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Activity of the beta-myosin heavy chain antisense promoter responds to diabetes and hypothyroidism.

Activity of the beta-myosin heavy chain antisense promoter responds to diabetes and hypothyroidism. Research Abstract Details 

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  • Activity of the beta-myosin heavy chain antisense promoter responds to diabetes and hypothyroidism. Abstract Text:

    julia gigerJulia Giger,anqi x qinAnqi X Qin,paul w bodellPaul W Bodell,kenneth m baldwinKenneth M Baldwin,fadia haddadFadia Haddad,

    Two genes encoding cardiac myosin heavy chain (MHC) isoforms, beta and alpha, are arranged in tandem 4.5 kb apart. We examined pre-mRNA and mature mRNA levels of beta and alpha genes in control, diabetic (streptozotocin), hypothyroid (propylthiouracil), and hyperthyroid rat hearts and analyzed the naturally occurring antisense (AS) beta RNA species that starts in the middle of the 4.5-kb intergenic region and extends upstream to the beta-gene promoter. The beta and alpha genes are expressed antithetically in control, diabetic, hypothyroid, and hyperthyroid hearts. Expression of AS beta-RNA was positively correlated with alpha-mRNA and negatively correlated with sense beta mRNA. These results support the novel idea of common promoter-regulatory elements situated in the intergenic region that likely control transcription of both sense alpha and AS beta genes and that AS beta transcription negatively regulates beta-MHC gene expression. To test whether an intergenic promoter drives transcription of AS beta RNA, a 1340-bp sequence of the intergenic region was inserted into a luciferase plasmid in the 3'-to-5' AS direction and was injected into rat ventricle. This promoter was activated in control heart and decreased greatly in response to propylthiouracil and streptozotocin and increased in hyperthyroid rats, similar in pattern to the endogenous AS beta RNA. When a putative retinoic acid receptor (RAR) site (a known thyroid hormone receptor cofactor) in this promoter was mutated, the reporter activity was almost abolished in control, propylthiouracil, and streptozotocin hearts. We conclude that there is an intergenic promoter that is active in the AS direction and that the putative RAR element is a vital regulatory site.

    Activity of the beta-myosin heavy chain antisense promoter responds to diabetes and hypothyroidism. Publishing Authors By Initials

    j gigerJ Giger,ax qinAX Qin,pw bodellPW Bodell,km baldwinKM Baldwin,f haddadF Haddad,

    For similar macromolecular substances: polymers: biopolymers: microfilament proteins: myosins: myosin type ii: cardiac myosins: ventricular myosins research abstracts see: macromolecular substances: polymers: biopolymers: microfilament proteins: myosins: myosin type ii: cardiac myosins: ventricular myosins research

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    Activity of the beta-myosin heavy chain antisense promoter responds to diabetes and hypothyroidism. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: American journal of physiology. Heart and circulat

    VOLUME: 292

    Page Numbers: H3065-71

    Journal Abbreviation: Am. J. Physiol. Heart Circ. Ph

    ISSN: 0363-6135

    DAY: 16

    MONTH: 02

    YEAR: 2007

    Activity of the beta-myosin heavy chain antisense promoter responds to diabetes and hypothyroidism. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901228

    Activity of the beta-myosin heavy chain antisense promoter responds to diabetes and hypothyroidism. Keywords Mesh Terms:

    KEYWORDS: Ventricular Myosins

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Activity of the beta-myosin heavy chain antisense promoter responds to diabetes and hypothyroidism. Information

    Substance Name: Ventricular Myosins

    Registry Number: EC 3.6.1.-

    Grant and Affiliation Information for Activity of the beta-myosin heavy chain antisense promoter responds to diabetes and hypothyroidism.

    AFFILIATION: Department of Physiology and Biophysics, University of California, Irvine, D-346, Med. Sci. I, Irvine, CA 92697, USA. jmeehan@uci.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: HL73473-01

    ACRONYM: HL

    MEDLINETA: Am J Physiol Heart Circ Physio

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