UB Paderborn / Katalog / Suche / in CDI

Sortiert nach

Einfacher Volltextzugriff von (fast) überall

Installieren Sie die LibKey Nomad-Browsererweiterung und erhalten Sie von vielen Webseiten einfachen Zugriff auf lizenzierte Volltexte oder Open Access Publikationen. Mehr erfahren...

Inwardly rectifying K+ channels are major contributors to flow‐induced vasodilatation in resistance arteries

The Journal of physiology, 2017-04, Vol.595 (7), p.2339-2364

2017

Volltextzugriff (PDF)

Early sensitization of myofilaments to Ca2+ prevents genetically linked dilated cardiomyopathy in mice

Cardiovascular research, 2017-07, Vol.113 (8), p.915-925

2017

Volltextzugriff (PDF)

Desensitization of myofilaments to Ca2+ as a therapeutic target for hypertrophic cardiomyopathy with mutations in thin filament proteins

Circulation. Cardiovascular genetics, 2014-04, Vol.7 (2), p.132

2014

Volltextzugriff (PDF)

Rescue of familial cardiomyopathies by modifications at the level of sarcomere and Ca2+ fluxes

Journal of molecular and cellular cardiology, 2010-05, Vol.48 (5), p.834-842

2010

Volltextzugriff (PDF)

Roles of phosphorylation of myosin binding protein-C and troponin I in mouse cardiac muscle twitch dynamics

The Journal of physiology, 2004-08, Vol.558 (3), p.927-941

2004

Volltextzugriff (PDF)

Neonatal gene transfer of Serca2a delays onset of hypertrophic remodeling and improves function in familial hypertrophic cardiomyopathy

Journal of molecular and cellular cardiology, 2010-12, Vol.49 (6), p.993-1002

2010

Volltextzugriff (PDF)

Long-term rescue of a familial hypertrophic cardiomyopathy caused by a mutation in the thin filament protein, tropomyosin, via modulation of a calcium cycling protein

Journal of molecular and cellular cardiology, 2011-11, Vol.51 (5), p.812-820

2011

Volltextzugriff (PDF)

Enhancing natriuretic peptide signaling in adipose tissue, but not in muscle, protects against diet-induced obesity and insulin resistance

Science signaling, 2017-07, Vol.10 (489)

2017

Volltextzugriff (PDF)

Effects of nicotine administration in a mouse model of familial hypertrophic cardiomyopathy, α-tropomyosin D175N

American journal of physiology. Heart and circulatory physiology, 2011-10, Vol.301 (4), p.H1646-H1655

2011

Volltextzugriff (PDF)

Charged residue changes in the carboxy‐terminus of α‐tropomyosin alter mouse cardiac muscle contractility

The Journal of physiology, 2004-04, Vol.556 (2), p.531-543

2004

Volltextzugriff (PDF)

Arginine-glycine-aspartic acid (RGD)-containing peptides inhibit the force production of mouse papillary muscle bundles via alpha 5 beta 1 integrin

The Journal of physiology, 2005-04, Vol.564 (Pt 2), p.603-617

2005

Volltextzugriff (PDF)

Arginine–glycine–aspartic acid (RGD)‐containing peptides inhibit the force production of mouse papillary muscle bundles via α5β1 integrin

The Journal of physiology, 2005-04, Vol.564 (2), p.603-617

2005

Volltextzugriff (PDF)

Changes in end-to-end interactions of tropomyosin affect mouse cardiac muscle dynamics

American journal of physiology. Heart and circulatory physiology, 2006-08, Vol.291 (2), p.H552-H563

2006

Volltextzugriff (PDF)

Shear‐stress sensitive endothelial K channels play major role in flow‐induced vasodilation

The FASEB journal, 2017-04, Vol.31 (S1)

2017

Volltextzugriff (PDF)

Charged residue alterations in the inner‐core domain and carboxy‐terminus of α‐tropomyosin differentially affect mouse cardiac muscle contractility

The Journal of physiology, 2004-12, Vol.561 (3), p.777-791

2004

Volltextzugriff (PDF)

Inwardly rectifying K super(+) channels are major contributors to flow-induced vasodilatation in resistance arteries

The Journal of physiology, 2017-04, Vol.595 (7), p.2339-2364

2017

Volltextzugriff (PDF)

Rescue of a Dilated Cardiomyopathy Mouse Model Caused by a Mutation in Tropomyosin (E54K) by Expression of Slow Skeletal Troponin I

Biophysical journal, 2012-01, Vol.102 (3), p.560a-560a

2012

Volltextzugriff (PDF)

Effects of nicotine administration in a mouse model of familial hypertrophic cardiomyopathy, [alpha]-tropomyosin D175N

American journal of physiology. Heart and circulatory physiology, 2011-10, Vol.301 (4), p.H1646

2011

Volltextzugriff (PDF)

Desensitization of Myofilaments to Ca 2+ as a Therapeutic Target for Hypertrophic Cardiomyopathy With Mutations in Thin Filament Proteins

Circulation. Cardiovascular genetics, 2014-04, Vol.7 (2), p.132-143

2014

Volltextzugriff (PDF)

Effects of nicotine administration in a mouse model of familial hypertrophic cardiomyopathy, α-tropomyosin D175N

