Requirement of protein kinase D1 for pathological cardiac remodeling. - Test2 - elhamkhani - TriplyDB

Requirement of protein kinase D1 for pathological cardiac remodeling.

Requirement of protein kinase D1 for pathological cardiac remodeling.

http://www.wikidata.org/entity/Q36498485

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Protein kinase D in vascular biology and angiogenesis Protein kinase D regulates RhoA activity via rhotekin phosphorylation.Histone deacetylase signaling in cardioprotection Protein Kinase D1 Signaling in Angiogenic Gene Expression and VEGF-Mediated Angiogenesis PKD signaling and pancreatitis Genome-Wide Gene Expression Analysis Shows AKAP13-Mediated PKD1 Signaling Regulates the Transcriptional Response to Cardiac Hypertrophy AKAP13 Rho-GEF and PKD-binding domain deficient mice develop normally but have an abnormal response to β-adrenergic-induced cardiac hypertrophy Post-translational modifications regulate class IIa histone deacetylase (HDAC) function in health and disease Protein kinase D increases maximal Ca2+-activated tension of cardiomyocyte contraction by phosphorylation of cMyBP-C-Ser315 Distinct sarcomeric substrates are responsible for protein kinase D-mediated regulation of cardiac myofilament Ca2+ sensitivity and cross-bridge cycling Beta-catenin phosphorylated at threonine 120 antagonizes generation of active beta-catenin by spatial localization in trans-Golgi network A targeted library screen reveals a new inhibitor scaffold for protein kinase D Unique functions for protein kinase D1 and protein kinase D2 in mammalian cells Protein kinase D1 (PKD1) activation mediates a compensatory protective response during early stages of oxidative stress-induced neuronal degeneration Design, Synthesis, and Biological Evaluation of PKD Inhibitors.Regulation of PTEN activity by p38δ-PKD1 signaling in neutrophils confers inflammatory responses in the lung.Expression patterns of protein kinase D 3 during mouse development Potent and selective disruption of protein kinase D functionality by a benzoxoloazepinolone.Protein kinase D1 mediates class IIa histone deacetylase phosphorylation and nuclear extrusion in intestinal epithelial cells: role in mitogenic signaling PLCε, PKD1, and SSH1L transduce RhoA signaling to protect mitochondria from oxidative stress in the heart.Molecular Signals Elicited by GPCR Agonists in Hypertension, Cardiovascular Remodeling: Are MMPs and ADAMs Elusive Therapeutic Targets?Protein kinase D2 is an essential regulator of murine myoblast differentiation.The C-terminus of the long AKAP13 isoform (AKAP-Lbc) is critical for development of compensatory cardiac hypertrophy.Splice variants of enigma homolog, differentially expressed during heart development, promote or prevent hypertrophy.Protein kinase D as a potential new target for cancer therapy.Essential role of sympathetic endothelin A receptors for adverse cardiac remodeling Heterogeneous myocyte enhancer factor-2 (Mef2) activation in myocytes predicts focal scarring in hypertrophic cardiomyopathy.Role of protein kinase D signaling in pancreatic cancer Novel function of cardiac protein kinase D1 as a dynamic regulator of Ca2+ sensitivity of contraction Small heat shock protein 20 (Hsp20) facilitates nuclear import of protein kinase D 1 (PKD1) during cardiac hypertrophy Protein kinase Cθ is required for cardiomyocyte survival and cardiac remodeling.Protein kinase D controls voluntary-running-induced skeletal muscle remodelling Calcium-mediated histone modifications regulate alternative splicing in cardiomyocytes.The scaffold protein muscle A-kinase anchoring protein β orchestrates cardiac myocyte hypertrophic signaling required for the development of heart failure.Synthesis and Structure-Activity Relationships of Benzothienothiazepinone Inhibitors of Protein Kinase D Protein kinase D: coupling extracellular stimuli to the regulation of cell physiology G protein βγ subunits regulate cardiomyocyte hypertrophy through a perinuclear Golgi phosphatidylinositol 4-phosphate hydrolysis pathway.Therapeutic efficacy of cardiosphere-derived cells in a transgenic mouse model of non-ischaemic dilated cardiomyopathy.Protein kinase D signaling: multiple biological functions in health and disease.Spatiotemporally distinct protein kinase D activation in adult cardiomyocytes in response to phenylephrine and endothelin

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Requirement of protein kinase D1 for pathological cardiac remodeling.

http://www.wikidata.org/entity/Q36498485

description

2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年學術文章

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2008年學術文章

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2008年學術文章

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name

Requirement of protein kinase D1 for pathological cardiac remodeling.

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Requirement of protein kinase D1 for pathological cardiac remodeling.

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type

label

Requirement of protein kinase D1 for pathological cardiac remodeling.

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Requirement of protein kinase D1 for pathological cardiac remodeling.

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prefLabel

Requirement of protein kinase D1 for pathological cardiac remodeling.

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Requirement of protein kinase D1 for pathological cardiac remodeling.

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Proceedings of the National Academy of Sciences of the United States of America

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Requirement of protein kinase D1 for pathological cardiac remodeling.

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P2093

Eric N Olson

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James A Richardson

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Jens Fielitz

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John M Shelton

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Joseph A Hill

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Mi-Sung Kim

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Rhonda Bassel-Duby

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Xiaoxia Qi

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P2860

Signal-dependent nuclear export of a histone deacetylase regulates muscle differentiation

Activation of the myocyte enhancer factor-2 transcription factor by calcium/calmodulin-dependent protein kinase-stimulated binding of 14-3-3 to histone deacetylase 5

Class II histone deacetylases: versatile regulators

Targeted disruption of NFATc3, but not NFATc4, reveals an intrinsic defect in calcineurin-mediated cardiac hypertrophic growth

The transcriptional coactivator CAMTA2 stimulates cardiac growth by opposing class II histone deacetylases

PKCu is a novel, atypical member of the protein kinase C family

Protein kinases C and D mediate agonist-dependent cardiac hypertrophy through nuclear export of histone deacetylase 5

Class II histone deacetylases act as signal-responsive repressors of cardiac hypertrophy

Protein kinase D is a novel mediator of cardiac troponin I phosphorylation and regulates myofilament function

Impaired cardiac hypertrophic response in Calcineurin Abeta -deficient mice

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5565089

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18287012

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