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COVID-19 and Toll-Like Receptor 4 (TLR4): SARS-CoV-2 May Bind and Activate TLR4 to Increase ACE2 Expression, Facilitating Entry and Causing Hyperinflammation

Mediators of inflammation, 2021, Vol.2021, p.8874339-18

2021

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Signalling mechanisms in the cardiovascular protective effects of estrogen: With a focus on rapid/membrane signalling

Current research in physiology, 2021-01, Vol.4, p.103-118

2021

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p42/p44-MAPK and PI3K are sufficient for IL-6 family cytokines/gp130 to signal to hypertrophy and survival in cardiomyocytes in the absence of JAK/STAT activation

Cellular signalling, 2013-04, Vol.25 (4), p.898-909

2013

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TRPA1 is essential for the vascular response to environmental cold exposure

Nature communications, 2014-12, Vol.5 (1), p.5732, Article 5732

2014

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Protein Kinase Cε-Calcineurin Cosignaling Downstream of Toll-Like Receptor 4 Downregulates Fibrosis and Induces Wound Healing Gene Expression in Cardiac Myofibroblasts

Molecular and Cellular Biology, 2014-02, Vol.34 (4), p.574-594

2014

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Superoxide generation and leukocyte accumulation: key elements in the mediation of leukotriene B4‐induced itch by transient receptor potential ankyrin 1 and transient receptor potential vanilloid 1

The FASEB journal, 2013-04, Vol.27 (4), p.1664-1673

2013

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The POU4F2/Brn-3b transcription factor is required for the hypertrophic response to angiotensin II in the heart

Cell death & disease, 2019-08, Vol.10 (8), p.621-18, Article 621

2019

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Protein sulfenation as a redox sensor: proteomics studies using a novel biotinylated dimedone analogue

Molecular & cellular proteomics, 2007-09, Vol.6 (9), p.1473-1484

2007

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Expression and regulation of type 2A protein phosphatases and alpha4 signalling in cardiac health and hypertrophy

Basic research in cardiology, 2017-07, Vol.112 (4), p.37-37, Article 37

2017

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Essential but partially redundant roles for POU4F1/Brn-3a and POU4F2/Brn-3b transcription factors in the developing heart

Cell death & disease, 2017-06, Vol.8 (6), p.e2861-e2861

2017

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Proliferation-associated POU4F2/Brn-3b transcription factor expression is regulated by oestrogen through ERα and growth factors via MAPK pathway

Breast cancer research : BCR, 2011-01, Vol.13 (1), p.R5-R5, Article R5

2011

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The role of differential activation of p38‐mitogen‐activated protein kinase in preconditioned ventricular myocytes

The FASEB journal, 2000-11, Vol.14 (14), p.2237-2246

2000

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MAPKAPK-2 Modulates p38-MAPK Localization and Small Heat Shock Protein Phosphorylation but Does Not Mediate the Injury Associated with p38-MAPK Activation during Myocardial Ischemia

Cell stress & chaperones, 2009-09, Vol.14 (5), p.477-489

2009

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TRPA1 activation leads to neurogenic vasodilatation: involvement of reactive oxygen nitrogen species in addition to CGRP and NO

British journal of pharmacology, 2016-08, Vol.173 (15), p.2419-2433

2016

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Cardiac Expression of Brn-3a and Brn-3b POU Transcription Factors and Regulation of Hsp27 Gene Expression

Cell stress & chaperones, 2008-09, Vol.13 (3), p.297-312

2008

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Activation of Akt during Simulated Ischemia/Reperfusion in Cardiac Myocytes

Biochemical and biophysical research communications, 2000-04, Vol.270 (3), p.947-952

2000

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Sustained activation of p42/p44 mitogen-activated protein kinase during recovery from simulated ischaemia mediates adaptive cytoprotection in cardiomyocytes

Biochemical journal, 2000-09, Vol.350 Pt 3 (3), p.891-899

2000

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Superoxide generation and leukocyte accumulation: key elements in the mediation of leukotriene B 4 ‐induced itch by transient receptor potential ankyrin 1 and transient receptor potential vanilloid 1

The FASEB journal, 2013-04, Vol.27 (4), p.1664-1673

2013

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Loss of Protein Kinase Novel 1 (PKN1) is associated with mild systolic and diastolic contractile dysfunction, increased phospholamban Thr17 phosphorylation, and exacerbated ischaemia-reperfusion injury

Cardiovascular research, 2018-01, Vol.114 (1), p.138-157

2018

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Targeting p38-MAPK in the ischaemic heart: kill or cure?

