N-Terminal Proteoforms in Human Disease

被引：32

作者：

Bogaert, Annelies ^{[1
,2
]}

Fernandez, Esperanza ^{[1
,2
]}

Gevaert, Kris ^{[1
,2
]}

机构：

[1] VIB, VIB Ctr Med Biotechnol, B-9000 Ghent, Belgium

[2] Univ Ghent, Dept Biomol Med, B-9000 Ghent, Belgium

来源：

TRENDS IN BIOCHEMICAL SCIENCES | 2020年 / 45卷 / 04期

基金：

欧盟地平线“2020”;

关键词：

ALTERNATIVE TRANSLATION INITIATION; ALPHA-SYNUCLEIN; MESSENGER-RNAS; MUTANT P53; ACETYLATION; CELLS; IRES; AGGREGATION; PROTEOME; ISOFORMS;

D O I：

10.1016/j.tibs.2019.12.009

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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 altemative 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.

引用

页码：308 / 320

页数：13

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