Functionally redundant control of cardiac hypertrophic signaling by inositol 1,4,5-trisphosphate receptors.

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Functionally redundant control of cardiac hypertrophic signaling by inositol 1,4,5-trisphosphate receptors.

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2017 nî lūn-bûn

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Functionally redundant control ...... 1,4,5-trisphosphate receptors.

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Functionally redundant control ...... 1,4,5-trisphosphate receptors.

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Functionally redundant control ...... 1,4,5-trisphosphate receptors.

@en

Functionally redundant control ...... 1,4,5-trisphosphate receptors.

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Functionally redundant control ...... 1,4,5-trisphosphate receptors.

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Functionally redundant control ...... 1,4,5-trisphosphate receptors.

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P1476

Functionally redundant control ...... 1,4,5-trisphosphate receptors

@en

P2093

Anja Karlstaedt

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Heinrich Taegtmeyer

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Javier Amione-Guerra

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Keith A Youker

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M Iveth Garcia

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P2860

Increased InsP3Rs in the junctional sarcoplasmic reticulum augment Ca2+ transients and arrhythmias associated with cardiac hypertrophy

Epigenetic mechanisms underlying cardiac degeneration and regeneration

Local control of nuclear calcium signaling in cardiac myocytes by perinuclear microdomains of sarcolemmal insulin-like growth factor 1 receptors

Calcium oscillations increase the efficiency and specificity of gene expression

Ultrasensitive fluorescent proteins for imaging neuronal activity

Methods in cardiomyocyte isolation, culture, and gene transfer.

No contribution of IP3-R(2) to disease phenotype in models of dilated cardiomyopathy or pressure overload hypertrophy.

Calcineurin/NFAT coupling participates in pathological, but not physiological, cardiac hypertrophy.

The IP3 receptor regulates cardiac hypertrophy in response to select stimuli.

Cytochrome c binds to inositol (1,4,5) trisphosphate receptors, amplifying calcium-dependent apoptosis.

P304

95-103

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P31

scholarly article

P356

10.1016/J.YJMCC.2017.09.006

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P478

112

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P50

Darren F. Boehning

Jessica Chen

P577

2017-09-18T00:00:00Z

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P698

28923351

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P932

5793903

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