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Results: 5

1.
Figure 5

Figure 5. From: Positive Transcription Elongation Factor b (P-TEFb) Activity in Compensatory Myocardial Hypertrophy is Regulated by Cardiac Lineage Protein-1.

Mason trichrome staining of representative ventricular transverse sections of the indicated genotypes (three-month old mice) illustrating the absence of any marked increase in interstitial collagen (which stains blue).

Jorge Espinoza-Derout, et al. Circ Res. ;104(12):1347-1354.
2.
Figure 4

Figure 4. From: Positive Transcription Elongation Factor b (P-TEFb) Activity in Compensatory Myocardial Hypertrophy is Regulated by Cardiac Lineage Protein-1.

Glucose transporters GLUT1/GLUT4 ratio in MHC-Cyclin T1/CLP-1+/− mice. A, Western blot shows expression levels of GLUT1, GLUT4, and GAPDH in heart lysates of the indicated genotypes. B, quantification of GLUT1/GLUT4 ratio. Data are expressed as mean ± SE of five independent experiments of three-month old mice. *P < 0.05 versus control; P < 0.05 versus MHC-Cyclin T1.

Jorge Espinoza-Derout, et al. Circ Res. ;104(12):1347-1354.
3.
Figure 3

Figure 3. From: Positive Transcription Elongation Factor b (P-TEFb) Activity in Compensatory Myocardial Hypertrophy is Regulated by Cardiac Lineage Protein-1.

Phosphorylation levels of CTD RNA Pol II in MHC-Cyclin T1 and MHC-Cyclin T1/CLP-1+/− mice. A, anti-Ser2 Pol II immunoblot of heart lysates showing phosphorylation levels of RNA Pol II in MHC-Cyclin T1 and MHC-Cyclin T1/CLP-1+/− mice. B, anti-Ser5 Pol II immunoblot heart lysates showing phosphorylation levels of CTD RNA Pol II. C, anti-RNA Pol II immunoblot heart lysates showing total protein levels of RNA Pol II. Data are expressed as mean ± SE of five independent experiments. *P < 0.05 versus control. *P < 0.05 versus control; P < 0.05 versus MHC-Cyclin T1.

Jorge Espinoza-Derout, et al. Circ Res. ;104(12):1347-1354.
4.

Figure 2. From: Positive Transcription Elongation Factor b (P-TEFb) Activity in Compensatory Myocardial Hypertrophy is Regulated by Cardiac Lineage Protein-1.

Exacerbated hypertrophy response in MHC-Cyclin T1/CLP-1+/− mice. A, photograph of adult mice hearts of the indicated genotypes. B, heart/body weight ratios in MHC-Cyclin T1 and MHC-Cyclin T1/CLP-1+/− mice. The data shown are means +/− SE of the Δheart/body ratio. *P < 0.05 versus wild type of three-month old mice (n =13). C, Western blots showing levels of CLP-1, Cyclin T1 and cdk9 hearts of the indicated genotypes of three-month old mice. GAPDH was used as loading control (n = 5). *P < 0.05 versus control; P < 0.05 versus MHC-Cyclin T1.

Jorge Espinoza-Derout, et al. Circ Res. ;104(12):1347-1354.
5.

Figure 1. From: Positive Transcription Elongation Factor b (P-TEFb) Activity in Compensatory Myocardial Hypertrophy is Regulated by Cardiac Lineage Protein-1.

Postnatal changes in the P-TEFb complex in wild type and calcineurin (MHC-CnA) transgenic mice. A, immunoblot with anti-CLP-1 and anti-cyclin T1 antibodies of the heart lysates from wild-type (WT) and MHC-CnA (+) mice. GAPDH was used as loading control (n = 6). B, Association of CLP-1 with P-TEFb in postnatal wild type and MHC-CnA mice as a function of age. Heart lysates from wild type (WT) and MHC-CnA (+) of 1 week, 1 month and 4 month old mice were immunoprecipitated with Cyclin T1 antibody and probed with anti-CLP-1 and anti-Cyclin T1 antibodies. Input is non-immunoprecipitated cell lysates. The data is representative three of independent experiments. C, Phosphorylation of Ser2 RNA Pol II and total RNA Pol II in postnatal wild type and CnA transgenic mice. Immunoblot incubated with anti-phosphorylated Ser2 RNA Pol II and anti-total Pol II of cell lysates of hearts from wild-type (WT) and MHC-CnA (+) of 1 week, 1 month, and 4 months old mice (n =4). Data are expressed as mean ± SE . *P < 0.05 versus control.

Jorge Espinoza-Derout, et al. Circ Res. ;104(12):1347-1354.

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