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Oxidized phospholipids in Doxorubicin-induced cardiotoxicity

Chemico-biological interactions, 2019-04, Vol.303, p.35-39

2019

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The Breast Tumor Microenvironment: A Key Player in Metastatic Spread

Cancers, 2021-09, Vol.13 (19), p.4798

2021

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Connexin43 phosphorylation and cytoprotection in the heart

Biochimica et biophysica acta, 2012-08, Vol.1818 (8), p.2009-2013

2012

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Navigating the Blood-Brain Barrier: Challenges and Therapeutic Strategies in Breast Cancer Brain Metastases

International journal of molecular sciences, 2023-07, Vol.24 (15), p.12034

2023

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High molecular weight fibroblast growth factor-2 in the human heart is a potential target for prevention of cardiac remodeling

PloS one, 2014-05, Vol.9 (5), p.e97281-e97281

2014

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Elimination or neutralization of endogenous high-molecular-weight FGF2 mitigates doxorubicin-induced cardiotoxicity

American journal of physiology. Heart and circulatory physiology, 2019-02, Vol.316 (2), p.H279-H288

2019

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Phosphorylation of connexin-43 at serine 262 promotes a cardiac injury-resistant state

Cardiovascular research, 2009-09, Vol.83 (4), p.672-681

2009

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The role of connexins in controlling cell growth and gene expression

Progress in biophysics and molecular biology, 2007-05, Vol.94 (1), p.245-264

2007

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Calreticulin induces dilated cardiomyopathy

PloS one, 2013-02, Vol.8 (2), p.e56387-e56387

2013

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A Cardiac Mitochondrial FGFR1 Mediates the Antithetical Effects of FGF2 Isoforms on Permeability Transition

Cells (Basel, Switzerland), 2021-10, Vol.10 (10), p.2735

2021

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Preferential accumulation and export of high molecular weight FGF-2 by rat cardiac non-myocytes

Cardiovascular research, 2011-01, Vol.89 (1), p.139-147

2011

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Phosphorylation of serine 262 in the gap junction protein connexin-43 regulates DNA synthesis in cell-cell contact forming cardiomyocytes

Journal of cell science, 2004-01, Vol.117 (Pt 3), p.507-514

2004

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The FGF-2-triggered protection of cardiac subsarcolemmal mitochondria from calcium overload is mitochondrial connexin 43-dependent

Cardiovascular research, 2014-07, Vol.103 (1), p.72-80

2014

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Comparison of Fixation Methods for the Detection of Claudin 1 and E-Cadherin in Breast Cancer Cell Lines by Immunofluorescence

The journal of histochemistry and cytochemistry, 2022-02, Vol.70 (2), p.181-187

2022

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Non-mitogenic FGF2 protects cardiomyocytes from acute doxorubicin-induced toxicity independently of the protein kinase CK2/heme oxygenase-1 pathway

Cell and tissue research, 2018-12, Vol.374 (3), p.607-617

2018

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Elimination of endogenous high molecular weight FGF2 prevents pressure-overload-induced systolic dysfunction, linked to increased FGFR1 activity and NR1D1 expression

Cell and tissue research, 2021-09, Vol.385 (3), p.753-768

2021

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Fibroblast growth factor-2-mediated protection of cardiomyocytes from the toxic effects of doxorubicin requires the mTOR/Nrf-2/HO-1 pathway

Oncotarget, 2017-10, Vol.8 (50), p.87415-87430

2017

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Fibroblast growth factor-2 stimulates mitochondrial resistance to injury and phosphorylation of mitochondrial Connexin-43

Journal of molecular and cellular cardiology, 2008, Vol.44 (4), p.789-790

2008

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Administration of FGF-2 to the Heart Stimulates Connexin-43 Phosphorylation at Protein Kinase C Target Sites

Cell communication & adhesion, 2006, Vol.13 (1-2), p.13-19

2006

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Abstract 838: High Molecular Weight FGF2 Contributes to Pressure Overload Induced Systolic Dysfunction by a Mechanism Associated With Modulation of the NR1D1 Orphan Nuclear Receptor Expression

