Gene expression levels of DNA methyltransferase enzymes in Shank3-deficient mouse model of autism during early development
Author:
Affiliation:
1. Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences , Bratislava , Slovakia
2. Institute of Physiology, Faculty of Medicine , Comenius University , Bratislava , Slovakia
Abstract
Publisher
Walter de Gruyter GmbH
Subject
Endocrinology,Endocrinology, Diabetes and Metabolism
Link
https://www.sciendo.com/pdf/10.2478/enr-2021-0025
Reference13 articles.
1. Alex AM, Saradalekshmi KR, Shilen N, Suresh PA, Banerjee M. Genetic association of DNMT variants can play a critical role in defining the methylation patterns in autism. IUBMB Life 71, 901–907, 2019.10.1002/iub.2021
2. Beri S, Tonna N, Menozzi G, Bonaglia MC, Sala C, Giorda R. DNA methylation regulates tissue-specific expression of Shank3. J Neurochem 101, 1380–1391, 2007.10.1111/j.1471-4159.2007.04539.x
3. Feng J, Zhou Y, Campbell SL, Le T, Li E, Sweatt JD, Silva AJ, Fan G. Dnmt1 and Dnmt3a maintain DNA methylation and regulate synaptic function in adult forebrain neurons. Nat Neurosci 13, 423–430, 2010.10.1038/nn.2514
4. Garrido N, Cruz F, Egea RR, Simon C, Sadler-Riggleman I, Beck D, Nilsson E, Ben Maamar M, Skinner MK. Sperm DNA methylation epimutation biomarker for paternal offspring autism susceptibility. Clin Epigenetics 13, 6, 2021.10.1186/s13148-020-00995-2
5. Jobe EM, Zhao X. DNA methylation and adult neurogenesis. Brain Plast 3, 5–26, 2017.10.3233/BPL-160034
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