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phospho acc ser 79 rabbit mab  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc phospho acc ser 79 rabbit mab
    ( A ) Western blot analysis of female mouse livers fed HFD containing doxycycline (Doxy) to express constitutive active AMPK [a1(1-312); AMPK CA ] for 7 days compared to control livers. ( B ) Immunohistochemical analysis of livers from male control and AMPK CA mice fed HFD+Doxy for 7 months. Scale bars, 100 μm. Right: Quantification of the staining intensity for P-Thr 172 AMPK and P-Ser 79 ACC staining. n = 6 to 10. ±SEM, Welch t test. ( C ) Representative whole-mount (top) and MRI (bottom) image of male control and AMPK CA livers 9 months post–DEN injection. Yellow dashed lines indicate tumors. ( D ) Quantification of the tumor number in male control and AMPK CA livers 6 and 9 months post–DEN injection based on MRI images. 6 months: N = 5 to 7; 9 months: N = 16 to 17; Fisher least significant difference (LSD) test. ( E ) Quantification of the serum AFP levels in control and AMPK CA male mice 6 and 9 months post–DEN injection. n = 9 to 15. Fisher LSD test. * P < 0.05; *** P < 0.001; **** P < 0.0001.
    Phospho Acc Ser 79 Rabbit Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/phospho+acc+ser+79+rabbit+mab/pmc13068069-9-0-7
    Average 86 stars, based on 1 article reviews
    phospho acc ser 79 rabbit mab - by Bioz Stars, 2026-09
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    Images

    1) Product Images from "Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity"

    Article Title: Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity

    Journal: Science Advances

    doi: 10.1126/sciadv.aea8017

    ( A ) Western blot analysis of female mouse livers fed HFD containing doxycycline (Doxy) to express constitutive active AMPK [a1(1-312); AMPK CA ] for 7 days compared to control livers. ( B ) Immunohistochemical analysis of livers from male control and AMPK CA mice fed HFD+Doxy for 7 months. Scale bars, 100 μm. Right: Quantification of the staining intensity for P-Thr 172 AMPK and P-Ser 79 ACC staining. n = 6 to 10. ±SEM, Welch t test. ( C ) Representative whole-mount (top) and MRI (bottom) image of male control and AMPK CA livers 9 months post–DEN injection. Yellow dashed lines indicate tumors. ( D ) Quantification of the tumor number in male control and AMPK CA livers 6 and 9 months post–DEN injection based on MRI images. 6 months: N = 5 to 7; 9 months: N = 16 to 17; Fisher least significant difference (LSD) test. ( E ) Quantification of the serum AFP levels in control and AMPK CA male mice 6 and 9 months post–DEN injection. n = 9 to 15. Fisher LSD test. * P < 0.05; *** P < 0.001; **** P < 0.0001.
    Figure Legend Snippet: ( A ) Western blot analysis of female mouse livers fed HFD containing doxycycline (Doxy) to express constitutive active AMPK [a1(1-312); AMPK CA ] for 7 days compared to control livers. ( B ) Immunohistochemical analysis of livers from male control and AMPK CA mice fed HFD+Doxy for 7 months. Scale bars, 100 μm. Right: Quantification of the staining intensity for P-Thr 172 AMPK and P-Ser 79 ACC staining. n = 6 to 10. ±SEM, Welch t test. ( C ) Representative whole-mount (top) and MRI (bottom) image of male control and AMPK CA livers 9 months post–DEN injection. Yellow dashed lines indicate tumors. ( D ) Quantification of the tumor number in male control and AMPK CA livers 6 and 9 months post–DEN injection based on MRI images. 6 months: N = 5 to 7; 9 months: N = 16 to 17; Fisher least significant difference (LSD) test. ( E ) Quantification of the serum AFP levels in control and AMPK CA male mice 6 and 9 months post–DEN injection. n = 9 to 15. Fisher LSD test. * P < 0.05; *** P < 0.001; **** P < 0.0001.