Circulation research, 2019-08, Vol.125 (Suppl_1)

2019

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Inhibition of TGFβ signaling potentiates the FGF-2-induced stimulation of cardiomyocyte DNA synthesis

Cardiovascular research, 2004-12, Vol.64 (3), p.516-525

2004

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Abstract 374: FGF2 Isoform-selective as well as Non-selective Signals Protect Cardiomyocytes from Doxorubicin-induced Cell Death

Circulation research, 2016-07, Vol.119 (suppl_1)

2016

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Fibroblast growth factor‐2 exerts protective effects on cardiac mitochondria

The FASEB journal, 2012-04, Vol.26 (S1)

2012

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Abstract 165: The 18 kDa FGF-2 Prevents the Doxorubicin-induced Cardiac Damage and Amp-activated Kinase Activation, in vitro and in vivo

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

2015

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Ubiquitinated histone H2B is preferentially located in transcriptionally active chromatin

Biochemistry (Easton), 1989-02, Vol.28 (3), p.958-963

1989

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Oxidized phospholipids in Doxorubicin-induced cardiotoxicity

The Breast Tumor Microenvironment: A Key Player in Metastatic Spread

Connexin43 phosphorylation and cytoprotection in the heart

Navigating the Blood-Brain Barrier: Challenges and Therapeutic Strategies in Breast Cancer Brain Metastases

High molecular weight fibroblast growth factor-2 in the human heart is a potential target for prevention of cardiac remodeling

Elimination or neutralization of endogenous high-molecular-weight FGF2 mitigates doxorubicin-induced cardiotoxicity

Phosphorylation of connexin-43 at serine 262 promotes a cardiac injury-resistant state

The role of connexins in controlling cell growth and gene expression

Calreticulin induces dilated cardiomyopathy

A Cardiac Mitochondrial FGFR1 Mediates the Antithetical Effects of FGF2 Isoforms on Permeability Transition

Preferential accumulation and export of high molecular weight FGF-2 by rat cardiac non-myocytes

Phosphorylation of serine 262 in the gap junction protein connexin-43 regulates DNA synthesis in cell-cell contact forming cardiomyocytes

The FGF-2-triggered protection of cardiac subsarcolemmal mitochondria from calcium overload is mitochondrial connexin 43-dependent

Comparison of Fixation Methods for the Detection of Claudin 1 and E-Cadherin in Breast Cancer Cell Lines by Immunofluorescence

Non-mitogenic FGF2 protects cardiomyocytes from acute doxorubicin-induced toxicity independently of the protein kinase CK2/heme oxygenase-1 pathway

Elimination of endogenous high molecular weight FGF2 prevents pressure-overload-induced systolic dysfunction, linked to increased FGFR1 activity and NR1D1 expression

Fibroblast growth factor-2-mediated protection of cardiomyocytes from the toxic effects of doxorubicin requires the mTOR/Nrf-2/HO-1 pathway

Fibroblast growth factor-2 stimulates mitochondrial resistance to injury and phosphorylation of mitochondrial Connexin-43

Administration of FGF-2 to the Heart Stimulates Connexin-43 Phosphorylation at Protein Kinase C Target Sites

Abstract 838: High Molecular Weight FGF2 Contributes to Pressure Overload Induced Systolic Dysfunction by a Mechanism Associated With Modulation of the NR1D1 Orphan Nuclear Receptor Expression

Inhibition of TGFβ signaling potentiates the FGF-2-induced stimulation of cardiomyocyte DNA synthesis

Abstract 374: FGF2 Isoform-selective as well as Non-selective Signals Protect Cardiomyocytes from Doxorubicin-induced Cell Death

Fibroblast growth factor‐2 exerts protective effects on cardiac mitochondria

Abstract 165: The 18 kDa FGF-2 Prevents the Doxorubicin-induced Cardiac Damage and Amp-activated Kinase Activation, in vitro and in vivo

Ubiquitinated histone H2B is preferentially located in transcriptionally active chromatin

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