Functional effects of overexpressing junctin in mouse hearts

J. Neumann, P. Boknik, L. R. Jones

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

Junctin (JUN) is a protein localized to the junctional sarcoplasmic reticulum (SR) that binds to calsequestrin which is a high capacity Ca2+ binding protein of the SR. In order to understand the functional role of JUN, transgenic mice (TG) were generated overexpressing dog JUN under the control of the alpha myosin heavy chain promoter. JUN was measured by quantitative immunoblotting with an antibody specific to dog JUN. No dog JUN was detectable in control mouse hearts (Ctr), while in (TG) the level of JUN (in arbitrary units) amounted to 1.24 ± 0.09, 1.12 ± 0.13, 0.92 ± 0.10, 0.71 ± 0.07 in left atria, right atria, left ventricles and right ventricles, resp. (n = 7). Heart weights were unaltered (TG 116 ± 3.6 mg vs. Ctr: 106 ± 5.1 mg). No gross anatomical abnormalities were seen. Time of relaxation (left atria, 1 Hz) in the presence of 5.4 mM Ca2+ was prolonged in TG (55 ± 4 ms) vs. Ctr (45 ± 2.7 ms, n = 6-8). Thus, JUN may play an important role in the Ca2+ handling by the SR.

Original languageEnglish (US)
Pages (from-to)A280
JournalFASEB Journal
Volume11
Issue number3
StatePublished - Dec 1 1997
Externally publishedYes

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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