Targeted disruption of CRE-binding factor TREB5 gene leads to cellular necrosis in cardiac myocytes at the embryonic stage
T Masaki, M Yoshida, S Noguchi - Biochemical and biophysical research …, 1999 - Elsevier
T Masaki, M Yoshida, S Noguchi
Biochemical and biophysical research communications, 1999•ElsevierTREB5 (hXBP-1) is a basic region leucine zipper protein which binds to a CRE-like element
in both human T-cell leukemia virus type 1 and MHC class II genes. To study the function (s)
of TREB5 in normal development, we have generated TREB5 deficient mice by gene
targeting. Heterozygous mutant mice have not exhibited any obvious abnormalities;
however, homozygous mutant embryos die between embryonic days 10.5 and 14.5. The
major defect responsible for lethality is cellular necrosis of cardiac myocytes located at the …
in both human T-cell leukemia virus type 1 and MHC class II genes. To study the function (s)
of TREB5 in normal development, we have generated TREB5 deficient mice by gene
targeting. Heterozygous mutant mice have not exhibited any obvious abnormalities;
however, homozygous mutant embryos die between embryonic days 10.5 and 14.5. The
major defect responsible for lethality is cellular necrosis of cardiac myocytes located at the …
TREB5 (hXBP-1) is a basic region leucine zipper protein which binds to a CRE-like element in both human T-cell leukemia virus type 1 and MHC class II genes. To study the function(s) of TREB5 in normal development, we have generated TREB5 deficient mice by gene targeting. Heterozygous mutant mice have not exhibited any obvious abnormalities; however, homozygous mutant embryos die between embryonic days 10.5 and 14.5. The major defect responsible for lethality is cellular necrosis of cardiac myocytes located at the atrium and the truncus arteriosus with its following ventricle. Necrotic alteration was not observed in either the endocardial cushion or the conotruncal ridge. These results indicate that TREB5 plays an essential role in maintenance and/or growth of cardiac myocytes during cardiogenesis.
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