Current opinion in pharmacology, 2008-04, Vol.8 (2), p.141-146

2008

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PKC-dependent delayed metabolic preconditioning is independent of transient MAPK activation

American journal of physiology. Heart and circulatory physiology, 2000-08, Vol.279 (2), p.H492-H501

2000

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Protein Sulfenation as a Redox Sensor

Molecular & cellular proteomics, 2007-09, Vol.6 (9), p.1473-1484

2007

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Hsp-27 induction requires POU4F2/Brn-3b TF in doxorubicin-treated breast cancer cells, whereas phosphorylation alters its cellular localisation following drug treatment

Cell stress & chaperones, 2011-07, Vol.16 (4), p.427-439

2011

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Mechanisms of MAPK kinase-independent p38-MAPK activation

Journal of molecular and cellular cardiology, 2008, Vol.44 (4), p.770-771

2008

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MR-less surface-based amyloid assessment based on 11C PiB PET

PloS one, 2014, Vol.9 (1), p.e84777-e84777

2014

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COVID-19 and Toll-Like Receptor 4 (TLR4): SARS-CoV-2 May Bind and Activate TLR4 to Increase ACE2 Expression, Facilitating Entry and Causing Hyperinflammation

Signalling mechanisms in the cardiovascular protective effects of estrogen: With a focus on rapid/membrane signalling

p42/p44-MAPK and PI3K are sufficient for IL-6 family cytokines/gp130 to signal to hypertrophy and survival in cardiomyocytes in the absence of JAK/STAT activation

TRPA1 is essential for the vascular response to environmental cold exposure

Protein Kinase Cε-Calcineurin Cosignaling Downstream of Toll-Like Receptor 4 Downregulates Fibrosis and Induces Wound Healing Gene Expression in Cardiac Myofibroblasts

Superoxide generation and leukocyte accumulation: key elements in the mediation of leukotriene B4‐induced itch by transient receptor potential ankyrin 1 and transient receptor potential vanilloid 1

The POU4F2/Brn-3b transcription factor is required for the hypertrophic response to angiotensin II in the heart

Protein sulfenation as a redox sensor: proteomics studies using a novel biotinylated dimedone analogue

Expression and regulation of type 2A protein phosphatases and alpha4 signalling in cardiac health and hypertrophy

Essential but partially redundant roles for POU4F1/Brn-3a and POU4F2/Brn-3b transcription factors in the developing heart

Proliferation-associated POU4F2/Brn-3b transcription factor expression is regulated by oestrogen through ERα and growth factors via MAPK pathway

The role of differential activation of p38‐mitogen‐activated protein kinase in preconditioned ventricular myocytes

MAPKAPK-2 Modulates p38-MAPK Localization and Small Heat Shock Protein Phosphorylation but Does Not Mediate the Injury Associated with p38-MAPK Activation during Myocardial Ischemia

TRPA1 activation leads to neurogenic vasodilatation: involvement of reactive oxygen nitrogen species in addition to CGRP and NO

Cardiac Expression of Brn-3a and Brn-3b POU Transcription Factors and Regulation of Hsp27 Gene Expression

Activation of Akt during Simulated Ischemia/Reperfusion in Cardiac Myocytes

Sustained activation of p42/p44 mitogen-activated protein kinase during recovery from simulated ischaemia mediates adaptive cytoprotection in cardiomyocytes

Superoxide generation and leukocyte accumulation: key elements in the mediation of leukotriene B 4 ‐induced itch by transient receptor potential ankyrin 1 and transient receptor potential vanilloid 1

Loss of Protein Kinase Novel 1 (PKN1) is associated with mild systolic and diastolic contractile dysfunction, increased phospholamban Thr17 phosphorylation, and exacerbated ischaemia-reperfusion injury

Targeting p38-MAPK in the ischaemic heart: kill or cure?

PKC-dependent delayed metabolic preconditioning is independent of transient MAPK activation

Protein Sulfenation as a Redox Sensor

Hsp-27 induction requires POU4F2/Brn-3b TF in doxorubicin-treated breast cancer cells, whereas phosphorylation alters its cellular localisation following drug treatment

Mechanisms of MAPK kinase-independent p38-MAPK activation

MR-less surface-based amyloid assessment based on 11C PiB PET

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