Publication Name	World Journal of Biological Chemistry
Manuscript ID	18439
Country	Germany

Received	2015-04-21 09:27
Peer-Review Started	2015-04-24 14:54
To Make the First Decision	2015-06-03 14:19
Return for Revision	2015-06-09 10:15
Revised	2015-06-19 23:57
Second Decision	2015-07-02 09:40
Accepted by Journal Editor-in-Chief	2015-07-02 16:17
Accepted by Company Editor-in-Chief	2015-07-14 09:54
Articles in Press	2015-07-14 09:54
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2015-08-14 10:08
Publish the Manuscript Online	2015-08-26 11:07

ISSN	1949-8454 (online)
Open Access	This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
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Category	Endocrinology & Metabolism
Manuscript Type	Review
Article Title	Role of ZAC1 in transient neonatal diabetes mellitus and glucose metabolism
Manuscript Source	Invited Manuscript
All Author List	Anke Hoffmann and Dietmar Spengler
Funding Agency and Grant Number	Funding Agency Grant Number Max Planck Institute of Psychiatry
Corresponding Author	Dietmar Spengler, MD, Max Planck Institute of Psychiatry, Translational Research, Kraepelinstrasse 2-10, 80804 Munich, Germany. spengler@psych.mpg.de
Key Words	Diabetes mellitus; ZAC1; Transient neonatal diabetes mellitus 1; Genomic imprinting; Insulin; Glucose; Target genes; Tailored therapy
Core Tip	Accidents of nature leading to rare genetic diseases can provide important insights into the molecular and cellular foundations of related common diseases. Various genetic anomalies at chromosome 6q24 manifest with life-threatening transient neonatal diabetes mellitus (TNDM1). All of these genetic defects share overexpress-ion of the maternally imprinted transcriptional regulator ZAC1. Genome-wide expression profiling identified a number of downstream target genes sharing a critical role in insulin secretion, β-cell proliferation, and survival. Importantly, Zac1 overexpression in β-cells spares the effects of G-protein signaling on insulin secretion opening the prospect for tailored therapy in TNDM1 patients.
Publish Date	2015-08-26 11:07
Citation	Hoffmann A, Spengler D. Role of ZAC1 in transient neonatal diabetes mellitus and glucose metabolism. World J Biol Chem 2015; 6(3): 95-109
URL	http://www.wjgnet.com/1949-8454/full/v6/i3/95.htm
DOI	http://dx.doi.org/10.4331/wjbc.v6.i3.95

Full Article (PDF)	WJBC-6-95.pdf
Full Article (Word)	WJBC-6-95.doc
Manuscript File	18439-Review.docx
Answering Reviewers	18439-Answering reviewers.pdf
Audio Core Tip	18439-Audio core tip.wav
Conflict-of-Interest Disclosure Form	18439-Conflict-of-interest statement.pdf
Copyright License Agreement	18439-Copyright assignment.pdf
Peer-review Report	18439-Peer-review(s).pdf
Journal Editor-in-Chief Review Report	18439-Journal editor-in-chief review report.pdf
Scientific Misconduct Check	18439-Scientific misconduct check.pdf
Scientific Editor Work List	18439-Scientific editor work list .pdf