    Techniques Used: Western Blot, Control, Immunohistochemical staining, Staining, Injection

    ( A ) Quantification of the tumor size from MRI imaging at 6 and 9 months. n = 10 to 448. Log normal Welch t test. ( B ) Immunohistochemical analysis of BrdU incorporation in tumor tissue from control and AMPK CA livers following a 4-hour BrdU pulse (10 mg/kg). Scale bars, 100 μm. Right: Quantification of the number of positive cells per area. n = 13 to 17. Welch t test. ( C ) Gene expression of Ampka1 normalized to Actin in nontumor and tumor tissue. n = 5 to 6. ±SEM, Fisher LSD test. ( D ) Immunohistochemical analysis of P-Ser 79 ACC in nontumor and tumor tissue from control and AMPK CA livers. Scale bars, 100 μm. ( E ) Quantification of the staining intensity of P-Ser 79 ACC. n = 5 to 14. Fisher LSD test. ( F ) Immunohistochemical analysis of P-Thr 172 AMPK in nontumor and tumor tissue from control and AMPK CA livers. Scale bars, 100 μm. ( G ) Quantification of the staining intensity. n = 6 to 11. Fisher LSD test. ( H ) Western blot analysis of nontumor (NT) and tumor (T) tissue. VINCULIN as loading control. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.
    Figure Legend Snippet: ( A ) Quantification of the tumor size from MRI imaging at 6 and 9 months. n = 10 to 448. Log normal Welch t test. ( B ) Immunohistochemical analysis of BrdU incorporation in tumor tissue from control and AMPK CA livers following a 4-hour BrdU pulse (10 mg/kg). Scale bars, 100 μm. Right: Quantification of the number of positive cells per area. n = 13 to 17. Welch t test. ( C ) Gene expression of Ampka1 normalized to Actin in nontumor and tumor tissue. n = 5 to 6. ±SEM, Fisher LSD test. ( D ) Immunohistochemical analysis of P-Ser 79 ACC in nontumor and tumor tissue from control and AMPK CA livers. Scale bars, 100 μm. ( E ) Quantification of the staining intensity of P-Ser 79 ACC. n = 5 to 14. Fisher LSD test. ( F ) Immunohistochemical analysis of P-Thr 172 AMPK in nontumor and tumor tissue from control and AMPK CA livers. Scale bars, 100 μm. ( G ) Quantification of the staining intensity. n = 6 to 11. Fisher LSD test. ( H ) Western blot analysis of nontumor (NT) and tumor (T) tissue. VINCULIN as loading control. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

    Techniques Used: Imaging, Immunohistochemical staining, BrdU Incorporation Assay, Control, Gene Expression, Staining, Western Blot

    Related Articles

    Western Blot:

    Article Title: Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity
    Article Snippet: Phospho-ACC (Ser 79 ) Rabbit mAb , Cell Signaling Technology , 11818.

    Control:

    Article Title: Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity
    Article Snippet: Phospho-ACC (Ser 79 ) Rabbit mAb , Cell Signaling Technology , 11818.

    Immunohistochemical staining:

    Article Title: Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity
    Article Snippet: Phospho-ACC (Ser 79 ) Rabbit mAb , Cell Signaling Technology , 11818.

    Staining:

    Article Title: Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity
    Article Snippet: Phospho-ACC (Ser 79 ) Rabbit mAb , Cell Signaling Technology , 11818.

    Injection:

    Article Title: Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity
    Article Snippet: Phospho-ACC (Ser 79 ) Rabbit mAb , Cell Signaling Technology , 11818.

    Imaging:

    Article Title: Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity
    Article Snippet: Phospho-ACC (Ser 79 ) Rabbit mAb , Cell Signaling Technology , 11818.

    BrdU Incorporation Assay:

    Article Title: Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity
    Article Snippet: Phospho-ACC (Ser 79 ) Rabbit mAb , Cell Signaling Technology , 11818.

    Gene Expression:

    Article Title: Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity
    Article Snippet: Phospho-ACC (Ser 79 ) Rabbit mAb , Cell Signaling Technology , 11818.



