- Location
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
2044-5040
- Extent
-
Online-Ressource
- Language
-
Englisch
- Notes
-
online resource.
- Bibliographic citation
-
Altered sodium channel-protein associations in critical illness myopathy ; volume:2 ; number:1 ; day:30 ; month:8 ; year:2012 ; pages:1-13 ; date:12.2012
Skeletal muscle ; 2, Heft 1 (30.8.2012), 1-13, 12.2012
- Creator
-
Kraner, Susan D.
Novak, Kevin R.
Wang, Qingbo
Peng, Junmin
Rich, Mark M.
- Contributor
-
SpringerLink (Online service)
- DOI
-
10.1186/2044-5040-2-17
- URN
-
urn:nbn:de:101:1-2021081020384690714223
- Rights
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
14.08.2025, 11:03 AM CEST
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Kraner, Susan D.
- Novak, Kevin R.
- Wang, Qingbo
- Peng, Junmin
- Rich, Mark M.
- SpringerLink (Online service)
Other Objects (12)
Critical Illness Myopathy: Diagnostic Approach and Resulting Therapeutic Implications
Altered myogenesis and premature senescence underlie human TRIM32-related myopathy
RNA-sequencing reveals altered skeletal muscle contraction, E3 ligases, autophagy, apoptosis, and chaperone expression in patients with critical illness myopathy
Sodium channel slow inactivation interferes with open channel block
Risk factors in critical illness myopathy during the early course of critical illness: a prospective observational study
Critical Illness Weakness, Polyneuropathy and Myopathy: Diagnosis, treatment, and long-term outcomes
Sodium channel biophysics, late sodium current and genetic arrhythmic syndromes
ClC-1 chloride channel and myotonia in proximal myotonic myopathy
Altered skeletal muscle (mitochondrial) properties in patients with mitochondrial DNA single deletion myopathy
Pharmacological modification of sodium channel Nav1.9 activity
Macrophages enhance sodium channel expression in cardiomyocytes
Cav3.2 calcium channel interactions with the epithelial sodium channel ENaC
Critical Illness Myopathy: Diagnostic Approach and Resulting Therapeutic Implications
Altered myogenesis and premature senescence underlie human TRIM32-related myopathy
RNA-sequencing reveals altered skeletal muscle contraction, E3 ligases, autophagy, apoptosis, and chaperone expression in patients with critical illness myopathy
Sodium channel slow inactivation interferes with open channel block
Risk factors in critical illness myopathy during the early course of critical illness: a prospective observational study
Critical Illness Weakness, Polyneuropathy and Myopathy: Diagnosis, treatment, and long-term outcomes
Sodium channel biophysics, late sodium current and genetic arrhythmic syndromes
ClC-1 chloride channel and myotonia in proximal myotonic myopathy
Altered skeletal muscle (mitochondrial) properties in patients with mitochondrial DNA single deletion myopathy
Pharmacological modification of sodium channel Nav1.9 activity
Macrophages enhance sodium channel expression in cardiomyocytes
Cav3.2 calcium channel interactions with the epithelial sodium channel ENaC
Critical Illness Myopathy: Diagnostic Approach and Resulting Therapeutic Implications
Altered myogenesis and premature senescence underlie human TRIM32-related myopathy
RNA-sequencing reveals altered skeletal muscle contraction, E3 ligases, autophagy, apoptosis, and chaperone expression in patients with critical illness myopathy
Sodium channel slow inactivation interferes with open channel block
Risk factors in critical illness myopathy during the early course of critical illness: a prospective observational study
Critical Illness Weakness, Polyneuropathy and Myopathy: Diagnosis, treatment, and long-term outcomes
Sodium channel biophysics, late sodium current and genetic arrhythmic syndromes
ClC-1 chloride channel and myotonia in proximal myotonic myopathy
Altered skeletal muscle (mitochondrial) properties in patients with mitochondrial DNA single deletion myopathy
Pharmacological modification of sodium channel Nav1.9 activity
Macrophages enhance sodium channel expression in cardiomyocytes