- Standort
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
2044-5040
- Umfang
-
Online-Ressource
- Sprache
-
Englisch
- Anmerkungen
-
online resource.
- Erschienen in
-
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
- Urheber
-
Kraner, Susan D.
Novak, Kevin R.
Wang, Qingbo
Peng, Junmin
Rich, Mark M.
- Beteiligte Personen und Organisationen
-
SpringerLink (Online service)
- DOI
-
10.1186/2044-5040-2-17
- URN
-
urn:nbn:de:101:1-2021081020384690714223
- Rechteinformation
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
-
14.08.2025, 11:03 MESZ
Datenpartner
Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Beteiligte
- Kraner, Susan D.
- Novak, Kevin R.
- Wang, Qingbo
- Peng, Junmin
- Rich, Mark M.
- SpringerLink (Online service)
Ähnliche Objekte (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
Risk factors in critical illness myopathy during the early course of critical illness: a prospective observational study
Sodium channel slow inactivation interferes with open channel block
Critical Illness Weakness, Polyneuropathy and Myopathy: Diagnosis, treatment, and long-term outcomes
ClC-1 chloride channel and myotonia in proximal myotonic myopathy
Sodium channel biophysics, late sodium current and genetic arrhythmic syndromes
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
Risk factors in critical illness myopathy during the early course of critical illness: a prospective observational study
Sodium channel slow inactivation interferes with open channel block
Critical Illness Weakness, Polyneuropathy and Myopathy: Diagnosis, treatment, and long-term outcomes
ClC-1 chloride channel and myotonia in proximal myotonic myopathy
Sodium channel biophysics, late sodium current and genetic arrhythmic syndromes
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
Risk factors in critical illness myopathy during the early course of critical illness: a prospective observational study
Sodium channel slow inactivation interferes with open channel block
Critical Illness Weakness, Polyneuropathy and Myopathy: Diagnosis, treatment, and long-term outcomes
ClC-1 chloride channel and myotonia in proximal myotonic myopathy
Sodium channel biophysics, late sodium current and genetic arrhythmic syndromes
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