Upregulation of gamma-catenin compensates for the loss of beta-catenin in adult cardiomyocytes.

Upregulation of gamma-catenin compensates for the loss of beta-catenin in adult cardiomyocytes. Research Abstract Details 

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Upregulation of gamma-catenin compensates for the loss of beta-catenin in adult cardiomyocytes. Abstract Text:

Jibin Zhou,Jiaxiang Qu,Xian Ping Yi,Kelly Graber,Lu Huber,Xuejun Wang,A Martin Gerdes,Faqian Li,

Recent progresses in signal transduction have revealed that beta-catenin signaling controls embryonic development, tumorigenesis, cell shape, and polarity. The role of this pathway in myocyte shape regulation during cardiac hypertrophy and failure is, however, not clearly defined. Since homozygous knockout of beta-catenin is embryonically lethal, we have deleted beta-catenin genes specifically in the heart of adult mice by crossing loxP-flanked beta-catenin mice with transgenic mice expressing tamoxifen-activated MerCreMer protein (MCM) driven by the alpha-myosin heavy chain promoter. Administration of tamoxifen to homozygous loxP-flanked beta-catenin mice positive for MCM induces the deletion of beta-catenin only in cardiomyocytes. Immunolabeling with beta-catenin antibody demonstrates that 90% of cardiomyocytes completely lose their beta-catenin expression but maintain normal rod-shaped morphology. The intercalated disk of cardiomyocytes lacking beta-catenin is morphologically unremarkable with normal distribution of vinculin, N-cadherin, desmoplakin, ZO-1, connexin43, and alpha-, gamma-, and p120 catenins. The expression level of these proteins, except that of gamma-catenin, is also similar in tamoxifen-treated and control mice with both homozygous loxP-flanked beta-catenin genes and the MCM transgene. Western blot analyses reveal that gamma-catenin increases in the heart of beta-catenin knockout mice compared with controls. Confocal microscopy also demonstrates that gamma-catenin has significantly increased in the intercalated disk of cardiomyocytes lacking beta-catenin. Echocardiographic data indicate that the knockout mice maintain normal ventricular geometry and cardiac function. The results suggest that upregulation of gamma-catenin can compensate for the loss of beta-catenin in cardiomyocytes to maintain normal cardiac structure and function.

Upregulation of gamma-catenin compensates for the loss of beta-catenin in adult cardiomyocytes. Publishing Authors By Initials

J Zhou,J Qu,XP Yi,K Graber,L Huber,X Wang,AM Gerdes,F Li,

For similar proteins: armadillo domain proteins: gamma catenin research abstracts see: proteins: armadillo domain proteins: gamma catenin research

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Upregulation of gamma-catenin compensates for the loss of beta-catenin in adult cardiomyocytes. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: American journal of physiology. Heart and circulat

VOLUME: 292

Page Numbers: H270-6

Journal Abbreviation: Am. J. Physiol. Heart Circ. Ph

ISSN: 0363-6135

DAY: 25

MONTH: 08

YEAR: 2006

Upregulation of gamma-catenin compensates for the loss of beta-catenin in adult cardiomyocytes. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901228

Upregulation of gamma-catenin compensates for the loss of beta-catenin in adult cardiomyocytes. Keywords Mesh Terms:

KEYWORDS: gamma Catenin

MESH TERMS: metabolism

Chemical & Substance for Abstract: Upregulation of gamma-catenin compensates for the loss of beta-catenin in adult cardiomyocytes. Information

Substance Name: gamma Catenin

Registry Number: 0

Grant and Affiliation Information for Upregulation of gamma-catenin compensates for the loss of beta-catenin in adult cardiomyocytes.

AFFILIATION: Cardiovascular Research Institute, South Dakota Health Research Foundation, 1100 East 21st St., Suite 700, Sioux Falls, SD 57105, USA.

Country: United States

AGENCY: United States NCRR

GRANT: P20 RR017662

ACRONYM: RR

MEDLINETA: Am J Physiol Heart Circ Physio

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