Abstract
Focusing on the interactomes of Homo sapiens, Saccharomyces cerevisiae, and Escherichia coli, we investigated interactions between controlling proteins. In particular, we determined critical, intermittent, and redundant proteins based on their tendency to participate in minimum dominating sets. Independently of the organisms considered, we found that interactions that involved critical nodes had the most prominent effects on the topology of their corresponding networks. Furthermore, we observed that phosphorylation and regulatory events were considerably enriched when the corresponding transcription factors and kinases were critical proteins, while such interactions were depleted when they were redundant proteins. Moreover, interactions involving critical proteins were enriched with essential genes, disease genes, and drug targets, suggesting that such characteristics may be key for the detection of novel drug targets as well as assess their efficacy.
| Original language | English (US) |
|---|---|
| Article number | 1700056 |
| Journal | Proteomics |
| Volume | 17 |
| Issue number | 10 |
| DOIs | |
| State | Published - May 1 2017 |
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Keywords
- Critical proteins
- Network control
- Protein–protein interactions
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
Cite this
Links between critical proteins drive the controllability of protein interaction networks. / Wuchty, Stefan; Boltz, Toni; Küçük-McGinty, Hande.
In: Proteomics, Vol. 17, No. 10, 1700056, 01.05.2017.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Links between critical proteins drive the controllability of protein interaction networks
AU - Wuchty, Stefan
AU - Boltz, Toni
AU - Küçük-McGinty, Hande
PY - 2017/5/1
Y1 - 2017/5/1
N2 - Focusing on the interactomes of Homo sapiens, Saccharomyces cerevisiae, and Escherichia coli, we investigated interactions between controlling proteins. In particular, we determined critical, intermittent, and redundant proteins based on their tendency to participate in minimum dominating sets. Independently of the organisms considered, we found that interactions that involved critical nodes had the most prominent effects on the topology of their corresponding networks. Furthermore, we observed that phosphorylation and regulatory events were considerably enriched when the corresponding transcription factors and kinases were critical proteins, while such interactions were depleted when they were redundant proteins. Moreover, interactions involving critical proteins were enriched with essential genes, disease genes, and drug targets, suggesting that such characteristics may be key for the detection of novel drug targets as well as assess their efficacy.
AB - Focusing on the interactomes of Homo sapiens, Saccharomyces cerevisiae, and Escherichia coli, we investigated interactions between controlling proteins. In particular, we determined critical, intermittent, and redundant proteins based on their tendency to participate in minimum dominating sets. Independently of the organisms considered, we found that interactions that involved critical nodes had the most prominent effects on the topology of their corresponding networks. Furthermore, we observed that phosphorylation and regulatory events were considerably enriched when the corresponding transcription factors and kinases were critical proteins, while such interactions were depleted when they were redundant proteins. Moreover, interactions involving critical proteins were enriched with essential genes, disease genes, and drug targets, suggesting that such characteristics may be key for the detection of novel drug targets as well as assess their efficacy.
KW - Critical proteins
KW - Network control
KW - Protein–protein interactions
UR - http://www.scopus.com/inward/record.url?scp=85019003172&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85019003172&partnerID=8YFLogxK
U2 - 10.1002/pmic.201700056
DO - 10.1002/pmic.201700056
M3 - Article
C2 - 28397356
AN - SCOPUS:85019003172
VL - 17
JO - Proteomics
JF - Proteomics
SN - 1615-9853
IS - 10
M1 - 1700056
ER -