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 journal › Journal article › Research › peer-review
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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