Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-10-27
pubmed:abstractText
The selective estrogen receptor modulator, tamoxifen, has been shown to reduce DNA methylation at Insulin-like growth factor 2/H19 differentially methylated region (Igf2/H19 DMR) in the spermatozoa of the Holtzman rats. Since imprint at this locus is acquired during spermatogenesis in the male germ-line, we hypothesized role for estrogen signaling in the methylation dynamics in the testis. The present study was designed to identify putative estrogen response elements (ERE) at Igf2/H19 DMR and their interaction with DNA methylation pathway. Here, we demonstrate presence of functional ERE at 2637/2655 base pair on Igf2/H19 DMR in testicular germ cells, which was found to bind to estrogen receptor beta (ER beta) in the chromatin immunoprecipitation assay. Tamoxifen attenuated ER beta-ERE association thereby acting as an estrogen antagonist at this locus. Further mechanistic study involving colocalization and immunoprecipitation assay revealed interaction of ER beta and Dnmt1 in the testis. The study provides evidence for the role for estrogen in acquisition of imprint at Igf2/H19 DMR in testis and help in understanding molecular mechanism of environmental estrogens impacting male fertility.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1872-8057
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
314
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
110-7
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Potential role of estrogen in regulation of the insulin-like growth factor2-H19 locus in the rat testis.
pubmed:affiliation
Division of Neuroendocrinology, National Institute for Research in Reproductive Health, Indian Council of Medical Research, JM Road, Parel, Mumbai, Maharashtra 400 012, India.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't