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    ( A ) Western blot analysis of female mouse livers fed HFD containing doxycycline (Doxy) to express constitutive active AMPK [a1(1-312); AMPK CA ] for 7 days compared to control livers. ( B ) Immunohistochemical analysis of livers from male control and AMPK CA mice fed HFD+Doxy for 7 months. Scale bars, 100 μm. Right: Quantification of the staining intensity for P-Thr 172 AMPK and P-Ser 79 ACC staining. n = 6 to 10. ±SEM, Welch t test. ( C ) Representative whole-mount (top) and MRI (bottom) image of male control and AMPK CA livers 9 months post–DEN injection. Yellow dashed lines indicate tumors. ( D ) Quantification of the tumor number in male control and AMPK CA livers 6 and 9 months post–DEN injection based on MRI images. 6 months: N = 5 to 7; 9 months: N = 16 to 17; Fisher least significant difference (LSD) test. ( E ) Quantification of the serum AFP levels in control and AMPK CA male mice 6 and 9 months post–DEN injection. n = 9 to 15. Fisher LSD test. * P < 0.05; *** P < 0.001; **** P < 0.0001.
    Phospho Acc Ser 79 Rabbit Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    AMPK expression and the development of atrial fibrillation in AMPK double-KO sarcolipin-Cre Prkaa1 fl/fl Prkaa2 fl/fl (AMPK-dKO) compared with littermate control Prkaa1 fl/fl Prkaa2 fl/fl (CON) mice. ( A ) Representative immunoblots with antibodies recognizing the AMPK α2 subunit, both α1 and α2 AMPK subunits (AMPKα), the downstream AMPK target acetyl-CoA carboxylase (ACC), and the phosphorylated form of ACC <t>(pACC)</t> in the left atria (LA), right atria (RA), and left ventricle. ( B ) Corresponding densitometric quantification of the immunoreactive bands. Values are mean ± SEM of n = 6–8 per group. ** P < 0.01, *** P < 0.001 versus CON by unpaired Student’s t test. ( C ) Representative in vivo ECG (lead II) tracings showing normal sinus rhythm in a CON and atrial fibrillation in an atrial AMPK-dKO mouse at 6 weeks of age. Insets show magnified views that demonstrate highly organized atrial P-wave electrical activity in CON and course fibrillatory waves in AMPK-dKO mice. Scale bars: 100 ms. ( D ) Kaplan-Meier analysis showing the 6-month event-free survival from atrial fibrillation in CON ( n = 18) versus AMPK-dKO mice ( n = 23), P < 0.001. ( E ) Graphs show heart rate variability in representative examples of CON mice in sinus rhythm and AMPK-dKO mice in atrial fibrillation, comparing sequential R-R intervals during 60-second recordings ( n = 533 intervals for CON and n = 454 intervals for AMPK-dKO mice).
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    AMPK expression and the development of atrial fibrillation in AMPK double-KO sarcolipin-Cre Prkaa1 fl/fl Prkaa2 fl/fl (AMPK-dKO) compared with littermate control Prkaa1 fl/fl Prkaa2 fl/fl (CON) mice. ( A ) Representative immunoblots with antibodies recognizing the AMPK α2 subunit, both α1 and α2 AMPK subunits (AMPKα), the downstream AMPK target acetyl-CoA carboxylase (ACC), and the phosphorylated form of ACC <t>(pACC)</t> in the left atria (LA), right atria (RA), and left ventricle. ( B ) Corresponding densitometric quantification of the immunoreactive bands. Values are mean ± SEM of n = 6–8 per group. ** P < 0.01, *** P < 0.001 versus CON by unpaired Student’s t test. ( C ) Representative in vivo ECG (lead II) tracings showing normal sinus rhythm in a CON and atrial fibrillation in an atrial AMPK-dKO mouse at 6 weeks of age. Insets show magnified views that demonstrate highly organized atrial P-wave electrical activity in CON and course fibrillatory waves in AMPK-dKO mice. Scale bars: 100 ms. ( D ) Kaplan-Meier analysis showing the 6-month event-free survival from atrial fibrillation in CON ( n = 18) versus AMPK-dKO mice ( n = 23), P < 0.001. ( E ) Graphs show heart rate variability in representative examples of CON mice in sinus rhythm and AMPK-dKO mice in atrial fibrillation, comparing sequential R-R intervals during 60-second recordings ( n = 533 intervals for CON and n = 454 intervals for AMPK-dKO mice).
