Regulation of the Expression of DAPK1 by SUMO Pathway
Identifieur interne : 000474 ( Main/Merge ); précédent : 000473; suivant : 000475Regulation of the Expression of DAPK1 by SUMO Pathway
Auteurs : Qingshui Wang ; Xiuli Zhang ; Ling Chen ; Shuyun Weng ; Yun Xia ; Yan Ye ; Ke Li ; Ziqiang Liao ; Pengchen Chen ; Khaldoon Alsamman ; Chen Meng ; Craig Stevens ; Ted R. Hupp ; Yao LinSource :
- Biomolecules [ 2218-273X ] ; 2019.
Abstract
Death Associated Protein Kinase 1 (DAPK1) is an important signaling kinase mediating the biological effect of multiple natural biomolecules such as IFN-γ, TNF-α, curcumin, etc. DAPK1 is degraded through both ubiquitin-proteasomal and lysosomal degradation pathways. To investigate the crosstalk between these two DAPK1 degradation pathways, we carried out a screen using a set of ubiquitin E2 siRNAs at the presence of Tuberous Sclerous 2 (TSC2) and identified that the small ubiquitin-like molecule (SUMO) pathway is able to regulate the protein levels of DAPK1. Inhibition of the SUMO pathway enhanced DAPK1 protein levels and the minimum domain of DAPK1 protein required for this regulation is the kinase domain, suggesting that the SUMO pathway regulates DAPK1 protein levels independent of TSC2. Suppression of the SUMO pathway did not enhance DAPK1 protein stability. In addition, mutation of the potential SUMO conjugation sites on DAPK1 kinase domain did not alter its protein stability or response to SUMO pathway inhibition. These data suggested that the SUMO pathway does not regulate DAPK1 protein degradation. The exact molecular mechanism underlying this regulation is yet to be discovered.
Url:
DOI: 10.3390/biom9040151
PubMed: 30999631
PubMed Central: 6523460
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PMC:6523460Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Regulation of the Expression of DAPK1 by SUMO Pathway</title>
<author><name sortKey="Wang, Qingshui" sort="Wang, Qingshui" uniqKey="Wang Q" first="Qingshui" last="Wang">Qingshui Wang</name>
<affiliation><nlm:aff id="af1-biomolecules-09-00151">Provincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou 350117, China;<email>wangqingshui@fjnu.edu.cn</email>
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<author><name sortKey="Zhang, Xiuli" sort="Zhang, Xiuli" uniqKey="Zhang X" first="Xiuli" last="Zhang">Xiuli Zhang</name>
<affiliation><nlm:aff id="af1-biomolecules-09-00151">Provincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou 350117, China;<email>wangqingshui@fjnu.edu.cn</email>
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<author><name sortKey="Chen, Ling" sort="Chen, Ling" uniqKey="Chen L" first="Ling" last="Chen">Ling Chen</name>
<affiliation><nlm:aff id="af1-biomolecules-09-00151">Provincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou 350117, China;<email>wangqingshui@fjnu.edu.cn</email>
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<author><name sortKey="Weng, Shuyun" sort="Weng, Shuyun" uniqKey="Weng S" first="Shuyun" last="Weng">Shuyun Weng</name>
<affiliation><nlm:aff id="af1-biomolecules-09-00151">Provincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou 350117, China;<email>wangqingshui@fjnu.edu.cn</email>
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<author><name sortKey="Xia, Yun" sort="Xia, Yun" uniqKey="Xia Y" first="Yun" last="Xia">Yun Xia</name>
<affiliation><nlm:aff id="af1-biomolecules-09-00151">Provincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou 350117, China;<email>wangqingshui@fjnu.edu.cn</email>
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<author><name sortKey="Ye, Yan" sort="Ye, Yan" uniqKey="Ye Y" first="Yan" last="Ye">Yan Ye</name>
<affiliation><nlm:aff id="af1-biomolecules-09-00151">Provincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou 350117, China;<email>wangqingshui@fjnu.edu.cn</email>
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<author><name sortKey="Li, Ke" sort="Li, Ke" uniqKey="Li K" first="Ke" last="Li">Ke Li</name>
<affiliation><nlm:aff id="af1-biomolecules-09-00151">Provincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou 350117, China;<email>wangqingshui@fjnu.edu.cn</email>
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<author><name sortKey="Liao, Ziqiang" sort="Liao, Ziqiang" uniqKey="Liao Z" first="Ziqiang" last="Liao">Ziqiang Liao</name>
<affiliation><nlm:aff id="af1-biomolecules-09-00151">Provincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou 350117, China;<email>wangqingshui@fjnu.edu.cn</email>
