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CD2-associated protein (CD2AP) expression in podocytes rescues lethality of CD2AP deficiency

Standard

CD2-associated protein (CD2AP) expression in podocytes rescues lethality of CD2AP deficiency. / Grunkemeyer, James A; Kwoh, Christopher; Huber, Tobias B; Shaw, Andrey S.

in: J BIOL CHEM, Jahrgang 280, Nr. 33, 19.08.2005, S. 29677-81.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Grunkemeyer, JA, Kwoh, C, Huber, TB & Shaw, AS 2005, 'CD2-associated protein (CD2AP) expression in podocytes rescues lethality of CD2AP deficiency', J BIOL CHEM, Jg. 280, Nr. 33, S. 29677-81. https://doi.org/10.1074/jbc.M504004200

APA

Grunkemeyer, J. A., Kwoh, C., Huber, T. B., & Shaw, A. S. (2005). CD2-associated protein (CD2AP) expression in podocytes rescues lethality of CD2AP deficiency. J BIOL CHEM, 280(33), 29677-81. https://doi.org/10.1074/jbc.M504004200

Vancouver

Grunkemeyer JA, Kwoh C, Huber TB, Shaw AS. CD2-associated protein (CD2AP) expression in podocytes rescues lethality of CD2AP deficiency. J BIOL CHEM. 2005 Aug 19;280(33):29677-81. https://doi.org/10.1074/jbc.M504004200

Bibtex

@article{144fba8850c04fbaa0c4bf47f4825401,
title = "CD2-associated protein (CD2AP) expression in podocytes rescues lethality of CD2AP deficiency",
abstract = "Mice born without CD2-associated protein (CD2AP) develop renal failure and nephrotic syndrome about 4 weeks after birth and die around 6 weeks of age. Although CD2AP is widely expressed, the severity of the renal failure precludes a clear determination of the role of CD2AP in other tissues. Here we generated transgenic mice expressing CD2AP using a podocyte-specific promoter. Podocyte-specific expression of CD2AP prevented the development of proteinuria, demonstrating that the renal failure is solely due to loss of CD2AP in podocytes and not in other renal or in immune cells. CD2AP-deficient mice are long-lived and appear phenotypically normal. Histological analysis demonstrated testicular abnormalities that were age-related. CIN85, a paralog of CD2AP, is poorly expressed in both the podocyte and the basal seminiferous tubule, suggesting that the loss of CD2AP in specific tissues may be compensated for by CIN85.",
keywords = "Adaptor Proteins, Signal Transducing, Animals, Cytoskeletal Proteins, Epithelial Cells, Infertility, Male, Kidney Glomerulus, Male, Mice, Mice, Transgenic, Phenotype, Proteins, Renal Insufficiency, Testis, Journal Article",
author = "Grunkemeyer, {James A} and Christopher Kwoh and Huber, {Tobias B} and Shaw, {Andrey S}",
year = "2005",
month = aug,
day = "19",
doi = "10.1074/jbc.M504004200",
language = "English",
volume = "280",
pages = "29677--81",
journal = "J BIOL CHEM",
issn = "0021-9258",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "33",

}

RIS

TY - JOUR

T1 - CD2-associated protein (CD2AP) expression in podocytes rescues lethality of CD2AP deficiency

AU - Grunkemeyer, James A

AU - Kwoh, Christopher

AU - Huber, Tobias B

AU - Shaw, Andrey S

PY - 2005/8/19

Y1 - 2005/8/19

N2 - Mice born without CD2-associated protein (CD2AP) develop renal failure and nephrotic syndrome about 4 weeks after birth and die around 6 weeks of age. Although CD2AP is widely expressed, the severity of the renal failure precludes a clear determination of the role of CD2AP in other tissues. Here we generated transgenic mice expressing CD2AP using a podocyte-specific promoter. Podocyte-specific expression of CD2AP prevented the development of proteinuria, demonstrating that the renal failure is solely due to loss of CD2AP in podocytes and not in other renal or in immune cells. CD2AP-deficient mice are long-lived and appear phenotypically normal. Histological analysis demonstrated testicular abnormalities that were age-related. CIN85, a paralog of CD2AP, is poorly expressed in both the podocyte and the basal seminiferous tubule, suggesting that the loss of CD2AP in specific tissues may be compensated for by CIN85.

AB - Mice born without CD2-associated protein (CD2AP) develop renal failure and nephrotic syndrome about 4 weeks after birth and die around 6 weeks of age. Although CD2AP is widely expressed, the severity of the renal failure precludes a clear determination of the role of CD2AP in other tissues. Here we generated transgenic mice expressing CD2AP using a podocyte-specific promoter. Podocyte-specific expression of CD2AP prevented the development of proteinuria, demonstrating that the renal failure is solely due to loss of CD2AP in podocytes and not in other renal or in immune cells. CD2AP-deficient mice are long-lived and appear phenotypically normal. Histological analysis demonstrated testicular abnormalities that were age-related. CIN85, a paralog of CD2AP, is poorly expressed in both the podocyte and the basal seminiferous tubule, suggesting that the loss of CD2AP in specific tissues may be compensated for by CIN85.

KW - Adaptor Proteins, Signal Transducing

KW - Animals

KW - Cytoskeletal Proteins

KW - Epithelial Cells

KW - Infertility, Male

KW - Kidney Glomerulus

KW - Male

KW - Mice

KW - Mice, Transgenic

KW - Phenotype

KW - Proteins

KW - Renal Insufficiency

KW - Testis

KW - Journal Article

U2 - 10.1074/jbc.M504004200

DO - 10.1074/jbc.M504004200

M3 - SCORING: Journal article

C2 - 15951437

VL - 280

SP - 29677

EP - 29681

JO - J BIOL CHEM

JF - J BIOL CHEM

SN - 0021-9258

IS - 33

ER -