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Chronic Contractile Dysfunction without Hypertrophy Does Not Provoke a Compensatory Transcriptional Response in Mouse Hearts

PloS one, 2016-06, Vol.11 (6), p.e0158317-e0158317

2016

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Tissue-specific splicing of an Ndufs6 gene-trap insertion generates a mitochondrial complex I deficiency-specific cardiomyopathy

Proceedings of the National Academy of Sciences - PNAS, 2012-04, Vol.109 (16), p.6165-6170

2012

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Novel Therapeutic Targets in Heart Failure: The Phospholipase Cβ1b-Shank3 Interface

Clinical Medicine Insights: Therapeutics, 2015-05, Vol.2015 (7), p.11

2015

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Phospholipase Cβ1b directly binds the SH3 domain of Shank3 for targeting and activation in cardiomyocytes

Biochemical and biophysical research communications, 2015-06, Vol.461 (3), p.519-524

2015

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The phosphatidylinositol(4,5)bisphosphate-binding sequence of transient receptor potential channel canonical 4α is critical for its contribution to cardiomyocyte hypertrophy

Molecular pharmacology, 2014-10, Vol.86 (4), p.399-405

2014

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Gq-initiated cardiomyocyte hypertrophy is mediated by phospholipase Cβ1b

The FASEB journal, 2009-10, Vol.23 (10), p.3564-3570

2009

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Regulation of autophagy in cardiomyocytes by Ins(1,4,5)P3 and IP3 -receptors

Journal of molecular and cellular cardiology, 2013-01, Vol.54, p.19-24

2013

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Scaffolding protein Homer 1c mediates hypertrophic responses downstream of Gq in cardiomyocytes

The FASEB journal, 2012-02, Vol.26 (2), p.596-603

2012

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The atypical ‘b’ splice variant of phospholipase Cβ1 promotes cardiac contractile dysfunction

Journal of molecular and cellular cardiology, 2015-07, Vol.84, p.95-103

2015

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Expressing an inhibitor of PLCβ1b sustains contractile function following pressure overload

Journal of molecular and cellular cardiology, 2016-04, Vol.93, p.12-17

2016

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The extreme C‐terminal region of phospholipase Cβ1 determines subcellular localization and function; the “b” splice variant mediates α1‐adrenergic receptor responses in cardiomyocytes

The FASEB journal, 2008-08, Vol.22 (8), p.2768-2774

2008

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Selective activation of the “b” splice variant of phospholipase Cβ1 in chronically dilated human and mouse atria

Journal of molecular and cellular cardiology, 2009-11, Vol.47 (5), p.676-683

2009

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Ins(1,4,5)P3 regulates phospholipase Cβ1 expression in cardiomyocytes

Journal of molecular and cellular cardiology, 2008-11, Vol.45 (5), p.679-684

2008

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Mitochondrial cytochrome c release is caspase-dependent and does not involve mitochondrial permeability transition in didemnin B-induced apoptosis

Oncogene, 2001-07, Vol.20 (30), p.4085-4094

2001

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The Phosphatidylinositol(4,5) Bis phosphate–Binding Sequence of Transient Receptor Potential Channel Canonical 4 α Is Critical for Its Contribution to Cardiomyocyte Hypertrophy

Molecular pharmacology, 2014-10, Vol.86 (4), p.399-405

2014

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Abstract 337: Reversal of Pathological Responses to Pressure Overload by Inhibition of Phospholipase Cbeta1b

Circulation research, 2015-07, Vol.117 (suppl_1)

2015

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Novel Therapeutic Targets in Heart Failure: The Phospholipase Cb1b-Shank3 Interface

Clinical Medicine Insights: Therapeutics, 2015-12, Vol.2015

2015

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Abstract P225: Possible Involvement of Homer-1b/c in Gq-Mediated Hypertrophy in Cardiomyocytes

Circulation research, 2011-12, Vol.109 (suppl_1)

2011

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Abstract 33: Contractile Dysfunction In The Mouse Heart Caused By Phospholipase C beta1b Mediated Activation Of Protein Kinase Calpha

Circulation research, 2014-07, Vol.115 (suppl_1)

2014

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Novel Therapeutic Targets in Heart Failure: The Phospholipase C[beta]1b-Shank3 Interface

