Functional characterization of mouse fetal TnI gene promoters in myocardial cells

J. Du, C. Nan, J. J. Huang, Chi Zhang, J. Liu, P. Jia, M. Abers, X. P. Huang

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Two major troponin I (TnI) genes, fetal TnI (ssTnI) and adult TnI (cTnI), are expressed in the mammalian heart under the control of a developmentally regulated program. In this study, the up-stream domain (∼1,800 bp) of mouse fetal TnI gene has been cloned and characterized. There is a high homology of this region among mouse, rat and human. Analysis of the sequence revealed several putative regulatory domains and binding sites (Sp1 binding sites, GATA binding site, MyoD, CREB, MEF2, AP1, NFκB, etc). Transfection assays indicated that conserved GA-rich sequences, CREB and a CCAAT box within the first 300 bp upstream of the transcription start site were critical for the gene expression. Electrophoretic mobility shift assays (EMSAs) and chromatin immunoprecipitation (ChIP) assays revealed binding proteins to CREB site in nuclear extracts from myocardial cells. An inhibitory domain was revealed within the sequence between -1,700 to -1,780. Thyroid hormone (T3) caused a significant inhibitory effect on ssTnI expression in myocardial cells whereas this effect was not evident in CHO cells.

Original languageEnglish
Pages (from-to)605-613
Number of pages9
JournalJournal of Biomedical Science
Volume15
Issue number5
DOIs
StatePublished - Sep 1 2008
Externally publishedYes

Fingerprint

Troponin I
Genes
Assays
Binding Sites
CREB-Binding Protein
Electrophoretic mobility
CHO Cells
Chromatin Immunoprecipitation
Transcription Initiation Site
Triiodothyronine
Electrophoretic Mobility Shift Assay
Cell Extracts
Gene expression
Chromatin
Transfection
Sequence Analysis
Rats
Carrier Proteins
Gene Expression

Keywords

  • Gene regulation
  • Myocardium
  • Myofibril protein
  • Slow skeletal troponin I
  • Thyroid hormone

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Du, J., Nan, C., Huang, J. J., Zhang, C., Liu, J., Jia, P., ... Huang, X. P. (2008). Functional characterization of mouse fetal TnI gene promoters in myocardial cells. Journal of Biomedical Science, 15(5), 605-613. https://doi.org/10.1007/s11373-008-9246-y

Functional characterization of mouse fetal TnI gene promoters in myocardial cells. / Du, J.; Nan, C.; Huang, J. J.; Zhang, Chi; Liu, J.; Jia, P.; Abers, M.; Huang, X. P.

In: Journal of Biomedical Science, Vol. 15, No. 5, 01.09.2008, p. 605-613.

Research output: Contribution to journalArticle

Du, J, Nan, C, Huang, JJ, Zhang, C, Liu, J, Jia, P, Abers, M & Huang, XP 2008, 'Functional characterization of mouse fetal TnI gene promoters in myocardial cells', Journal of Biomedical Science, vol. 15, no. 5, pp. 605-613. https://doi.org/10.1007/s11373-008-9246-y
Du, J. ; Nan, C. ; Huang, J. J. ; Zhang, Chi ; Liu, J. ; Jia, P. ; Abers, M. ; Huang, X. P. / Functional characterization of mouse fetal TnI gene promoters in myocardial cells. In: Journal of Biomedical Science. 2008 ; Vol. 15, No. 5. pp. 605-613.
@article{6c715c8c279644719c9ced812da4931c,
title = "Functional characterization of mouse fetal TnI gene promoters in myocardial cells",
abstract = "Two major troponin I (TnI) genes, fetal TnI (ssTnI) and adult TnI (cTnI), are expressed in the mammalian heart under the control of a developmentally regulated program. In this study, the up-stream domain (∼1,800 bp) of mouse fetal TnI gene has been cloned and characterized. There is a high homology of this region among mouse, rat and human. Analysis of the sequence revealed several putative regulatory domains and binding sites (Sp1 binding sites, GATA binding site, MyoD, CREB, MEF2, AP1, NFκB, etc). Transfection assays indicated that conserved GA-rich sequences, CREB and a CCAAT box within the first 300 bp upstream of the transcription start site were critical for the gene expression. Electrophoretic mobility shift assays (EMSAs) and chromatin immunoprecipitation (ChIP) assays revealed binding proteins to CREB site in nuclear extracts from myocardial cells. An inhibitory domain was revealed within the sequence between -1,700 to -1,780. Thyroid hormone (T3) caused a significant inhibitory effect on ssTnI expression in myocardial cells whereas this effect was not evident in CHO cells.",
keywords = "Gene regulation, Myocardium, Myofibril protein, Slow skeletal troponin I, Thyroid hormone",
author = "J. Du and C. Nan and Huang, {J. J.} and Chi Zhang and J. Liu and P. Jia and M. Abers and Huang, {X. P.}",
year = "2008",
month = "9",
day = "1",
doi = "10.1007/s11373-008-9246-y",
language = "English",
volume = "15",
pages = "605--613",
journal = "Journal of Biomedical Science",
issn = "1021-7770",
publisher = "BioMed Central",
number = "5",

