Team:SMMU-China/Description

1 Heart failure
2 CaRTIN
References

Description

1 Heart failure

What is heart failure?

The main function of the heart is to pump blood, providing power to promote blood circulation to meet the metabolic needs of tissue cells throughout the body.

Heart failure is when the heart's systolic or diastolic function declines, resulting in a failure of cardiac output to meet the body's metabolic needs. Heart failure is the severe and terminal stage of various heart diseases. According to the patients at all stages, patients including hypertension, coronary heart disease and diabetes are at risk of heart failure.

Figure 1.

2 CaRTIN

What is RyR2? What is it made up of?

To identify the epitopes recognized by AR185, phage clones were isolated by panning the PhD.-7 phage display peptide library with AR185. Three rounds of selection were performed, and, at each round, the library was pre-cleared with a control AR177 nanobody. After the third round of panning, the binding of the isolated phage clones to AR185 was determined by ELISA. Sequence analysis of AR185-positive phage clones identified five and six distinct amino acid sequences, respectively (fig. S2). Alignment of these sequences revealed the consensus motifs DKLAC, which could be aligned with the (2725) DKLAN (2729) sequence located at P2 Domain of RyR2.

References

  1. W. Chen et al., Outline of the report on cardiovascular diseases in China, 2014. 18, F2 (2016).
  2. B. Ziaeian, G. C. J. N. R. C. Fonarow, Epidemiology and aetiology of heart failure. 13, 368 (2016).
  3. C. W. Yancy et al., 2016 ACC/AHA/HFSA Focused Update on New Pharmacological Therapy for Heart Failure: An Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure. 68, 1476-1488 (2016).
  4. J. S. Hulot, K. Ishikawa, R. J. J. E. H. J. Hajjar, Gene therapy for the treatment of heart failure: promise postponed. 37, 1651-1658 (2016).
  5. M. Luo, M. E. J. C. R. Anderson, Mechanisms of Altered Ca^2^+ Handling in Heart Failure. 113, 690-708 (2013).
  6. F. V. J. J. o. B. C. Petegem, Ryanodine Receptors: Structure and Function. 287, 31624-31632 (2012).
  7. G. W. Cho, F. Altamirano, J. A. J. B.-M. B. o. D. Hill, Chronic heart failure: Ca2+, catabolism, and catastrophic cell death. 1862, 763-777 (2016).
  8. J. Roussel et al., Palmitoyl-carnitine increases RyR2 oxidation and sarcoplasmic reticulum Ca 2 + leak in cardiomyocytes: Role of adenine nucleotide translocase. 1852, 749-758 (2015).
  9. M. Munkvik et al., Training effects on skeletal muscle calcium handling in human chronic heart failure. 42, 847-855 (2010).
  10. S. O. Marx et al., PKA Phosphorylation Dissociates FKBP12.6 from the Calcium Release Channel (Ryanodine Receptor). 101, 365-376 (2000).
  11. X. H. Wehrens et al., Ryanodine receptor/calcium release channel PKA phosphorylation: a critical mediator of heart failure progression. Proc Natl Acad Sci U S A 103, 511-518 (2006).
  12. J. Shan et al., Role of chronic ryanodine receptor phosphorylation in heart failure and β-adrenergic receptor blockade in mice. 120, 4375-4387 (2010).
  13. H. Zhang et al., Hyperphosphorylation of the cardiac ryanodine receptor at serine 2808 is not involved in cardiac dysfunction after myocardial infarction. 110, 831 (2012).
  14. S. R. J. C. R. Houser, Role of RyR2 phosphorylation in heart failure and arrhythmias: protein kinase A-mediated hyperphosphorylation of the ryanodine receptor at serine 2808 does not alter cardiac contractility or cause heart failure and arrhythmias. 114, 1320-1327 (2014).
  15. S. Steeland, R. E. Vandenbroucke, C. J. D. D. T. Libert, Nanobodies as therapeutics: big opportunities for small antibodies. 21, 1076-1113 (2016).
  16. F. Peyvandi et al., Caplacizumab reduces the frequency of major thromboembolic events, exacerbations, and death in patients with acquired thrombotic thrombocytopenic purpura. 15, 1448-1452 (2017).
  17. T. Dörner et al., in European Congress of Rheumatology, 14–17 June. (2017), pp. 575.572-575.
  18. Safety and efficacy of multiple ascending doses of subcutaneous M1095, an anti-interleukin-17A/F bispecific nanobody, in patients with moderate-to-severe psoriasis %J Retour Au Numéro. (2017).
  19. L. D. Wang, D. X. Feng, S. M. Zhang, B. M. J. L. i. B. University, Research Progress of Nanobody. (2016).
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