Document Detail


Identification and expression of HDAC4 targeted by miR-1and miR-133a during early development in Paralichthys olivaceus.
MedLine Citation:
PMID:  25193329     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Histone deacetylase4, which is a class II histone deacetylase, plays a critical role in development, differentiation of muscle, cell proliferation and metabolism. In our study, we obtained the full-length HDAC4 cDNA, which included the coding region of 3171bp, an 180bp 5'untranslated region (UTR) and a 760bp 3'UTR.The deduced HDAC4 protein contained all known functional domains identified in other organisms. The phylogenetic analysis indicated that P. olivaceus HDAC4 had the highest identity with the T.rubripes. Tissue distribution analysis indicated that HDAC4 is abundantly expressed in muscle, and its levels are significantly higher in muscle than in other tissues (P<0.01). HDAC4 mRNA levels at 3 dph (days post hatching) and 36 dph were higher than that at other stages. Exogenous thyroid hormones either directly or indirectly promoted the expression of HDAC4 mRNA during metamorphosis, indicating that HDAC4 might directly or indirectly be regulated by thyroid hormone during muscle development in metamorphosis. To identify the miRNAs targeting HDAC4, we performed a luciferase reporter assay and verified that HDAC4 is a common target gene of miR-1 and miR-133a indicating that HDAC4 might be involved in a signal pathway of microRNA regulating muscle development.
Authors:
Hongmei Zhang; Yuanshuai Fu; Yanfang Su; Zhiyi Shi; Junling Zhang
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-9-1
Journal Detail:
Title:  Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology     Volume:  -     ISSN:  1879-1107     ISO Abbreviation:  Comp. Biochem. Physiol. B, Biochem. Mol. Biol.     Publication Date:  2014 Sep 
Date Detail:
Created Date:  2014-9-6     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9516061     Medline TA:  Comp Biochem Physiol B Biochem Mol Biol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014. Published by Elsevier Inc.
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