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Par3A is dispensable for the function of the glomerular filtration barrier of the kidney

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Par3A is dispensable for the function of the glomerular filtration barrier of the kidney. / Koehler, Sybille; Tellkamp, Frederik; Niessen, Carien M; Bloch, Wilhelm; Kerjaschki, Dontscho; Schermer, Bernhard; Benzing, Thomas; Brinkkoetter, Paul T.

In: AM J PHYSIOL-RENAL, Vol. 311, No. 1, 01.07.2016, p. F112-9.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Koehler, S, Tellkamp, F, Niessen, CM, Bloch, W, Kerjaschki, D, Schermer, B, Benzing, T & Brinkkoetter, PT 2016, 'Par3A is dispensable for the function of the glomerular filtration barrier of the kidney', AM J PHYSIOL-RENAL, vol. 311, no. 1, pp. F112-9. https://doi.org/10.1152/ajprenal.00171.2016

APA

Koehler, S., Tellkamp, F., Niessen, C. M., Bloch, W., Kerjaschki, D., Schermer, B., Benzing, T., & Brinkkoetter, P. T. (2016). Par3A is dispensable for the function of the glomerular filtration barrier of the kidney. AM J PHYSIOL-RENAL, 311(1), F112-9. https://doi.org/10.1152/ajprenal.00171.2016

Vancouver

Koehler S, Tellkamp F, Niessen CM, Bloch W, Kerjaschki D, Schermer B et al. Par3A is dispensable for the function of the glomerular filtration barrier of the kidney. AM J PHYSIOL-RENAL. 2016 Jul 1;311(1):F112-9. https://doi.org/10.1152/ajprenal.00171.2016

Bibtex

@article{5bca17adde66402fa803814b02e54cba,
title = "Par3A is dispensable for the function of the glomerular filtration barrier of the kidney",
abstract = "Polarity signaling through the atypical PKC (aPKC)-Par polarity complex is essential for the development and maintenance of the podocyte architecture and the function of the glomerular filtration barrier of the kidney. To study the contribution of Par3A in this complex, we generated a novel Pard3 podocyte-specific knockout mouse model by targeting exon 6 of the Pard3 gene. Genetic deletion of Pard3a did not impair renal function, neither at birth nor later in life. Even challenging the animals did not result in glomerular disease. Despite its well-established role in aPKC-mediated signaling, Par3A appears to be dispensable for the function of the glomerular filtration barrier. Moreover, its homolog Pard3b, and not Pard3a, is the dominant Par3 gene expressed in podocytes and found at the basis of the slit diaphragm, where it partially colocalizes with podocin. In conclusion, Par3A function is either dispensable for slit diaphragm integrity, or compensatory mechanisms and a high redundancy of the different polarity proteins, including Par3B, Lgl, or PALS1, maintain the function of the glomerular filtration barrier, even in the absence of Par3A.",
keywords = "Adaptor Proteins, Signal Transducing, Animals, Cell Adhesion Molecules/genetics, Cell Cycle Proteins, Cells, Cultured, Female, Glomerular Filtration Barrier/physiology, Kidney/pathology, Lipopolysaccharides/toxicity, Male, Membrane Proteins/genetics, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Nucleoside-Phosphate Kinase/genetics, Podocytes/drug effects, Primary Cell Culture, Serum Albumin, Bovine/toxicity",
author = "Sybille Koehler and Frederik Tellkamp and Niessen, {Carien M} and Wilhelm Bloch and Dontscho Kerjaschki and Bernhard Schermer and Thomas Benzing and Brinkkoetter, {Paul T}",
note = "Copyright {\textcopyright} 2016 the American Physiological Society.",
year = "2016",
month = jul,
day = "1",
doi = "10.1152/ajprenal.00171.2016",
language = "English",
volume = "311",
pages = "F112--9",
journal = "AM J PHYSIOL-RENAL",
issn = "1931-857X",
publisher = "AMER PHYSIOLOGICAL SOC",
number = "1",

}

RIS

TY - JOUR

T1 - Par3A is dispensable for the function of the glomerular filtration barrier of the kidney

AU - Koehler, Sybille

AU - Tellkamp, Frederik

AU - Niessen, Carien M

AU - Bloch, Wilhelm

AU - Kerjaschki, Dontscho

AU - Schermer, Bernhard

AU - Benzing, Thomas

AU - Brinkkoetter, Paul T

N1 - Copyright © 2016 the American Physiological Society.

PY - 2016/7/1

Y1 - 2016/7/1

N2 - Polarity signaling through the atypical PKC (aPKC)-Par polarity complex is essential for the development and maintenance of the podocyte architecture and the function of the glomerular filtration barrier of the kidney. To study the contribution of Par3A in this complex, we generated a novel Pard3 podocyte-specific knockout mouse model by targeting exon 6 of the Pard3 gene. Genetic deletion of Pard3a did not impair renal function, neither at birth nor later in life. Even challenging the animals did not result in glomerular disease. Despite its well-established role in aPKC-mediated signaling, Par3A appears to be dispensable for the function of the glomerular filtration barrier. Moreover, its homolog Pard3b, and not Pard3a, is the dominant Par3 gene expressed in podocytes and found at the basis of the slit diaphragm, where it partially colocalizes with podocin. In conclusion, Par3A function is either dispensable for slit diaphragm integrity, or compensatory mechanisms and a high redundancy of the different polarity proteins, including Par3B, Lgl, or PALS1, maintain the function of the glomerular filtration barrier, even in the absence of Par3A.

AB - Polarity signaling through the atypical PKC (aPKC)-Par polarity complex is essential for the development and maintenance of the podocyte architecture and the function of the glomerular filtration barrier of the kidney. To study the contribution of Par3A in this complex, we generated a novel Pard3 podocyte-specific knockout mouse model by targeting exon 6 of the Pard3 gene. Genetic deletion of Pard3a did not impair renal function, neither at birth nor later in life. Even challenging the animals did not result in glomerular disease. Despite its well-established role in aPKC-mediated signaling, Par3A appears to be dispensable for the function of the glomerular filtration barrier. Moreover, its homolog Pard3b, and not Pard3a, is the dominant Par3 gene expressed in podocytes and found at the basis of the slit diaphragm, where it partially colocalizes with podocin. In conclusion, Par3A function is either dispensable for slit diaphragm integrity, or compensatory mechanisms and a high redundancy of the different polarity proteins, including Par3B, Lgl, or PALS1, maintain the function of the glomerular filtration barrier, even in the absence of Par3A.

KW - Adaptor Proteins, Signal Transducing

KW - Animals

KW - Cell Adhesion Molecules/genetics

KW - Cell Cycle Proteins

KW - Cells, Cultured

KW - Female

KW - Glomerular Filtration Barrier/physiology

KW - Kidney/pathology

KW - Lipopolysaccharides/toxicity

KW - Male

KW - Membrane Proteins/genetics

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Mice, Transgenic

KW - Nucleoside-Phosphate Kinase/genetics

KW - Podocytes/drug effects

KW - Primary Cell Culture

KW - Serum Albumin, Bovine/toxicity

U2 - 10.1152/ajprenal.00171.2016

DO - 10.1152/ajprenal.00171.2016

M3 - SCORING: Journal article

C2 - 27122542

VL - 311

SP - F112-9

JO - AM J PHYSIOL-RENAL

JF - AM J PHYSIOL-RENAL

SN - 1931-857X

IS - 1

ER -