A proteomic study of the regulatory role for STAT-1 in cytokine-induced beta-cell death

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Standard

A proteomic study of the regulatory role for STAT-1 in cytokine-induced beta-cell death. / Rondas, Dieter; Gudmundsdottir, Valborg; D'Hertog, Wannes; Crèvecoeur, Inne; Waelkens, Etienne; Brunak, Soren; Mathieu, Chantal; Overbergh, Lut.

In: Proteomics - Clinical Applications, Vol. 9, No. 9-10, 10.2015, p. 938–952.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Rondas, D, Gudmundsdottir, V, D'Hertog, W, Crèvecoeur, I, Waelkens, E, Brunak, S, Mathieu, C & Overbergh, L 2015, 'A proteomic study of the regulatory role for STAT-1 in cytokine-induced beta-cell death', Proteomics - Clinical Applications, vol. 9, no. 9-10, pp. 938–952. https://doi.org/10.1002/prca.201400124

APA

Rondas, D., Gudmundsdottir, V., D'Hertog, W., Crèvecoeur, I., Waelkens, E., Brunak, S., Mathieu, C., & Overbergh, L. (2015). A proteomic study of the regulatory role for STAT-1 in cytokine-induced beta-cell death. Proteomics - Clinical Applications, 9(9-10), 938–952. https://doi.org/10.1002/prca.201400124

Vancouver

Rondas D, Gudmundsdottir V, D'Hertog W, Crèvecoeur I, Waelkens E, Brunak S et al. A proteomic study of the regulatory role for STAT-1 in cytokine-induced beta-cell death. Proteomics - Clinical Applications. 2015 Oct;9(9-10):938–952. https://doi.org/10.1002/prca.201400124

Author

Rondas, Dieter ; Gudmundsdottir, Valborg ; D'Hertog, Wannes ; Crèvecoeur, Inne ; Waelkens, Etienne ; Brunak, Soren ; Mathieu, Chantal ; Overbergh, Lut. / A proteomic study of the regulatory role for STAT-1 in cytokine-induced beta-cell death. In: Proteomics - Clinical Applications. 2015 ; Vol. 9, No. 9-10. pp. 938–952.

Bibtex

@article{2353d191b4dc432bb707e46b6228ff11,
title = "A proteomic study of the regulatory role for STAT-1 in cytokine-induced beta-cell death",
abstract = "PURPOSE: Signal transducer and activator of transcription 1 (STAT-1) plays a crucial role in cytokine-induced beta-cell destruction. However, its precise downstream pathways have not been completely clarified. We performed a proteome analysis of cytokine-exposed C57Bl/6 and STAT-1(-/-) mouse islets and prioritized proteins for their potential in relation to type 1 diabetes (T1D).EXPERIMENTAL DESIGN: Differential proteins were identified using a combination of 2D-DIGE and MALDI-TOF/TOF analysis and were subjected to ingenuity pathway analysis (IPA). Protein-protein interaction networks were created and a phenome-interactome ranking of the differential proteins based on their assignment to T1D was performed.RESULTS: Numerous STAT-1-regulated proteins were identified and divided in different groups according to their biological function. The largest group of proteins was the one involved in protein synthesis and processing. Network analysis revealed a complex interaction between proteins from different functional groups and IPA analysis confirmed the protective effect of STAT-1 deletion on cytokine-induced beta-cell death. Finally, a central role in this STAT-1-regulated mechanism was assigned to small ubiquitin-related modifier 4 (SUMO4).CONCLUSIONS AND CLINICAL RELEVANCE: These findings confirm a central role for STAT-1 in pancreatic islet inflammation induced destruction and most importantly elucidate the underlying proteomic pathways involved.",
author = "Dieter Rondas and Valborg Gudmundsdottir and Wannes D'Hertog and Inne Cr{\`e}vecoeur and Etienne Waelkens and Soren Brunak and Chantal Mathieu and Lut Overbergh",
note = "{\textcopyright} 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.",
year = "2015",
month = oct,
doi = "10.1002/prca.201400124",
language = "English",
volume = "9",
pages = "938–952",
journal = "Proteomics - Clinical Applications",
issn = "1862-8346",
publisher = "Wiley - V C H Verlag GmbH & Co. KGaA",
number = "9-10",

