Literature DB >> 12593842

Smooth muscle uses another promoter to express primarily a form of human Cav1.2 L-type calcium channel different from the principal heart form.

Nehad Saada1, Bosong Dai, Clement Echetebu, Sushil K Sarna, Philip Palade.   

Abstract

Several different first exons and amino termini have been reported for the cardiac Ca channel known as alpha(1C) or Ca(V)1.2. The aim of this study was to investigate whether the expression of this channel is regulated by different promoters in smooth muscle cells and in heart in humans. Ribonuclease protection assay (RPA) indicates that the longer first exon 1a is found in certain human smooth muscle-containing tissues, notably bladder and fetal aorta, but that it is not expressed to any significant degree in lung or intestine. On the other hand, all four smooth muscle-containing tissues examined strongly express transcripts containing exon 1b, first reported cloned from human fibroblast cells. In addition, primary cultures of human colonic myocytes and coronary artery smooth muscle cells express predominantly transcripts containing exon 1b. The promoter immediately upstream of exon 1b was cloned, and it displays functional promoter activity when luciferase-expressing constructs were transfected into three different cultured smooth muscle cells: primary human coronary artery smooth muscles cells, primary human colonocytes, and the fetal rat aorta-derived A7r5 cell line. These results indicate that expression in smooth muscle is primarily driven by a promoter different from that which drives expression in cardiac myocytes.

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Year:  2003        PMID: 12593842     DOI: 10.1016/s0006-291x(03)00097-4

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN: 0006-291X            Impact factor:   3.575


  17 in total

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2.  The L-type calcium channel alpha 1C subunit gene undergoes extensive, uncoordinated alternative splicing.

Authors:  Q Ivy Fan; Kathleen M Vanderpool; Hui-San Chung; James D Marsh
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Review 3.  Vascular calcium channels and high blood pressure: pathophysiology and therapeutic implications.

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4.  Disrupting calcium channel expression to lower blood pressure: new targeting of a well-known channel.

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5.  Vascular smooth muscle-specific knockdown of the noncardiac form of the L-type calcium channel by microRNA-based short hairpin RNA as a potential antihypertensive therapy.

Authors:  Sung W Rhee; Joseph R Stimers; Wenze Wang; Li Pang
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Review 6.  Regulation of Coronary Blood Flow.

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Journal:  Compr Physiol       Date:  2017-03-16       Impact factor: 9.090

7.  Regulation of maximal open probability is a separable function of Ca(v)beta subunit in L-type Ca2+ channel, dependent on NH2 terminus of alpha1C (Ca(v)1.2alpha).

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8.  Developmental origins of colon smooth muscle dysfunction in IBS-like rats.

Authors:  Qingjie Li; John H Winston; Sushil K Sarna
Journal:  Am J Physiol Gastrointest Liver Physiol       Date:  2013-07-25       Impact factor: 4.052

9.  Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice.

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Journal:  Mol Cell Biochem       Date:  2016-08-13       Impact factor: 3.396

10.  Protein and gene expression of Ca2+ channel isoforms in murine colon: effect of inflammation.

Authors:  Minho Kang; Nemat Morsy; Xiaochun Jin; Florea Lupu; Hamid I Akbarali
Journal:  Pflugers Arch       Date:  2004-12       Impact factor: 3.657

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