Specific disruption of smooth muscle caldesmon expression in mice

Guo, Hongqiu; Wang, C.-L. Albert

doi:10.1016/j.bbrc.2005.03.089

Cited by 16 publications

(22 citation statements)

References 17 publications

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“…The regulation of caldesmon is complex as further illustrated by the findings in the SM-B knockout mouse in which caldesmon expression is decreased in bladder smooth muscle in the absence of any obstruction [80]. Further clarification of caldesmon’s role in the regulation of bladder contractility will come as the voiding phenotype of this knockout mouse is characterized [81]. …”

Section: Alterations In the Thin Contractile Filamentsmentioning

confidence: 99%

Alterations in the contractile phenotype of the bladder: lessons for understanding physiological and pathological remodelling of smooth muscle

Zderic

Chacko

2012

J Cellular Molecular Medi

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The contractile properties of the urinary bladder are changed by the conditions of normal development and partial bladder outlet obstruction. This change in the contractile phenotype is accompanied by changes in the regulatory cascades and filaments that regulate contractility. This review focuses on such changes during the course of normal development and in response to obstruction. Our goal is to discuss the experimental evidence that has accumulated from work in animal models and correlate these findings with the human voiding phenotype.

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Section: Alterations In the Thin Contractile Filamentsmentioning

confidence: 99%

Alterations in the contractile phenotype of the bladder: lessons for understanding physiological and pathological remodelling of smooth muscle

Zderic

Chacko

2012

J Cellular Molecular Medi

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“…In brief, the gene of interest (or parts of it) is flanked Diminished recovery from endotoxic shock, overexpression of some LPS inducible genes. Yoo et al (2002) Caldesmon exon 3b* Unclear phenotype Guo and Wang (2005) See text for details. Models marked by an asterisk are not further discussed, as they do not show a phenotype in vivo and are described in only one or two references.…”

Section: Jensen Et Al (2000)mentioning

confidence: 99%

The impact of alternative splicing in vivo: Mouse models show the way

Möröy

Heyd²

2007

RNA

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Alternative splicing is widely believed to have a major impact on almost all biological processes since it increases proteome complexity and thereby controls protein function. Recently, gene targeting in mice has been used to create in vivo models to study the regulation and consequences of alternative splicing. The evidence accumulated so far argues for a nonredundant, highly specific role of individual splicing factors in mammalian development, and furthermore, demonstrates the importance of distinct protein isoforms in vivo. In this review, we will compare phenotypes of mouse models for alternative splicing to crystallize common themes and to put them into perspective with the available in vitro data.

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“…When the expression of h-CaD was abolished in mice, l-CaD became upregulated only in phasic muscles. 19 This may suggest that CaD (of either isoform) is "indispensable" in phasic smooth muscles and that l-CaD can at least partially substitute hCaD for its function. On the other hand, tonic smooth muscles, which contain less h-CaD in the wild-type, did not show isoform switchover in the h-CaD-deficient animals, probably because the basal level of l-CaD was sufficient to carry out h-CaD's function.…”

Section: Cellular Content Of H-cadmentioning

confidence: 99%

“…Recently, the expression of smooth muscle CaD was successfully abrogated in mice without blocking the expression of nonmuscle CaD. 19 Such a strategy was achieved by disrupting the CaD gene (on mouse chromosome 6) at exon 3 beyond the splicing site. The homozygous mice thus obtained indeed lack h-CaD, but still express l-CaD.…”

Section: Introductionmentioning

confidence: 99%

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Caldesmon and the Regulation of Cytoskeletal Functions

Wang

2008

Advances in Experimental Medicine and Biology

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Caldesmon (CaD) is an extraordinary actin-binding protein, because in addition to actin, it also binds myosin, calmodulin and tropomyosin. As a component of the smooth muscle and nonmuscle contractile apparatus CaD inhibits the actomyosin ATPase activity and its inhibitory action is modulated by both Ca 2+ and phosphorylation. The multiplicity of binding partners and diverse biochemical properties suggest CaD is a potent and versatile regulatory protein both in contractility and cell motility. However, after decades of investigation in numerous laboratories, hard evidence is still lacking to unequivocally identify its in vivo functions, although indirect evidence is mounting to support an important role in connection with the actin cytoskeleton. This chapter reviews the highlights of the past findings and summarizes the current views on this protein, with emphasis of its interaction with tropomyosin.

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Specific disruption of smooth muscle caldesmon expression in mice

Cited by 16 publications

References 17 publications

Alterations in the contractile phenotype of the bladder: lessons for understanding physiological and pathological remodelling of smooth muscle

Alterations in the contractile phenotype of the bladder: lessons for understanding physiological and pathological remodelling of smooth muscle

The impact of alternative splicing in vivo: Mouse models show the way

Caldesmon and the Regulation of Cytoskeletal Functions

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