American journal of physiology. Heart and circulatory physiology, 2011, Vol.70 (4)

2011

Volltextzugriff (PDF)

VS-501: A NOVEL, NON-ABSORBED, CALCIUM- AND ALUMINUM-FREE, HIGHLY EFFECTIVE PHOSPHATE BINDER DERIVED FROM NATURAL PLANT POLYMER

Pharmacology research & perspectives, 2014-06, Vol.2 (3)

2014

Volltextzugriff (PDF)

Arginine-glycine-aspartic acid (RGD)-containing peptides inhibit the force production of mouse papillary muscle bundles via alpha sub(5) beta sub(1) integrin

The Journal of physiology, 2005-04, Vol.564 (2)

2005

Volltextzugriff (PDF)

Changes in end-to-end interactions of tropomyosin affect mouse cardiac muscle dynamics

American journal of physiology. Heart and circulatory physiology, 2006-08, Vol.291 (2), p.21

2006

Volltextzugriff (PDF)

VS‐501: a novel, nonabsorbed, calcium‐ and aluminum‐free, highly effective phosphate binder derived from natural plant polymer

Pharmacology research & perspectives, 2014-06, Vol.2 (3), p.n/a

2014

Volltextzugriff (PDF)

Changes in end-to-end interactions of tropomyosin affect mouse cardiac muscle dynamics

American Journal of Physiology: Cell Physiology, 2006-08, Vol.291 (2), p.H552-H563

2006

Volltextzugriff (PDF)

1 – 25 von 48

Suche als RSS-Feed

Suchergebnisse filtern

Filter anzeigen

Nur zeigen

Geprüft (Peer-Review)
(44)
Mit Volltextzugriff
(39)

Publikationsform

Artikel
(47)
Dissertationen
(1)

Sprache

Englisch
(48)
Japanisch
(3)

Erscheinungsjahr

n.n

Thema

15 weitere anzeigen...

Weniger anzeigen...

Neu hinzugefügt

... seit 90 Tagen
(1)

Menü

Weitere Dienste

Einstellungen

Inwardly rectifying K+ channels are major contributors to flow‐induced vasodilatation in resistance arteries

Early sensitization of myofilaments to Ca2+ prevents genetically linked dilated cardiomyopathy in mice

Desensitization of myofilaments to Ca2+ as a therapeutic target for hypertrophic cardiomyopathy with mutations in thin filament proteins

Rescue of familial cardiomyopathies by modifications at the level of sarcomere and Ca2+ fluxes

Roles of phosphorylation of myosin binding protein-C and troponin I in mouse cardiac muscle twitch dynamics

Neonatal gene transfer of Serca2a delays onset of hypertrophic remodeling and improves function in familial hypertrophic cardiomyopathy

Long-term rescue of a familial hypertrophic cardiomyopathy caused by a mutation in the thin filament protein, tropomyosin, via modulation of a calcium cycling protein

Enhancing natriuretic peptide signaling in adipose tissue, but not in muscle, protects against diet-induced obesity and insulin resistance

Effects of nicotine administration in a mouse model of familial hypertrophic cardiomyopathy, α-tropomyosin D175N

Charged residue changes in the carboxy‐terminus of α‐tropomyosin alter mouse cardiac muscle contractility

Arginine-glycine-aspartic acid (RGD)-containing peptides inhibit the force production of mouse papillary muscle bundles via alpha 5 beta 1 integrin

Arginine–glycine–aspartic acid (RGD)‐containing peptides inhibit the force production of mouse papillary muscle bundles via α5β1 integrin

Changes in end-to-end interactions of tropomyosin affect mouse cardiac muscle dynamics

Shear‐stress sensitive endothelial K channels play major role in flow‐induced vasodilation

Charged residue alterations in the inner‐core domain and carboxy‐terminus of α‐tropomyosin differentially affect mouse cardiac muscle contractility

Inwardly rectifying K super(+) channels are major contributors to flow-induced vasodilatation in resistance arteries

Rescue of a Dilated Cardiomyopathy Mouse Model Caused by a Mutation in Tropomyosin (E54K) by Expression of Slow Skeletal Troponin I

Effects of nicotine administration in a mouse model of familial hypertrophic cardiomyopathy, [alpha]-tropomyosin D175N

Desensitization of Myofilaments to Ca 2+ as a Therapeutic Target for Hypertrophic Cardiomyopathy With Mutations in Thin Filament Proteins

Effects of nicotine administration in a mouse model of familial hypertrophic cardiomyopathy, α-tropomyosin D175N

VS-501: A NOVEL, NON-ABSORBED, CALCIUM- AND ALUMINUM-FREE, HIGHLY EFFECTIVE PHOSPHATE BINDER DERIVED FROM NATURAL PLANT POLYMER

Arginine-glycine-aspartic acid (RGD)-containing peptides inhibit the force production of mouse papillary muscle bundles via alpha sub(5) beta sub(1) integrin

Changes in end-to-end interactions of tropomyosin affect mouse cardiac muscle dynamics

VS‐501: a novel, nonabsorbed, calcium‐ and aluminum‐free, highly effective phosphate binder derived from natural plant polymer

Changes in end-to-end interactions of tropomyosin affect mouse cardiac muscle dynamics

Suchergebnisse filtern