{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T19:49:45Z","timestamp":1769629785731,"version":"3.49.0"},"reference-count":110,"publisher":"MDPI AG","issue":"18","license":[{"start":{"date-parts":[[2019,9,7]],"date-time":"2019-09-07T00:00:00Z","timestamp":1567814400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Schwiete Stiftung","award":["project Nr. 06\/2015"],"award-info":[{"award-number":["project Nr. 06\/2015"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Since diabetes is a global epidemic, the development of novel therapeutic strategies for the treatment of this disease is of major clinical interest. Diabetes is differentiated in two types: type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). T1DM arises from an autoimmune destruction of insulin-producing \u03b2-cells whereas T2DM is characterized by an insulin resistance, an impaired insulin reaction of the target cells, and\/or dysregulated insulin secretion. In the past, a growing number of studies have reported on the important role of the protein kinase CK2 in the regulation of the survival and endocrine function of pancreatic \u03b2-cells. In fact, inhibition of CK2 is capable of reducing cytokine-induced loss of \u03b2-cells and increases insulin expression as well as secretion by various pathways that are regulated by reversible phosphorylation of proteins. Moreover, CK2 inhibition modulates pathways that are involved in the development of diabetes and prevents signal transduction, leading to late complications such as diabetic retinopathy. Hence, targeting CK2 may represent a novel therapeutic strategy for the treatment of diabetes.<\/jats:p>","DOI":"10.3390\/ijms20184398","type":"journal-article","created":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T04:12:40Z","timestamp":1568002360000},"page":"4398","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["Protein Kinase CK2\u2014A Putative Target for the Therapy of Diabetes Mellitus?"],"prefix":"10.3390","volume":"20","author":[{"given":"Emmanuel","family":"Ampofo","sequence":"first","affiliation":[{"name":"Institute for Clinical &amp; Experimental Surgery, Saarland University, 66424 Homburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lisa","family":"Nalbach","sequence":"additional","affiliation":[{"name":"Institute for Clinical &amp; Experimental Surgery, Saarland University, 66424 Homburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael D.","family":"Menger","sequence":"additional","affiliation":[{"name":"Institute for Clinical &amp; Experimental Surgery, Saarland University, 66424 Homburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mathias","family":"Montenarh","sequence":"additional","affiliation":[{"name":"Medical Biochemistry and Molecular Biology, Saarland University, 66424 Homburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7115-0485","authenticated-orcid":false,"given":"Claudia","family":"G\u00f6tz","sequence":"additional","affiliation":[{"name":"Medical Biochemistry and Molecular Biology, Saarland University, 66424 Homburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2019,9,7]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"847","DOI":"10.1016\/j.bbamcr.2009.01.013","article-title":"Extraordinary pleiotropy of protein kinase CK2 revealed by weblogo phosphoproteome analysis","volume":"1793","author":"Salvi","year":"2009","journal-title":"Biochim. 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