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July 1, 1995Genes & DevelopmentOpen Access

Myogenic and morphogenetic defects in the heart tubes of murine embryos lacking the homeo box gene Nkx2-5.

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Key result

Targeted interruption of Nkx2-5 in murine embryos resulted in abnormal heart morphogenesis, lack of looping morphogenesis, loss of MLC2V expression, and embryonic lethality at 9-10 days postcoitum.

Population

Murine embryos and ES cell-derived cardiocytes

Comparison

Targeted interruption of the homeobox gene Nkx2-5 vs Normal/wild-type murine embryos (implied)

Design

Preclinical

Follow-up

9-10 days postcoitum

Authors

ILIan LyonsAustralian National UniversityLPLinda M. ParsonsPeter MacCallum Cancer CentreLHLynne HartleyWalter and Eliza Hall Institute of Medical Research

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Overview

Nkx2-5 disruption causes lethal cardiac defects in mice; leaves open its role in human congenital heart disease.

Structured PICO

P
Population
Murine embryos and ES cell-derived cardiocytes
I
Intervention
Targeted interruption of the homeobox gene Nkx2-5
C
Comparator
Normal/wild-type murine embryos (implied)
O
Outcome
Heart morphogenesis, growth, and embryonic survivalsurrogate

The homeobox gene Nkx2-5 is essential for normal heart morphogenesis, myogenesis, and ventricular specialization in murine embryos.

Cite This Study

Lyons et al. (1995) studied Nkx2-5 gene knockout in murine embryos. Targeted interruption of Nkx2-5 vs. Normal embryos was evaluated on Heart morphogenesis, growth retardation, and embryonic lethality. Targeted interruption of Nkx2-5 in murine embryos resulted in abnormal heart morphogenesis, lack of looping morphogenesis, loss of MLC2V expression, and embryonic lethality at 9-10 days postcoitum.

synapsesocial.com/papers/6a0d51f2cae7912d2fa4e738https://doi.org/10.1101/gad.9.13.1654

Topics

Congenital heart disease adults
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