}

TY - JOUR

T1 - Functional characterization of mouse fetal TnI gene promoters in myocardial cells

AU - Du, J.

AU - Nan, C.

AU - Huang, J. J.

AU - Zhang, Chi

AU - Liu, J.

AU - Jia, P.

AU - Abers, M.

AU - Huang, X. P.

PY - 2008/9/1

Y1 - 2008/9/1

N2 - Two major troponin I (TnI) genes, fetal TnI (ssTnI) and adult TnI (cTnI), are expressed in the mammalian heart under the control of a developmentally regulated program. In this study, the up-stream domain (∼1,800 bp) of mouse fetal TnI gene has been cloned and characterized. There is a high homology of this region among mouse, rat and human. Analysis of the sequence revealed several putative regulatory domains and binding sites (Sp1 binding sites, GATA binding site, MyoD, CREB, MEF2, AP1, NFκB, etc). Transfection assays indicated that conserved GA-rich sequences, CREB and a CCAAT box within the first 300 bp upstream of the transcription start site were critical for the gene expression. Electrophoretic mobility shift assays (EMSAs) and chromatin immunoprecipitation (ChIP) assays revealed binding proteins to CREB site in nuclear extracts from myocardial cells. An inhibitory domain was revealed within the sequence between -1,700 to -1,780. Thyroid hormone (T3) caused a significant inhibitory effect on ssTnI expression in myocardial cells whereas this effect was not evident in CHO cells.

AB - Two major troponin I (TnI) genes, fetal TnI (ssTnI) and adult TnI (cTnI), are expressed in the mammalian heart under the control of a developmentally regulated program. In this study, the up-stream domain (∼1,800 bp) of mouse fetal TnI gene has been cloned and characterized. There is a high homology of this region among mouse, rat and human. Analysis of the sequence revealed several putative regulatory domains and binding sites (Sp1 binding sites, GATA binding site, MyoD, CREB, MEF2, AP1, NFκB, etc). Transfection assays indicated that conserved GA-rich sequences, CREB and a CCAAT box within the first 300 bp upstream of the transcription start site were critical for the gene expression. Electrophoretic mobility shift assays (EMSAs) and chromatin immunoprecipitation (ChIP) assays revealed binding proteins to CREB site in nuclear extracts from myocardial cells. An inhibitory domain was revealed within the sequence between -1,700 to -1,780. Thyroid hormone (T3) caused a significant inhibitory effect on ssTnI expression in myocardial cells whereas this effect was not evident in CHO cells.

KW - Gene regulation

KW - Myocardium

KW - Myofibril protein

KW - Slow skeletal troponin I

KW - Thyroid hormone

UR - http://www.scopus.com/inward/record.url?scp=51349117727&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=51349117727&partnerID=8YFLogxK

U2 - 10.1007/s11373-008-9246-y

DO - 10.1007/s11373-008-9246-y

M3 - Article

VL - 15

SP - 605

EP - 613

JO - Journal of Biomedical Science

JF - Journal of Biomedical Science

SN - 1021-7770

IS - 5

ER -