of the phospholamban promoter associated with hypertrophic cardiomyopathy. PMID: 12705874
  46. SERCA2a and phospholamban bind to S100A1 in the human heart PMID: 12804600
  47. The frequency-dependent phosphorylation of Ser16-PLB may favor an increase in Ca2+ transient and force generation in humans. PMID: 14530977
  48. This study concludes that phospholamban (PLB) increases the maximal activity (Vmax) of calcium (Ca2+)-ATPase, and that the magnitude of this effect is sensitive to mutation. A region of mutant PLB responsible for this regulatory property is identified. PMID: 15736939
  49. The unusual bellflower-like assembly is held together by leucine/isoleucine zipper motifs along the membrane-spanning helices. PMID: 16043693
  50. the nonreversible superinhibitory function of mutant PLN-R14Del may lead to inherited dilated cardiomyopathy and premature death in both humans and mice PMID: 16432188
  51. Human PLN may play a more inhibitory role than that of other species in Ca2+ cycling. Expression of human PLN in the mouse is compensated by alterations in Ca2+-handling proteins and cardiac remodeling in an effort to normalize cardiac contractility. PMID: 16476846
  52. Mutations in the phospholamban gene are not a frequent cause of hypertrophic and idiopathic dilated cardiomyopathy. PMID: 16829191
  53. Phospholamban in the human esophagus might be of less importance for regulation of SERCA than in heart. Lower expression of calsequestrin and calreticulin might contribute to increased lower esophageal sphincter pressure in achalasia. PMID: 17009399
  54. Gene expression of PLB was studied in children with congenital heart defects. PMID: 17515962
  55. A truncation mutant was identified in PLN. PMID: 17655857
  56. The structure and dynamics of PLN pentamer was compared in its unphosphorylated and pseudo-phosphorylatd states. PMID: 17766390
  57. analysis of phospholamban in oriented lipid bilayers using 15N solid-state NMR spectroscopy PMID: 17905829
  58. G147D PPI-1 can attenuate responses of cardiomyocytes to beta-adrenergic agonists by decreasing PLN phosphorylation and therefore may contribute to deteriorated function in heart failure. PMID: 18192322
  59. findings suggest that the g.203A>C genetic variant in the human phospholamban promoter may contribute to depressed contractility and accelerate functional deterioration in heart failure PMID: 18241046
  60. analysis of how mutations increase phospholamban oligomerization and alter the structure of its regulatory complex PMID: 18708665
  61. A weak inhibitor transgene PLN(Arg9Cys) is diminished in its ability to modify the level of sarco(endo)plasmic reticulum ccalcium-ATPase activity, leading to heart failure despite fast sarcoplasmic reticulum calcium ion reuptake. PMID: 19139388
  62. Attenuated R amplitudes were identified as an early ECG phenotype in a family with familial dilated cardiomyopathy due to the PLN-R14Del mutation. PMID: 19324307
  63. PLN is a key regulator of cardiac diastolic function and is involved in regulating intracellular calcium cycling, it has only recently been identified as a susceptibility locus for QT interval PMID: 19587794
  64. Data do not support a role for the phospholamban -36A>C alteration in modulating the heart failure phenotype. PMID: 19638213
  65. These data demonstrate that alphaKAP exhibits a novel interaction with SERCA2a and may serve to spatially position CaMKII isoforms at the SR and to uniquely modulate the phosphorylation of PLN. PMID: 19671701
  66. Three steps in the kinetic reaction with calcium-dependent ATPase (SERCA) are affected by the presence of PLB: binding of the first calcium ion, a subsequent conformational change in SERCA, and binding of the second calcium ion. PMID: 19708671
  67. Meta-analysis and genome-wide association study of gene-disease association and gene-gene interaction. (HuGE Navigator) PMID: 19587794

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Involvement in disease Cardiomyopathy, dilated 1P (CMD1P); Cardiomyopathy, familial hypertrophic 18 (CMH18)
Subcellular Location Endoplasmic reticulum membrane, Single-pass membrane protein, Sarcoplasmic reticulum membrane, Single-pass membrane protein, Mitochondrion membrane, Single-pass membrane protein, Membrane, Single-pass membrane protein
Protein Families Phospholamban family
Tissue Specificity Heart muscle (at protein level).
Database Links

HGNC: 9080

OMIM: 172405

KEGG: hsa:5350

STRING: 9606.ENSP00000350132

UniGene: Hs.170839

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