Clinical medicine insights. Therapeutics, 2015-01, Vol.7, p.11

2015

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The extreme C‐terminal region of phospholipase Cβ1 determines subcellular localization and function; the “b” splice variant mediates α 1 ‐adrenergic receptor responses in cardiomyocytes

The FASEB journal, 2008-08, Vol.22 (8), p.2768-2774

2008

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Phospholipase Cβlb associates with a Shank3 complex at the cardiac sarcolemma

The FASEB journal, 2011-03, Vol.25 (3), p.1040-1047

2011

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Regulation of autophagy in cardiomyocytes by Ins(1,4,5)P(3) and IP(3)-receptors

Journal of molecular and cellular cardiology, 2013-01, Vol.54, p.19-24

2013

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Ins(1,4,5)P 3 regulates phospholipase Cβ1 expression in cardiomyocytes

Journal of molecular and cellular cardiology, 2008, Vol.45 (5), p.679-684

2008

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The extreme C-terminal region of phospholipase Cbeta1 determines subcellular localization and function; the "b" splice variant mediates alpha1-adrenergic receptor responses in cardiomyocytes

The FASEB journal, 2008-08, Vol.22 (8), p.2768-2774

2008

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Chronic Contractile Dysfunction without Hypertrophy Does Not Provoke a Compensatory Transcriptional Response in Mouse Hearts

Tissue-specific splicing of an Ndufs6 gene-trap insertion generates a mitochondrial complex I deficiency-specific cardiomyopathy

Novel Therapeutic Targets in Heart Failure: The Phospholipase Cβ1b-Shank3 Interface

Phospholipase Cβ1b directly binds the SH3 domain of Shank3 for targeting and activation in cardiomyocytes

The phosphatidylinositol(4,5)bisphosphate-binding sequence of transient receptor potential channel canonical 4α is critical for its contribution to cardiomyocyte hypertrophy

Gq-initiated cardiomyocyte hypertrophy is mediated by phospholipase Cβ1b

Regulation of autophagy in cardiomyocytes by Ins(1,4,5)P3 and IP3 -receptors

Scaffolding protein Homer 1c mediates hypertrophic responses downstream of Gq in cardiomyocytes

The atypical ‘b’ splice variant of phospholipase Cβ1 promotes cardiac contractile dysfunction

Expressing an inhibitor of PLCβ1b sustains contractile function following pressure overload

The extreme C‐terminal region of phospholipase Cβ1 determines subcellular localization and function; the “b” splice variant mediates α1‐adrenergic receptor responses in cardiomyocytes

Selective activation of the “b” splice variant of phospholipase Cβ1 in chronically dilated human and mouse atria

Ins(1,4,5)P3 regulates phospholipase Cβ1 expression in cardiomyocytes

Mitochondrial cytochrome c release is caspase-dependent and does not involve mitochondrial permeability transition in didemnin B-induced apoptosis

The Phosphatidylinositol(4,5) Bis phosphate–Binding Sequence of Transient Receptor Potential Channel Canonical 4 α Is Critical for Its Contribution to Cardiomyocyte Hypertrophy

Abstract 337: Reversal of Pathological Responses to Pressure Overload by Inhibition of Phospholipase Cbeta1b

Novel Therapeutic Targets in Heart Failure: The Phospholipase Cb1b-Shank3 Interface

Abstract P225: Possible Involvement of Homer-1b/c in Gq-Mediated Hypertrophy in Cardiomyocytes

Abstract 33: Contractile Dysfunction In The Mouse Heart Caused By Phospholipase C beta1b Mediated Activation Of Protein Kinase Calpha

Novel Therapeutic Targets in Heart Failure: The Phospholipase C[beta]1b-Shank3 Interface

The extreme C‐terminal region of phospholipase Cβ1 determines subcellular localization and function; the “b” splice variant mediates α 1 ‐adrenergic receptor responses in cardiomyocytes

Phospholipase Cβlb associates with a Shank3 complex at the cardiac sarcolemma

Regulation of autophagy in cardiomyocytes by Ins(1,4,5)P(3) and IP(3)-receptors

Ins(1,4,5)P 3 regulates phospholipase Cβ1 expression in cardiomyocytes

The extreme C-terminal region of phospholipase Cbeta1 determines subcellular localization and function; the "b" splice variant mediates alpha1-adrenergic receptor responses in cardiomyocytes

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