}

RIS

TY - JOUR

T1 - A proteomic study of the regulatory role for STAT-1 in cytokine-induced beta-cell death

AU - Rondas, Dieter

AU - Gudmundsdottir, Valborg

AU - D'Hertog, Wannes

AU - Crèvecoeur, Inne

AU - Waelkens, Etienne

AU - Brunak, Soren

AU - Mathieu, Chantal

AU - Overbergh, Lut

N1 - © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

PY - 2015/10

Y1 - 2015/10

N2 - PURPOSE: Signal transducer and activator of transcription 1 (STAT-1) plays a crucial role in cytokine-induced beta-cell destruction. However, its precise downstream pathways have not been completely clarified. We performed a proteome analysis of cytokine-exposed C57Bl/6 and STAT-1(-/-) mouse islets and prioritized proteins for their potential in relation to type 1 diabetes (T1D).EXPERIMENTAL DESIGN: Differential proteins were identified using a combination of 2D-DIGE and MALDI-TOF/TOF analysis and were subjected to ingenuity pathway analysis (IPA). Protein-protein interaction networks were created and a phenome-interactome ranking of the differential proteins based on their assignment to T1D was performed.RESULTS: Numerous STAT-1-regulated proteins were identified and divided in different groups according to their biological function. The largest group of proteins was the one involved in protein synthesis and processing. Network analysis revealed a complex interaction between proteins from different functional groups and IPA analysis confirmed the protective effect of STAT-1 deletion on cytokine-induced beta-cell death. Finally, a central role in this STAT-1-regulated mechanism was assigned to small ubiquitin-related modifier 4 (SUMO4).CONCLUSIONS AND CLINICAL RELEVANCE: These findings confirm a central role for STAT-1 in pancreatic islet inflammation induced destruction and most importantly elucidate the underlying proteomic pathways involved.

AB - PURPOSE: Signal transducer and activator of transcription 1 (STAT-1) plays a crucial role in cytokine-induced beta-cell destruction. However, its precise downstream pathways have not been completely clarified. We performed a proteome analysis of cytokine-exposed C57Bl/6 and STAT-1(-/-) mouse islets and prioritized proteins for their potential in relation to type 1 diabetes (T1D).EXPERIMENTAL DESIGN: Differential proteins were identified using a combination of 2D-DIGE and MALDI-TOF/TOF analysis and were subjected to ingenuity pathway analysis (IPA). Protein-protein interaction networks were created and a phenome-interactome ranking of the differential proteins based on their assignment to T1D was performed.RESULTS: Numerous STAT-1-regulated proteins were identified and divided in different groups according to their biological function. The largest group of proteins was the one involved in protein synthesis and processing. Network analysis revealed a complex interaction between proteins from different functional groups and IPA analysis confirmed the protective effect of STAT-1 deletion on cytokine-induced beta-cell death. Finally, a central role in this STAT-1-regulated mechanism was assigned to small ubiquitin-related modifier 4 (SUMO4).CONCLUSIONS AND CLINICAL RELEVANCE: These findings confirm a central role for STAT-1 in pancreatic islet inflammation induced destruction and most importantly elucidate the underlying proteomic pathways involved.

U2 - 10.1002/prca.201400124

DO - 10.1002/prca.201400124

M3 - Journal article

C2 - 25712914

VL - 9

SP - 938

EP - 952

JO - Proteomics - Clinical Applications

JF - Proteomics - Clinical Applications

SN - 1862-8346

IS - 9-10

ER -

ID: 139977426