Disruption of the Murine Calpain Small Subunit Gene, <i>Capn4</i>: Calpain Is Essential for Embryonic Development but Not for Cell Growth and Division

Arthur, J. Simon C.; Elce, John S.; Hegadorn, Carol; Williams, Karen; Greer, Peter A.

doi:10.1128/mcb.20.12.4474-4481.2000

Cited by 307 publications

(297 citation statements)

References 68 publications

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“…(Carmeliet et al, 1999) L1-CAM Cell-cell adhesion Total Malformations of the nervous system, decreased nerve sensitivity, weak and uncoordinated hindlegs. (Dahme et al, 1997) Ate1 Arginyltransferase Total Embryonic lethality at E12-17 with defects in cardiovascular development and angiogenesis (Kwon et al, 2002) Calpain IV (Capn4) Protease Total Embryonic lethality at midgestation with defects in the cardiovascular system, (Arthur et al, 2000) Birth Defects Res C Embryo Today. Author manuscript; available in PMC 2009 June 1.…”

Section: Note On Nomenclaturementioning

confidence: 99%

Cell biology of embryonic migration

Kurosaka¹,

Kashina²

2008

Birth Defects Research Pt C

113

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Cell migration is an evolutionarily conserved mechanism that underlies the development and functioning of uni-and multicellular organisms and takes place in normal and pathogenic processes, including various events of embryogenesis, wound healing, immune response, cancer metastases, and angiogenesis. Despite the differences in the cell types that take part in different migratory events, it is believed that all of these migrations occur by similar molecular mechanisms, whose major components have been functionally conserved in evolution and whose perturbation leads to severe developmental defects. These mechanisms involve intricate cytoskeleton-based molecular machines that can sense the environment, respond to signals, and modulate the entire cell behavior. A big question that has concerned the researchers for decades relates to the coordination of cell migration in situ and its relation to the intracellular aspects of the cell migratory mechanisms. Traditionally, this question has been addressed by researchers that considered the intra-and extracellular mechanisms driving migration in separate sets of studies. As more data accumulate researchers are now able to integrate all of the available information and consider the intracellular mechanisms of cell migration in the context of the developing organisms that contain additional levels of complexity provided by extracellular regulation. This review provides a broad summary of the existing and emerging data in the cell and developmental biology fields regarding cell migration during development.

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Section: Note On Nomenclaturementioning

confidence: 99%

Cell biology of embryonic migration

Kurosaka¹,

Kashina²

2008

Birth Defects Research Pt C

113

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“…91,92 These observations could not be corroborated by genetic approaches because mice deficient in the regulatory subunit develop defects in vasculogenesis and erythropoiesis and die early during embryonic development, which impedes evaluation of the importance of this protease in epidermal differentiation. 93 m-Calpain-null mice have no apparent embryological or epidermal defects, suggesting that m-calpain compensates for m-calpain during development. 94 m-Calpain-deficient mice have not been generated so far.…”

Section: Calpainsmentioning

confidence: 99%

Death penalty for keratinocytes: apoptosis versus cornification

et al. 2005

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Homeostasis implies a balance between cell growth and cell death. This balance is essential for the development and maintenance of multicellular organisms. Homeostasis is controlled by several mechanisms including apoptosis, a process by which cells condemned to death are completely eliminated. However, in some cases, total destruction and removal of dead cells is not desirable, as when they fulfil a specific function such as formation of the skin barrier provided by corneocytes, also known as terminally differentiated keratinocytes. In this case, programmed cell death results in accumulation of functional cell corpses. Previously, this process has been associated with apoptotic cell death. In this overview, we discuss differences and similarities in the molecular regulation of epidermal programmed cell death and apoptosis. We conclude that despite earlier confusion, apoptosis and cornification occur through distinct molecular pathways, and that possibly antiapoptotic mechanisms are implicated in the terminal differentiation of keratinocytes.

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“…Knockout of calpain small subunit 1 (CSS1 or Capn4) in mice (Arthur et al, 2000) leads to reduced expression and activities of both calpain 1 and calpain 2 (Dourdin et al, 2001). Embryonic fibroblasts isolated from these mice exhibit decreased proteolysis of several reported substrates, including FAK, paxillin, spectrin, cortactin and talin 1.…”

Section: Calpain Substratesmentioning

confidence: 99%

Regulating cell migration: calpains make the cut

Franco

Huttenlocher

2005

Journal of Cell Science

435

406

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The calpain family of proteases has been implicated in cellular processes such as apoptosis, proliferation and cell migration. Calpains are involved in several key aspects of migration, including: adhesion and spreading; detachment of the rear; integrin- and growth-factor-mediated signaling; and membrane protrusion. Our understanding of how calpains are activated and regulated during cell migration has increased as studies have identified roles for calcium and phospholipid binding, autolysis, phosphorylation and inhibition by calpastatin in the modulation of calpain activity. Knockout and knockdown approaches have also contributed significantly to our knowledge of calpain biology, particularly with respect to the specific functions of different calpain isoforms. The mechanisms by which calpain-mediated proteolysis of individual substrates contributes to cell motility have begun to be addressed, and these efforts have revealed roles for proteolysis of specific substrates in integrin activation, adhesion complex turnover and membrane protrusion dynamics. Understanding these mechanisms should provide avenues for novel therapeutic strategies to treat pathological processes such as tumor metastasis and chronic inflammatory disease.

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Disruption of the Murine Calpain Small Subunit Gene, Capn4: Calpain Is Essential for Embryonic Development but Not for Cell Growth and Division

Cited by 307 publications

References 68 publications

Cell biology of embryonic migration

Cell biology of embryonic migration

Death penalty for keratinocytes: apoptosis versus cornification

Regulating cell migration: calpains make the cut

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