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PMID:9950951

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Citation

Sorenson, CM (1999) Nuclear localization of beta-catenin and loss of apical brush border actin in cystic tubules of bcl-2 -/- mice. Am. J. Physiol. 276:F210-7

Abstract

Tight regulation of the rates of cell proliferation and apoptosis is critical for normal nephrogenesis. Nephrogenesis is profoundly affected by the loss of bcl-2 expression. Bcl-2-deficient (bcl-2 -/-) mice are born with renal hypoplasia and succumb to renal failure secondary to renal multicystic disease. Cell-cell and cell-matrix interactions impact tissue architecture by modulating cell proliferation, migration, differentiation, and apoptosis. E-cadherin mediates calcium-dependent homotypic cell-cell interactions that are stabilized by its association with catenins and the actin cytoskeleton. The contribution of altered cell-cell interactions to renal cystic disease has not been delineated. Cystic kidneys from bcl-2 -/- mice displayed nuclear localization of beta-catenin and loss of apical brush border actin staining. The protein levels of alpha-catenin, beta-catenin, actin, and E-cadherin were not altered in cystic kidneys compared with normal kidneys. Therefore, an altered distribution of beta-catenin and actin, in kidneys from bcl-2 -/- mice, may indicate improper cell-cell interactions interfering with renal maturation and contributing to renal cyst formation.

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PubMed

Keywords

Actins/metabolism; Actins/physiology; Animals; Blotting, Western; Cadherins/metabolism; Cell Adhesion Molecules/metabolism; Cell Nucleus/metabolism; Cytoskeletal Proteins/metabolism; Immunohistochemistry; Kidney Tubules/metabolism; Mice/genetics; Microvilli/metabolism; Polycystic Kidney Diseases/genetics; Polycystic Kidney Diseases/metabolism; Proto-Oncogene Proteins c-bcl-2/deficiency; Proto-Oncogene Proteins c-bcl-2/genetics; Tissue Distribution; Trans-Activators; beta Catenin

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


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References

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