Quality control system response to stochastic growth of amyloid fibrils

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Quality control system response to stochastic growth of amyloid fibrils. / Pigolotti, S.; Lizana, L.; Sneppen, K.; Otzen, Daniel.

In: F E B S Letters, Vol. 587, No. 9, 02.05.2013, p. 1405-1410.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Pigolotti, S, Lizana, L, Sneppen, K & Otzen, D 2013, 'Quality control system response to stochastic growth of amyloid fibrils', F E B S Letters, vol. 587, no. 9, pp. 1405-1410. https://doi.org/10.1016/j.febslet.2013.03.018

APA

Pigolotti, S., Lizana, L., Sneppen, K., & Otzen, D. (2013). Quality control system response to stochastic growth of amyloid fibrils. F E B S Letters, 587(9), 1405-1410. https://doi.org/10.1016/j.febslet.2013.03.018

Vancouver

Pigolotti S, Lizana L, Sneppen K, Otzen D. Quality control system response to stochastic growth of amyloid fibrils. F E B S Letters. 2013 May 2;587(9):1405-1410. https://doi.org/10.1016/j.febslet.2013.03.018

Author

Pigolotti, S. ; Lizana, L. ; Sneppen, K. ; Otzen, Daniel. / Quality control system response to stochastic growth of amyloid fibrils. In: F E B S Letters. 2013 ; Vol. 587, No. 9. pp. 1405-1410.

Bibtex

@article{f05b355294204c4a87ec30fa9c19588b,
title = "Quality control system response to stochastic growth of amyloid fibrils",
abstract = "We introduce a stochastic model describing aggregation of misfolded proteins and degradation by the protein quality control system in a single cell. Aggregate growth is contrasted by the cell quality control system, that attacks them at different stages of the growth process, with an efficiency that decreases with their size. Model parameters are estimated from experimental data. Two qualitatively different behaviors emerge: a homeostatic state, where the quality control system is stable and aggregates of large sizes are not formed, and an oscillatory state, where the quality control system periodically breaks down, allowing for formation of large aggregates. We discuss how these periodic breakdowns may constitute a mechanism for the development of neurodegenerative diseases.",
author = "S. Pigolotti and L. Lizana and K. Sneppen and Daniel Otzen",
year = "2013",
month = may,
day = "2",
doi = "10.1016/j.febslet.2013.03.018",
language = "English",
volume = "587",
pages = "1405--1410",
journal = "F E B S Letters",
issn = "0014-5793",
publisher = "JohnWiley & Sons Ltd",
number = "9",

}

RIS

TY - JOUR

T1 - Quality control system response to stochastic growth of amyloid fibrils

AU - Pigolotti, S.

AU - Lizana, L.

AU - Sneppen, K.

AU - Otzen, Daniel

PY - 2013/5/2

Y1 - 2013/5/2

N2 - We introduce a stochastic model describing aggregation of misfolded proteins and degradation by the protein quality control system in a single cell. Aggregate growth is contrasted by the cell quality control system, that attacks them at different stages of the growth process, with an efficiency that decreases with their size. Model parameters are estimated from experimental data. Two qualitatively different behaviors emerge: a homeostatic state, where the quality control system is stable and aggregates of large sizes are not formed, and an oscillatory state, where the quality control system periodically breaks down, allowing for formation of large aggregates. We discuss how these periodic breakdowns may constitute a mechanism for the development of neurodegenerative diseases.

AB - We introduce a stochastic model describing aggregation of misfolded proteins and degradation by the protein quality control system in a single cell. Aggregate growth is contrasted by the cell quality control system, that attacks them at different stages of the growth process, with an efficiency that decreases with their size. Model parameters are estimated from experimental data. Two qualitatively different behaviors emerge: a homeostatic state, where the quality control system is stable and aggregates of large sizes are not formed, and an oscillatory state, where the quality control system periodically breaks down, allowing for formation of large aggregates. We discuss how these periodic breakdowns may constitute a mechanism for the development of neurodegenerative diseases.

UR - http://www.scopus.com/inward/record.url?scp=84876490034&partnerID=8YFLogxK

U2 - 10.1016/j.febslet.2013.03.018

DO - 10.1016/j.febslet.2013.03.018

M3 - Journal article

C2 - 23524241

AN - SCOPUS:84876490034

VL - 587

SP - 1405

EP - 1410

JO - F E B S Letters

JF - F E B S Letters

SN - 0014-5793

IS - 9

ER -

ID: 45590320