Literature DB >> 1650725

Muscle fibers from dysgenic mouse in vivo lack a surface component of peripheral couplings.

C Franzini-Armstrong1, M Pincon-Raymond, F Rieger.   

Abstract

We have studied the structure of developing normal and dysgenic (mdg/mdg) mouse muscle fibers in vivo, with special attention to the components of the junctions between the sarcoplasmic reticulum and either the surface membrane or the transverse tubules. Triads and dyads are rare in dysgenic muscle fibers, but have apparently normal disposition of feet and calsequestrin. Peripheral couplings in normal developing muscle fibers have junctional tetrads in their surface membrane in association with the junctional feet. Muscle fibers in dysgenic mice lack junctional tetrads. This provides indirect evidence for the identification of the components of junctional tetrads with dihydropyridine receptors, which are known to be absent in dysgenic muscle fibers.

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Year:  1991        PMID: 1650725     DOI: 10.1016/0012-1606(91)90238-x

Source DB:  PubMed          Journal:  Dev Biol        ISSN: 0012-1606            Impact factor:   3.582


  38 in total

1.  The structure of Ca(2+) release units in arthropod body muscle indicates an indirect mechanism for excitation-contraction coupling.

Authors:  Hiroaki Takekura; Clara Franzini-Armstrong
Journal:  Biophys J       Date:  2002-11       Impact factor: 4.033

Review 2.  DHP receptors and excitation-contraction coupling.

Authors:  G D Lamb
Journal:  J Muscle Res Cell Motil       Date:  1992-08       Impact factor: 2.698

3.  Functional crosstalk between cell-surface and intracellular channels mediated by junctophilins essential for neuronal functions.

Authors:  Sho Kakizawa; Shigeki Moriguchi; Atsushi Ikeda; Masamitsu Iino; Hiroshi Takeshima
Journal:  Cerebellum       Date:  2008       Impact factor: 3.847

4.  Tagging with green fluorescent protein reveals a distinct subcellular distribution of L-type and non-L-type Ca2+ channels expressed in dysgenic myotubes.

Authors:  M Grabner; R T Dirksen; K G Beam
Journal:  Proc Natl Acad Sci U S A       Date:  1998-02-17       Impact factor: 11.205

5.  Recovery of Ca2+ current, charge movements, and Ca2+ transients in myotubes deficient in dihydropyridine receptor beta 1 subunit transfected with beta 1 cDNA.

Authors:  M Beurg; M Sukhareva; C Strube; P A Powers; R G Gregg; R Coronado
Journal:  Biophys J       Date:  1997-08       Impact factor: 4.033

6.  Functional impact of the ryanodine receptor on the skeletal muscle L-type Ca(2+) channel.

Authors:  G Avila; R T Dirksen
Journal:  J Gen Physiol       Date:  2000-04       Impact factor: 4.086

7.  Transport of the alpha subunit of the voltage gated L-type calcium channel through the sarcoplasmic reticulum occurs prior to localization to triads and requires the beta subunit but not Stac3 in skeletal muscles.

Authors:  Jeremy W Linsley; I-Uen Hsu; Wenjia Wang; John Y Kuwada
Journal:  Traffic       Date:  2017-09       Impact factor: 6.215

8.  Alternate disposition of tetrads in peripheral couplings of skeletal muscle.

Authors:  C Franzini-Armstrong; J W Kish
Journal:  J Muscle Res Cell Motil       Date:  1995-06       Impact factor: 2.698

9.  Abnormal junctions between surface membrane and sarcoplasmic reticulum in skeletal muscle with a mutation targeted to the ryanodine receptor.

Authors:  H Takekura; M Nishi; T Noda; H Takeshima; C Franzini-Armstrong
Journal:  Proc Natl Acad Sci U S A       Date:  1995-04-11       Impact factor: 11.205

10.  An Ryr1I4895T mutation abolishes Ca2+ release channel function and delays development in homozygous offspring of a mutant mouse line.

Authors:  Elena Zvaritch; Frederic Depreux; Natasha Kraeva; Ryan E Loy; Sanjeewa A Goonasekera; Simona Boncompagni; Simona Boncompagi; Alexander Kraev; Anthony O Gramolini; Robert T Dirksen; Clara Franzini-Armstrong; Christine E Seidman; J G Seidman; David H Maclennan
Journal:  Proc Natl Acad Sci U S A       Date:  2007-11-14       Impact factor: 11.205

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