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    AMPK expression and the development of atrial fibrillation in AMPK double-KO sarcolipin-Cre Prkaa1 fl/fl Prkaa2 fl/fl (AMPK-dKO) compared with littermate control Prkaa1 fl/fl Prkaa2 fl/fl (CON) mice. ( A ) Representative immunoblots with antibodies recognizing the AMPK α2 subunit, both α1 and α2 AMPK subunits (AMPKα), the downstream AMPK target acetyl-CoA carboxylase (ACC), and the phosphorylated form of ACC <t>(pACC)</t> in the left atria (LA), right atria (RA), and left ventricle. ( B ) Corresponding densitometric quantification of the immunoreactive bands. Values are mean ± SEM of n = 6–8 per group. ** P < 0.01, *** P < 0.001 versus CON by unpaired Student’s t test. ( C ) Representative in vivo ECG (lead II) tracings showing normal sinus rhythm in a CON and atrial fibrillation in an atrial AMPK-dKO mouse at 6 weeks of age. Insets show magnified views that demonstrate highly organized atrial P-wave electrical activity in CON and course fibrillatory waves in AMPK-dKO mice. Scale bars: 100 ms. ( D ) Kaplan-Meier analysis showing the 6-month event-free survival from atrial fibrillation in CON ( n = 18) versus AMPK-dKO mice ( n = 23), P < 0.001. ( E ) Graphs show heart rate variability in representative examples of CON mice in sinus rhythm and AMPK-dKO mice in atrial fibrillation, comparing sequential R-R intervals during 60-second recordings ( n = 533 intervals for CON and n = 454 intervals for AMPK-dKO mice).
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    AMPK expression and the development of atrial fibrillation in AMPK double-KO sarcolipin-Cre Prkaa1 fl/fl Prkaa2 fl/fl (AMPK-dKO) compared with littermate control Prkaa1 fl/fl Prkaa2 fl/fl (CON) mice. ( A ) Representative immunoblots with antibodies recognizing the AMPK α2 subunit, both α1 and α2 AMPK subunits (AMPKα), the downstream AMPK target acetyl-CoA carboxylase (ACC), and the phosphorylated form of ACC <t>(pACC)</t> in the left atria (LA), right atria (RA), and left ventricle. ( B ) Corresponding densitometric quantification of the immunoreactive bands. Values are mean ± SEM of n = 6–8 per group. ** P < 0.01, *** P < 0.001 versus CON by unpaired Student’s t test. ( C ) Representative in vivo ECG (lead II) tracings showing normal sinus rhythm in a CON and atrial fibrillation in an atrial AMPK-dKO mouse at 6 weeks of age. Insets show magnified views that demonstrate highly organized atrial P-wave electrical activity in CON and course fibrillatory waves in AMPK-dKO mice. Scale bars: 100 ms. ( D ) Kaplan-Meier analysis showing the 6-month event-free survival from atrial fibrillation in CON ( n = 18) versus AMPK-dKO mice ( n = 23), P < 0.001. ( E ) Graphs show heart rate variability in representative examples of CON mice in sinus rhythm and AMPK-dKO mice in atrial fibrillation, comparing sequential R-R intervals during 60-second recordings ( n = 533 intervals for CON and n = 454 intervals for AMPK-dKO mice).
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    AMPK expression and the development of atrial fibrillation in AMPK double-KO sarcolipin-Cre Prkaa1 fl/fl Prkaa2 fl/fl (AMPK-dKO) compared with littermate control Prkaa1 fl/fl Prkaa2 fl/fl (CON) mice. ( A ) Representative immunoblots with antibodies recognizing the AMPK α2 subunit, both α1 and α2 AMPK subunits (AMPKα), the downstream AMPK target acetyl-CoA carboxylase (ACC), and the phosphorylated form of ACC <t>(pACC)</t> in the left atria (LA), right atria (RA), and left ventricle. ( B ) Corresponding densitometric quantification of the immunoreactive bands. Values are mean ± SEM of n = 6–8 per group. ** P < 0.01, *** P < 0.001 versus CON by unpaired Student’s t test. ( C ) Representative in vivo ECG (lead II) tracings showing normal sinus rhythm in a CON and atrial fibrillation in an atrial AMPK-dKO mouse at 6 weeks of age. Insets show magnified views that demonstrate highly organized atrial P-wave electrical activity in CON and course fibrillatory waves in AMPK-dKO mice. Scale bars: 100 ms. ( D ) Kaplan-Meier analysis showing the 6-month event-free survival from atrial fibrillation in CON ( n = 18) versus AMPK-dKO mice ( n = 23), P < 0.001. ( E ) Graphs show heart rate variability in representative examples of CON mice in sinus rhythm and AMPK-dKO mice in atrial fibrillation, comparing sequential R-R intervals during 60-second recordings ( n = 533 intervals for CON and n = 454 intervals for AMPK-dKO mice).
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    Image Search Results


