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The Human Angiotensin II Type 1 Receptor +1166 A/C Polymorphism Attenuates MicroRNA-155 Binding

The Journal of biological chemistry, 2007-08, Vol.282 (33), p.24262-24269

2007

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Chromosome 21-derived MicroRNAs Provide an Etiological Basis for Aberrant Protein Expression in Human Down Syndrome Brains

The Journal of biological chemistry, 2010-01, Vol.285 (2), p.1529-1543

2010

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miR-1 Overexpression Enhances Ca2+ Release and Promotes Cardiac Arrhythmogenesis by Targeting PP2A Regulatory Subunit B56α and Causing CaMKII-Dependent Hyperphosphorylation of RyR2

Circulation research, 2009-02, Vol.104 (4), p.514-521

2009

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Human chromosome 21-derived miRNAs are overexpressed in down syndrome brains and hearts

Biochemical and biophysical research communications, 2008-06, Vol.370 (3), p.473-477

2008

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TGF-β1 stimulates human AT1 receptor expression in lung fibroblasts by cross talk between the Smad, p38 MAPK, JNK, and PI3K signaling pathways

American journal of physiology. Lung cellular and molecular physiology, 2007-09, Vol.293 (3), p.L790-L799

2007

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The human angiotensin II type 1 receptor +1166 A/C polymorphism attenuates microRNA-155 binding

The Journal of biological chemistry, 2013-02, Vol.288 (6), p.4227-4227

2013

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Retraction notice to "Human chromosome 21-derived miRNAs are over-expressed in down syndrome brains and hearts" [Biochem. Biophys. Res. Commun. 370 (2008) 473–477]

Biochemical and biophysical research communications, 2013-07, Vol.436 (3), p.564-564

2013

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Chromosome 21-derived microRNAs provide an etiological basis for aberrant protein expression in human down syndrome brains

The Journal of biological chemistry, 2013-02, Vol.288 (6), p.4228-4228

2013

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miR-1 Overexpression Enhances Ca 2+ Release and Promotes Cardiac Arrhythmogenesis by Targeting PP2A Regulatory Subunit B56α and Causing CaMKII-Dependent Hyperphosphorylation of RyR2

Circulation research, 2009-02, Vol.104 (4), p.514-521

2009

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MiR-1 Overexpression Enhances Ca2+ Release and Promotes Cardiac Arrhythmogenesis by Targeting PP2A Regulatory Subunit B56a and Causing CaMKII-Dependent Hyperphosphorylation of RyR2

Circulation research, 2009, Vol.104 (4), p.514-521

2009

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TGF-ß1 stimulates human AT^sub 1^ receptor expression in lung fibroblasts by cross talk between the Smad, p38 MAPK, JNK, and PI3K signaling pathways

American journal of physiology. Lung cellular and molecular physiology, 2007-09, Vol.293 (3), p.L790

2007

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Abstract 5247: MiR-132 Regulates Angiotensin II Type 1 Receptor Expression Through a Protein Coding Region Binding Site

Circulation (New York, N.Y.), 2008-10, Vol.118 (suppl_18)

2008

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Abstract 5302: Control of Reversible Phosphorylation of Ryanodine Receptor by MiR-1 : Mechanism of Cardiac Arrhythmia

Circulation (New York, N.Y.), 2008-10, Vol.118 (suppl_18)

2008

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TGF-beta1 stimulates human AT1 receptor expression in lung fibroblasts by cross talk between the Smad, p38 MAPK, JNK, and PI3K signaling pathways

American journal of physiology. Lung cellular and molecular physiology, 2007-09, Vol.293 (3), p.L790-L799

2007

Volltextzugriff (PDF)

TGF-β1 stimulates human AT 1 receptor expression in lung fibroblasts by cross talk between the Smad, p38 MAPK, JNK, and PI3K signaling pathways

American journal of physiology. Lung cellular and molecular physiology, 2007-09, Vol.293 (3), p.L790-L799

2007

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RETRACTED: Human chromosome 21-derived miRNAs are overexpressed in down syndrome brains and hearts

Biochemical and biophysical research communications, 2008-06, Vol.370 (3), p.473-477

2008

Volltextzugriff (PDF)

TGF-β1 stimulates human AT1 receptor expression in lung fibroblasts by cross talk between the smad, p38 MAPK, JNK, and PI3K signaling pathways

American journal of physiology. Lung cellular and molecular physiology, 2007, Vol.37 (3)

