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| Caption | KLF5 is essential for pressure overload-induced hypertrophy. (A-D) Klf5tm1Rng/Klf5+ (Klf5+/-) and wild-type (WT) mice were subjected to low intensity transverse aortic constriction (LI-TAC) or sham operation. (A) Representative low-magnification views of hematoxylin and eosin (H&E)-stained heart sections from WT and mutant mice 2 weeks after the operations. Scale bar: 1 mm. (B and C) Heart weight/body (HW/BW) weight ratios (B) and relative cross-sectional areas of cardiomyocytes (C) from WT and mutant hearts. (D) Fractional areas of fibrosis in cross sections of hearts as determined by elastic picrosirius red staining. *P < 0.01 versus sham control of the same genotype; #P < 0.05 versus WT subjected to TAC. n= 7. (E) Expression of KLF5 in normal and hypertrophied hearts 4 days after LI-TAC. Cells were double stained for KLF5 (brown) and a cardiomyocyte marker, alphaMHC (red); nuclei were counterstained in blue. Scale bar: 20 um. | ||||
| Copyright | This image is from Takeda N, J Clin Invest 2010 Jan;120(1):254-65 and is displayed with the permission of the American Society for Clinical Investigation who owns the Copyright. J:156696 | ||||
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Associated Alleles |
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Associated Genotypes |
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 12/10/2024 MGI 6.24 |
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