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N-Terminal Proteoforms in Human Disease

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Abstract
The collection of chemically different protein variants, or proteoforms, by far exceeds the number of protein-coding genes in the human genome. Major contributors are alternative splicing and protein modifications. In this review, we focus on those proteoforms that differ at their N termini with a molecular link to disease. We describe the main underlying mechanisms that give rise to such N-terminal proteoforms, these being splicing, initiation of protein translation, and protein modifications. Given their role in several human diseases, it is becoming increasingly clear that several of these N-terminal proteoforms may have potential as therapeutic interventions and/or for diagnosing and prognosing their associated disease.
Keywords
Biochemistry, Molecular Biology

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Please use this url to cite or link to this publication:

MLA
Bogaert, Annelies, et al. “N-Terminal Proteoforms in Human Disease.” Trends in Biochemical Sciences, 2020.
APA
Bogaert, A., Fernandez Fernandez, M., & Gevaert, K. (2020). N-Terminal Proteoforms in Human Disease. Trends in Biochemical Sciences.
Chicago author-date
Bogaert, Annelies, Maria Fernandez Fernandez, and Kris Gevaert. 2020. “N-Terminal Proteoforms in Human Disease.” Trends in Biochemical Sciences.
Chicago author-date (all authors)
Bogaert, Annelies, Maria Fernandez Fernandez, and Kris Gevaert. 2020. “N-Terminal Proteoforms in Human Disease.” Trends in Biochemical Sciences.
Vancouver
1.
Bogaert A, Fernandez Fernandez M, Gevaert K. N-Terminal Proteoforms in Human Disease. Trends in Biochemical Sciences. 2020;
IEEE
[1]
A. Bogaert, M. Fernandez Fernandez, and K. Gevaert, “N-Terminal Proteoforms in Human Disease,” Trends in Biochemical Sciences, 2020.
@article{8647000,
  abstract     = {The collection of chemically different protein variants, or proteoforms, by far exceeds the number of protein-coding genes in the human genome. Major contributors are alternative splicing and protein modifications. In this review, we focus on those proteoforms that differ at their N termini with a molecular link to disease. We describe the main underlying mechanisms that give rise to such N-terminal proteoforms, these being splicing, initiation of protein translation, and protein modifications. Given their role in several human diseases, it is becoming increasingly clear that several of these N-terminal proteoforms may have potential as therapeutic interventions and/or for diagnosing and prognosing their associated disease.},
  author       = {Bogaert, Annelies and Fernandez Fernandez, Maria and Gevaert, Kris},
  issn         = {0968-0004},
  journal      = {Trends in Biochemical Sciences},
  keywords     = {Biochemistry,Molecular Biology},
  language     = {eng},
  title        = {N-Terminal Proteoforms in Human Disease},
  url          = {http://dx.doi.org/10.1016/j.tibs.2019.12.009},
  year         = {2020},
}

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