    ( A ) Western blot analysis of female mouse livers fed HFD containing doxycycline (Doxy) to express constitutive active AMPK [a1(1-312); AMPK CA ] for 7 days compared to control livers. ( B ) Immunohistochemical analysis of livers from male control and AMPK CA mice fed HFD+Doxy for 7 months. Scale bars, 100 μm. Right: Quantification of the staining intensity for P-Thr 172 AMPK and P-Ser 79 ACC staining. n = 6 to 10. ±SEM, Welch t test. ( C ) Representative whole-mount (top) and MRI (bottom) image of male control and AMPK CA livers 9 months post–DEN injection. Yellow dashed lines indicate tumors. ( D ) Quantification of the tumor number in male control and AMPK CA livers 6 and 9 months post–DEN injection based on MRI images. 6 months: N = 5 to 7; 9 months: N = 16 to 17; Fisher least significant difference (LSD) test. ( E ) Quantification of the serum AFP levels in control and AMPK CA male mice 6 and 9 months post–DEN injection. n = 9 to 15. Fisher LSD test. * P < 0.05; *** P < 0.001; **** P < 0.0001.

    Journal: Science Advances

    Article Title: Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity

    doi: 10.1126/sciadv.aea8017

    Figure Lengend Snippet: ( A ) Western blot analysis of female mouse livers fed HFD containing doxycycline (Doxy) to express constitutive active AMPK [a1(1-312); AMPK CA ] for 7 days compared to control livers. ( B ) Immunohistochemical analysis of livers from male control and AMPK CA mice fed HFD+Doxy for 7 months. Scale bars, 100 μm. Right: Quantification of the staining intensity for P-Thr 172 AMPK and P-Ser 79 ACC staining. n = 6 to 10. ±SEM, Welch t test. ( C ) Representative whole-mount (top) and MRI (bottom) image of male control and AMPK CA livers 9 months post–DEN injection. Yellow dashed lines indicate tumors. ( D ) Quantification of the tumor number in male control and AMPK CA livers 6 and 9 months post–DEN injection based on MRI images. 6 months: N = 5 to 7; 9 months: N = 16 to 17; Fisher least significant difference (LSD) test. ( E ) Quantification of the serum AFP levels in control and AMPK CA male mice 6 and 9 months post–DEN injection. n = 9 to 15. Fisher LSD test. * P < 0.05; *** P < 0.001; **** P < 0.0001.

    Article Snippet: Phospho-ACC (Ser 79 ) Rabbit mAb , Cell Signaling Technology , 11818.

    Techniques: Western Blot, Control, Immunohistochemical staining, Staining, Injection

    ( A ) Quantification of the tumor size from MRI imaging at 6 and 9 months. n = 10 to 448. Log normal Welch t test. ( B ) Immunohistochemical analysis of BrdU incorporation in tumor tissue from control and AMPK CA livers following a 4-hour BrdU pulse (10 mg/kg). Scale bars, 100 μm. Right: Quantification of the number of positive cells per area. n = 13 to 17. Welch t test. ( C ) Gene expression of Ampka1 normalized to Actin in nontumor and tumor tissue. n = 5 to 6. ±SEM, Fisher LSD test. ( D ) Immunohistochemical analysis of P-Ser 79 ACC in nontumor and tumor tissue from control and AMPK CA livers. Scale bars, 100 μm. ( E ) Quantification of the staining intensity of P-Ser 79 ACC. n = 5 to 14. Fisher LSD test. ( F ) Immunohistochemical analysis of P-Thr 172 AMPK in nontumor and tumor tissue from control and AMPK CA livers. Scale bars, 100 μm. ( G ) Quantification of the staining intensity. n = 6 to 11. Fisher LSD test. ( H ) Western blot analysis of nontumor (NT) and tumor (T) tissue. VINCULIN as loading control. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

    Journal: Science Advances

    Article Title: Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity

    doi: 10.1126/sciadv.aea8017

    Figure Lengend Snippet: ( A ) Quantification of the tumor size from MRI imaging at 6 and 9 months. n = 10 to 448. Log normal Welch t test. ( B ) Immunohistochemical analysis of BrdU incorporation in tumor tissue from control and AMPK CA livers following a 4-hour BrdU pulse (10 mg/kg). Scale bars, 100 μm. Right: Quantification of the number of positive cells per area. n = 13 to 17. Welch t test. ( C ) Gene expression of Ampka1 normalized to Actin in nontumor and tumor tissue. n = 5 to 6. ±SEM, Fisher LSD test. ( D ) Immunohistochemical analysis of P-Ser 79 ACC in nontumor and tumor tissue from control and AMPK CA livers. Scale bars, 100 μm. ( E ) Quantification of the staining intensity of P-Ser 79 ACC. n = 5 to 14. Fisher LSD test. ( F ) Immunohistochemical analysis of P-Thr 172 AMPK in nontumor and tumor tissue from control and AMPK CA livers. Scale bars, 100 μm. ( G ) Quantification of the staining intensity. n = 6 to 11. Fisher LSD test. ( H ) Western blot analysis of nontumor (NT) and tumor (T) tissue. VINCULIN as loading control. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

    Article Snippet: Phospho-ACC (Ser 79 ) Rabbit mAb , Cell Signaling Technology , 11818.

