Literature DB >> 19005011

Disruption of Myosin 1e promotes podocyte injury.

Mira Krendel1, Sangwon V Kim, Tim Willinger, Tong Wang, Michael Kashgarian, Richard A Flavell, Mark S Mooseker.   

Abstract

Myosin 1e (Myo1e) is one of two Src homology 3 domain-containing "long-tailed" type I myosins in vertebrates, whose functions in health and disease are incompletely understood. Here, we demonstrate that Myo1e localizes to podocytes in the kidney. We generated Myo1e-knockout mice and found that they exhibit proteinuria, signs of chronic renal injury, and kidney inflammation. At the ultrastructural level, renal tissue from Myo1e-null mice demonstrates changes characteristic of glomerular disease, including a thickened and disorganized glomerular basement membrane and flattened podocyte foot processes. These observations suggest that Myo1e plays an important role in podocyte function and normal glomerular filtration.

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Year:  2008        PMID: 19005011      PMCID: PMC2615733          DOI: 10.1681/ASN.2007111172

Source DB:  PubMed          Journal:  J Am Soc Nephrol        ISSN: 1046-6673            Impact factor:   10.121


  28 in total

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Authors:  J Bernstein
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4.  Periodate-lysine-paraformaldehyde fixative. A new fixation for immunoelectron microscopy.

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Review 6.  Myosin I: from yeast to human.

Authors:  S V Kim; R A Flavell
Journal:  Cell Mol Life Sci       Date:  2008-07       Impact factor: 9.261

7.  Mouse model of X-linked Alport syndrome.

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Review 8.  Pathophysiology of proteinuria.

Authors:  Giuseppe D'Amico; Claudio Bazzi
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Authors:  Clifford E Kashtan
Journal:  Curr Opin Pediatr       Date:  2004-04       Impact factor: 2.856

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Authors:  June Yao; Tu Cam Le; Claudine H Kos; Joel M Henderson; Phillip G Allen; Bradley M Denker; Martin R Pollak
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  51 in total

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Review 7.  Animal models of nephrotic syndrome.

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Review 8.  Recent advances of animal model of focal segmental glomerulosclerosis.

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9.  Myosin 1e is a component of the invadosome core that contributes to regulation of invadosome dynamics.

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10.  TGFβ-Induced Actin Cytoskeleton Rearrangement in Podocytes Is Associated with Compensatory Adaptation of Mitochondrial Energy Metabolism.

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