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SIRT3 Deacetylates and Activates OPA1 To Regulate Mitochondrial Dynamics during Stress

Molecular and Cellular Biology, 2014-03, Vol.34 (5), p.807-819

2014

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The nuclear and mitochondrial sirtuins, Sirt6 and Sirt3, regulate each other's activity and protect the heart from developing obesity‐mediated diabetic cardiomyopathy

The FASEB journal, 2019-10, Vol.33 (10), p.10872-10888

2019

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SIRT3 Is a Stress-Responsive Deacetylase in Cardiomyocytes That Protects Cells from Stress-Mediated Cell Death by Deacetylation of Ku70

Molecular and Cellular Biology, 2008-10, Vol.28 (20), p.6384-6401

2008

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Honokiol blocks and reverses cardiac hypertrophy in mice by activating mitochondrial Sirt3

Nature communications, 2015-04, Vol.6 (1), p.6656-6656, Article 6656

2015

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The sirtuin SIRT6 blocks IGF-Akt signaling and development of cardiac hypertrophy by targeting c-Jun

Nature medicine, 2012-11, Vol.18 (11), p.1643-1650

2012

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Honokiol, an activator of Sirtuin-3 (SIRT3) preserves mitochondria and protects the heart from doxorubicin-induced cardiomyopathy in mice

Oncotarget, 2017-05, Vol.8 (21), p.34082-34098

2017

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Sirt3 protects mitochondrial DNA damage and blocks the development of doxorubicin-induced cardiomyopathy in mice

American journal of physiology. Heart and circulatory physiology, 2016-04, Vol.310 (8), p.H962-H972

2016

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The histone deacetylase SIRT6 blocks myostatin expression and development of muscle atrophy

Scientific reports, 2017-09, Vol.7 (1), p.11877-18, Article 11877

2017

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The deacetylase SIRT1 promotes membrane localization and activation of Akt and PDK1 during tumorigenesis and cardiac hypertrophy

Science signaling, 2011-07, Vol.4 (182), p.ra46

2011

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SIRT3 blocks myofibroblast differentiation and pulmonary fibrosis by preventing mitochondrial DNA damage

American journal of physiology. Lung cellular and molecular physiology, 2017-01, Vol.312 (1), p.L68-L78

2017

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Exogenous NAD Blocks Cardiac Hypertrophic Response via Activation of the SIRT3-LKB1-AMP-activated Kinase Pathway

The Journal of biological chemistry, 2010-01, Vol.285 (5), p.3133-3144

2010

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HDAC4 and PCAF Bind to Cardiac Sarcomeres and Play a Role in Regulating Myofilament Contractile Activity

The Journal of biological chemistry, 2008-04, Vol.283 (15), p.10135-10146

2008

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SIRT1 Promotes Cell Survival under Stress by Deacetylation-Dependent Deactivation of Poly(ADP-Ribose) Polymerase 1

Molecular and Cellular Biology, 2009-08, Vol.29 (15), p.4116-4129

2009

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Histone Deacetylase 3 (HDAC3)-dependent Reversible Lysine Acetylation of Cardiac Myosin Heavy Chain Isoforms Modulates Their Enzymatic and Motor Activity

The Journal of biological chemistry, 2015-06, Vol.290 (25), p.15559-15569

2015

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Cellular mechanisms promoting cachexia and how they are opposed by sirtuins

Canadian journal of physiology and pharmacology, 2019-04, Vol.97 (4), p.235-245

2019

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Nampt secreted from cardiomyocytes promotes development of cardiac hypertrophy and adverse ventricular remodeling

American journal of physiology. Heart and circulatory physiology, 2013-02, Vol.304 (3), p.H415-H426

2013

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Translational control of FOG-2 expression in cardiomyocytes by microRNA-130a

PloS one, 2009-07, Vol.4 (7), p.e6161-e6161

2009

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Acetylation of a Conserved Lysine Residue in the ATP Binding Pocket of p38 Augments Its Kinase Activity during Hypertrophy of Cardiomyocytes

Molecular and Cellular Biology, 2011-06, Vol.31 (11), p.2349-2363

2011

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Skeletal muscle‐specific over‐expression of the nuclear sirtuin SIRT6 blocks cancer‐associated cachexia by regulating multiple targets

JCSM rapid communications, 2021-01, Vol.4 (1), p.40-56

2021

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HDAC3-dependent Reversible Lysine Acetylation of Cardiac Myosin Heavy Chain Isoforms Modulates Their Enzymatic and Motor Activity