    Techniques: Imaging, Immunohistochemical staining, BrdU Incorporation Assay, Control, Gene Expression, Staining, Western Blot

    AMPK expression and the development of atrial fibrillation in AMPK double-KO sarcolipin-Cre Prkaa1 fl/fl Prkaa2 fl/fl (AMPK-dKO) compared with littermate control Prkaa1 fl/fl Prkaa2 fl/fl (CON) mice. ( A ) Representative immunoblots with antibodies recognizing the AMPK α2 subunit, both α1 and α2 AMPK subunits (AMPKα), the downstream AMPK target acetyl-CoA carboxylase (ACC), and the phosphorylated form of ACC (pACC) in the left atria (LA), right atria (RA), and left ventricle. ( B ) Corresponding densitometric quantification of the immunoreactive bands. Values are mean ± SEM of n = 6–8 per group. ** P < 0.01, *** P < 0.001 versus CON by unpaired Student’s t test. ( C ) Representative in vivo ECG (lead II) tracings showing normal sinus rhythm in a CON and atrial fibrillation in an atrial AMPK-dKO mouse at 6 weeks of age. Insets show magnified views that demonstrate highly organized atrial P-wave electrical activity in CON and course fibrillatory waves in AMPK-dKO mice. Scale bars: 100 ms. ( D ) Kaplan-Meier analysis showing the 6-month event-free survival from atrial fibrillation in CON ( n = 18) versus AMPK-dKO mice ( n = 23), P < 0.001. ( E ) Graphs show heart rate variability in representative examples of CON mice in sinus rhythm and AMPK-dKO mice in atrial fibrillation, comparing sequential R-R intervals during 60-second recordings ( n = 533 intervals for CON and n = 454 intervals for AMPK-dKO mice).

    Journal: JCI Insight

    Article Title: Atrial AMP-activated protein kinase is critical for prevention of dysregulation of electrical excitability and atrial fibrillation

    doi: 10.1172/jci.insight.141213

    Figure Lengend Snippet: AMPK expression and the development of atrial fibrillation in AMPK double-KO sarcolipin-Cre Prkaa1 fl/fl Prkaa2 fl/fl (AMPK-dKO) compared with littermate control Prkaa1 fl/fl Prkaa2 fl/fl (CON) mice. ( A ) Representative immunoblots with antibodies recognizing the AMPK α2 subunit, both α1 and α2 AMPK subunits (AMPKα), the downstream AMPK target acetyl-CoA carboxylase (ACC), and the phosphorylated form of ACC (pACC) in the left atria (LA), right atria (RA), and left ventricle. ( B ) Corresponding densitometric quantification of the immunoreactive bands. Values are mean ± SEM of n = 6–8 per group. ** P < 0.01, *** P < 0.001 versus CON by unpaired Student’s t test. ( C ) Representative in vivo ECG (lead II) tracings showing normal sinus rhythm in a CON and atrial fibrillation in an atrial AMPK-dKO mouse at 6 weeks of age. Insets show magnified views that demonstrate highly organized atrial P-wave electrical activity in CON and course fibrillatory waves in AMPK-dKO mice. Scale bars: 100 ms. ( D ) Kaplan-Meier analysis showing the 6-month event-free survival from atrial fibrillation in CON ( n = 18) versus AMPK-dKO mice ( n = 23), P < 0.001. ( E ) Graphs show heart rate variability in representative examples of CON mice in sinus rhythm and AMPK-dKO mice in atrial fibrillation, comparing sequential R-R intervals during 60-second recordings ( n = 533 intervals for CON and n = 454 intervals for AMPK-dKO mice).

    Article Snippet: The following antibodies were used: AMPKα (D5A2), AMPKα2 (catalog 2757), phospho-AMPKα Thr 172 (D4D6D), ACC (C83B10), phospho-ACC Ser 79 (D7D11), connexin-43 (E7N2R), Nav1.5 (D9J7S), GAPDH (14C10) (all from Cell Signaling Technology), and Kir2.1 (N112B/1) (Abcam).

    Techniques: Expressing, Control, Western Blot, In Vivo, Activity Assay