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(C.M.)</nlm:aff>
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<author><name sortKey="Chen, Pengchen" sort="Chen, Pengchen" uniqKey="Chen P" first="Pengchen" last="Chen">Pengchen Chen</name>
<affiliation><nlm:aff id="af1-biomolecules-09-00151">Provincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou 350117, China;<email>wangqingshui@fjnu.edu.cn</email>
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</affiliation>
</author>
<author><name sortKey="Alsamman, Khaldoon" sort="Alsamman, Khaldoon" uniqKey="Alsamman K" first="Khaldoon" last="Alsamman">Khaldoon Alsamman</name>
<affiliation><nlm:aff id="af2-biomolecules-09-00151">Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Imam Abdulrahman bin Faisal University, Dammam 34212, Saudi Arabia;<email>kmalsamman@iau.edu.sa</email>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Meng, Chen" sort="Meng, Chen" uniqKey="Meng C" first="Chen" last="Meng">Chen Meng</name>
<affiliation><nlm:aff id="af1-biomolecules-09-00151">Provincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou 350117, China;<email>wangqingshui@fjnu.edu.cn</email>
(Q.W.);<email>15980239296@163.com</email>
(X.Z.);<email>chenling654321@163.com</email>
(L.C.);<email>wsy09080700@163.com</email>
(S.W.);<email>xiayunnyyl@163.com</email>
(Y.X.);<email>m18759141945@163.com</email>
(Y.Y.);<email>13107673087@163.com</email>
(K.L.);<email>liaoziqiangcontact@163.com</email>
(Z.L.);<email>yb77620@umac.mo</email>
(P.C.);<email>mmenger@126.com</email>
(C.M.)</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Stevens, Craig" sort="Stevens, Craig" uniqKey="Stevens C" first="Craig" last="Stevens">Craig Stevens</name>
<affiliation><nlm:aff id="af3-biomolecules-09-00151">School of Applied Sciences, Edinburgh Napier University, Edinburgh EH11 4BN, UK;<email>C.Stevens@napier.ac.uk</email>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Hupp, Ted R" sort="Hupp, Ted R" uniqKey="Hupp T" first="Ted R." last="Hupp">Ted R. Hupp</name>
<affiliation><nlm:aff id="af4-biomolecules-09-00151">Institute of Genetics and Molecular Medicine, Cell Signaling Unit, CRUK p53 Transduction Group, University of Edinburgh, EH4 2XR EH4 2XR, UK;<email>ted.hupp@ed.ac.uk</email>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Lin, Yao" sort="Lin, Yao" uniqKey="Lin Y" first="Yao" last="Lin">Yao Lin</name>
<affiliation><nlm:aff id="af1-biomolecules-09-00151">Provincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou 350117, China;<email>wangqingshui@fjnu.edu.cn</email>
(Q.W.);<email>15980239296@163.com</email>
(X.Z.);<email>chenling654321@163.com</email>
(L.C.);<email>wsy09080700@163.com</email>
(S.W.);<email>xiayunnyyl@163.com</email>
(Y.X.);<email>m18759141945@163.com</email>
(Y.Y.);<email>13107673087@163.com</email>
(K.L.);<email>liaoziqiangcontact@163.com</email>
(Z.L.);<email>yb77620@umac.mo</email>
(P.C.);<email>mmenger@126.com</email>
(C.M.)</nlm:aff>
</affiliation>
</author>
</analytic>
<series><title level="j">Biomolecules</title>
<idno type="eISSN">2218-273X</idno>
<imprint><date when="2019">2019</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>Death Associated Protein Kinase 1 (DAPK1) is an important signaling kinase mediating the biological effect of multiple natural biomolecules such as IFN-γ, TNF-α, curcumin, etc. DAPK1 is degraded through both ubiquitin-proteasomal and lysosomal degradation pathways. To investigate the crosstalk between these two DAPK1 degradation pathways, we carried out a screen using a set of ubiquitin E2 siRNAs at the presence of Tuberous Sclerous 2 (TSC2) and identified that the small ubiquitin-like molecule (SUMO) pathway is able to regulate the protein levels of DAPK1. Inhibition of the SUMO pathway enhanced DAPK1 protein levels and the minimum domain of DAPK1 protein required for this regulation is the kinase domain, suggesting that the SUMO pathway regulates DAPK1 protein levels independent of TSC2. Suppression of the SUMO pathway did not enhance DAPK1 protein stability. In addition, mutation of the potential SUMO conjugation sites on DAPK1 kinase domain did not alter its protein stability or response to SUMO pathway inhibition. These data suggested that the SUMO pathway does not regulate DAPK1 protein degradation. The exact molecular mechanism underlying this regulation is yet to be discovered.</p>
</div>
</front>
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