The Journal of biological chemistry, 2011-02, Vol.286 (7), p.5567-5577

2011

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The zinc finger and C-terminal domains of MTA proteins are required for FOG-2-mediated transcriptional repression via the NuRD complex

Journal of molecular and cellular cardiology, 2008-02, Vol.44 (2), p.352-360

2008

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Muscle‐Specific Over‐Expression of the NAD+‐Dependent Nuclear Sirtuin SIRT6, Suppresses Cancer‐Associated Cachexia

The FASEB journal, 2019-04, Vol.33 (S1), p.700.11-700.11

2019

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The protein deacetylase SIRT6 suppresses cardiomyocyte senescence by protecting mitochondria

The FASEB journal, 2019-04, Vol.33 (S1), p.693.7-693.7

2019

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The nuclear sirtuin SIRT6 plays a role in regulating cardiac branched‐chain amino acid catabolism

The FASEB journal, 2020-04, Vol.34 (S1), p.1-1

2020

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Abstract 12592: Nuclear Sirtuin Sirt6, Protects Mice From Endotoxin-Induced Septic Cardiomyopathy

Circulation (New York, N.Y.), 2022-11, Vol.146 (Suppl_1)

2022

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SIRT3 Deacetylates and Activates OPA1 To Regulate Mitochondrial Dynamics during Stress

The nuclear and mitochondrial sirtuins, Sirt6 and Sirt3, regulate each other's activity and protect the heart from developing obesity‐mediated diabetic cardiomyopathy

SIRT3 Is a Stress-Responsive Deacetylase in Cardiomyocytes That Protects Cells from Stress-Mediated Cell Death by Deacetylation of Ku70

Honokiol blocks and reverses cardiac hypertrophy in mice by activating mitochondrial Sirt3

The sirtuin SIRT6 blocks IGF-Akt signaling and development of cardiac hypertrophy by targeting c-Jun

Honokiol, an activator of Sirtuin-3 (SIRT3) preserves mitochondria and protects the heart from doxorubicin-induced cardiomyopathy in mice

Sirt3 protects mitochondrial DNA damage and blocks the development of doxorubicin-induced cardiomyopathy in mice

The histone deacetylase SIRT6 blocks myostatin expression and development of muscle atrophy

The deacetylase SIRT1 promotes membrane localization and activation of Akt and PDK1 during tumorigenesis and cardiac hypertrophy

SIRT3 blocks myofibroblast differentiation and pulmonary fibrosis by preventing mitochondrial DNA damage

Exogenous NAD Blocks Cardiac Hypertrophic Response via Activation of the SIRT3-LKB1-AMP-activated Kinase Pathway

HDAC4 and PCAF Bind to Cardiac Sarcomeres and Play a Role in Regulating Myofilament Contractile Activity

SIRT1 Promotes Cell Survival under Stress by Deacetylation-Dependent Deactivation of Poly(ADP-Ribose) Polymerase 1

Histone Deacetylase 3 (HDAC3)-dependent Reversible Lysine Acetylation of Cardiac Myosin Heavy Chain Isoforms Modulates Their Enzymatic and Motor Activity

Cellular mechanisms promoting cachexia and how they are opposed by sirtuins

Nampt secreted from cardiomyocytes promotes development of cardiac hypertrophy and adverse ventricular remodeling

Translational control of FOG-2 expression in cardiomyocytes by microRNA-130a

Acetylation of a Conserved Lysine Residue in the ATP Binding Pocket of p38 Augments Its Kinase Activity during Hypertrophy of Cardiomyocytes

Skeletal muscle‐specific over‐expression of the nuclear sirtuin SIRT6 blocks cancer‐associated cachexia by regulating multiple targets

HDAC3-dependent Reversible Lysine Acetylation of Cardiac Myosin Heavy Chain Isoforms Modulates Their Enzymatic and Motor Activity

The zinc finger and C-terminal domains of MTA proteins are required for FOG-2-mediated transcriptional repression via the NuRD complex

Muscle‐Specific Over‐Expression of the NAD+‐Dependent Nuclear Sirtuin SIRT6, Suppresses Cancer‐Associated Cachexia

The protein deacetylase SIRT6 suppresses cardiomyocyte senescence by protecting mitochondria

The nuclear sirtuin SIRT6 plays a role in regulating cardiac branched‐chain amino acid catabolism

Abstract 12592: Nuclear Sirtuin Sirt6, Protects Mice From Endotoxin-Induced Septic Cardiomyopathy

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