2007

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Human Chromosome 21-derived miRNAs are Over-expressed in Down Syndrome Brains and Hearts

Biochemical and biophysical research communications, 2008-04, Vol.370 (3), p.473-477

2008

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miR-1 overexpression enhances Ca(2+) release and promotes cardiac arrhythmogenesis by targeting PP2A regulatory subunit B56alpha and causing CaMKII-dependent hyperphosphorylation of RyR2

Circulation research, 2009-02, Vol.104 (4), p.514-521

2009

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Targeted deletion of fibrinogen like protein 1 reveals a novel role in energy substrate utilization

PloS one, 2013-03, Vol.8 (3), p.e58084

2013

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Targeted Deletion of Fibrinogen Like Protein 1 Reveals a Novel Role in Energy Substrate Utilization

PloS one, 2013-03, Vol.8 (3), p.e58084

2013

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Extending Volunteered Geographic Information (VGI) with Geospatial Software as a Service: Participatory Asset Mapping Infrastructures for Urban Health

Geospatial Technologies for Urban Health, p.209-230

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The Human Angiotensin II Type 1 Receptor +1166 A/C Polymorphism Attenuates MicroRNA-155 Binding

Chromosome 21-derived MicroRNAs Provide an Etiological Basis for Aberrant Protein Expression in Human Down Syndrome Brains

miR-1 Overexpression Enhances Ca2+ Release and Promotes Cardiac Arrhythmogenesis by Targeting PP2A Regulatory Subunit B56α and Causing CaMKII-Dependent Hyperphosphorylation of RyR2

Human chromosome 21-derived miRNAs are overexpressed in down syndrome brains and hearts

TGF-β1 stimulates human AT1 receptor expression in lung fibroblasts by cross talk between the Smad, p38 MAPK, JNK, and PI3K signaling pathways

The human angiotensin II type 1 receptor +1166 A/C polymorphism attenuates microRNA-155 binding

Retraction notice to "Human chromosome 21-derived miRNAs are over-expressed in down syndrome brains and hearts" [Biochem. Biophys. Res. Commun. 370 (2008) 473–477]

Chromosome 21-derived microRNAs provide an etiological basis for aberrant protein expression in human down syndrome brains

miR-1 Overexpression Enhances Ca 2+ Release and Promotes Cardiac Arrhythmogenesis by Targeting PP2A Regulatory Subunit B56α and Causing CaMKII-Dependent Hyperphosphorylation of RyR2

MiR-1 Overexpression Enhances Ca2+ Release and Promotes Cardiac Arrhythmogenesis by Targeting PP2A Regulatory Subunit B56a and Causing CaMKII-Dependent Hyperphosphorylation of RyR2

TGF-ß1 stimulates human AT^sub 1^ receptor expression in lung fibroblasts by cross talk between the Smad, p38 MAPK, JNK, and PI3K signaling pathways

Abstract 5247: MiR-132 Regulates Angiotensin II Type 1 Receptor Expression Through a Protein Coding Region Binding Site

Abstract 5302: Control of Reversible Phosphorylation of Ryanodine Receptor by MiR-1 : Mechanism of Cardiac Arrhythmia

TGF-beta1 stimulates human AT1 receptor expression in lung fibroblasts by cross talk between the Smad, p38 MAPK, JNK, and PI3K signaling pathways

TGF-β1 stimulates human AT 1 receptor expression in lung fibroblasts by cross talk between the Smad, p38 MAPK, JNK, and PI3K signaling pathways

RETRACTED: Human chromosome 21-derived miRNAs are overexpressed in down syndrome brains and hearts

TGF-β1 stimulates human AT1 receptor expression in lung fibroblasts by cross talk between the smad, p38 MAPK, JNK, and PI3K signaling pathways

Human Chromosome 21-derived miRNAs are Over-expressed in Down Syndrome Brains and Hearts

miR-1 overexpression enhances Ca(2+) release and promotes cardiac arrhythmogenesis by targeting PP2A regulatory subunit B56alpha and causing CaMKII-dependent hyperphosphorylation of RyR2

Targeted deletion of fibrinogen like protein 1 reveals a novel role in energy substrate utilization

Targeted Deletion of Fibrinogen Like Protein 1 Reveals a Novel Role in Energy Substrate Utilization

Extending Volunteered Geographic Information (VGI) with Geospatial Software as a Service: Participatory Asset Mapping Infrastructures for Urban Health

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