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Nerve-responsive troponin I slow promoter does not respond to unloading
Journal of applied physiology (1985), 1998-03, Vol.84 (3), p.1083-1087
Criswell, David S
Hodgson, Vanessa R. M
Hardeman, Edna C
Booth, Frank W
1998
Details
Autor(en) / Beteiligte
Criswell, David S
Hodgson, Vanessa R. M
Hardeman, Edna C
Booth, Frank W
Titel
Nerve-responsive troponin I slow promoter does not respond to unloading
Ist Teil von
Journal of applied physiology (1985), 1998-03, Vol.84 (3), p.1083-1087
Ort / Verlag
Legacy CDMS: Am Physiological Soc
Erscheinungsjahr
1998
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
1 Department of Integrative Biology, Pharmacology, and Physiology, University of Texas Medical School, Houston, Texas 77030; and 2 Muscle Development Unit, The Children's Medical Research Institute, Wentworthville, New South Wales 2145, Australia We examined the regulation of the troponin I slow (TnIs) promoter during skeletal muscle unloading-induced protein isoform transition, by using a transgenic mouse line harboring the 4,200 to +12 base pairs region of the human TnIs promoter. Eighteen female transgenic mice (~30 g body mass) were randomly divided into two groups: weight-bearing (WB) controls ( n = 9) and hindlimb unloaded (HU; n = 9). The HU mice were tail suspended for 7 days. Body mass was unchanged in the WB group but was reduced ( 6%; P < 0.05) after the HU treatment. Absolute soleus muscle mass ( 25%) and soleus mass relative to body mass ( 16%) were both lower ( P < 0.05) in the HU group compared with the WB mice. Northern blot analyses indicate that 7 days of HU result in a 64% decrease ( P < 0.05) in the abundance of endogenous TnIs mRNA (µg/mg muscle) in the mouse soleus. Furthermore, there is a trend for the abundance of the fast troponin I mRNA to be increased (+34%). Analysis of transgenic chloramphenicol acetyltransferase activity in the soleus muscle revealed no difference ( P > 0.05) between WB and HU groups. We conclude that additional elements are necessary for the TnIs gene to respond to an unloading-induced, slow-to-fast isoform transition stimulus. transgenic mice; skeletal muscle; hindlimb unloading JAP 84(3):1083-1087 0161-7567/98 $5.00 Copyright © 1998 the American Physiological Society
Sprache
Englisch
Identifikatoren
ISSN: 8750-7587
eISSN: 1522-1601
DOI: 10.1152/jappl.1998.84.3.1083
Titel-ID: cdi_pubmed_primary_9480972
Format
–
Schlagworte
Aerospace Medicine
,
Animals
,
Biological and medical sciences
,
Blotting, Northern
,
Body Weight - physiology
,
Chloramphenicol O-Acetyltransferase - biosynthesis
,
Chloramphenicol O-Acetyltransferase - genetics
,
Chloramphenicol O-Acetyltransferase - metabolism
,
DNA Probes
,
Female
,
Fundamental and applied biological sciences. Psychology
,
Hindlimb Suspension - physiology
,
Humans
,
Mice
,
Mice, Transgenic
,
Muscle, Skeletal - enzymology
,
Muscle, Skeletal - physiology
,
Organ Size - physiology
,
RNA - biosynthesis
,
Space life sciences
,
Striated muscle. Tendons
,
Transcription, Genetic
,
Troponin I - genetics
,
Troponin I - physiology
,
Vertebrates: osteoarticular system, musculoskeletal system
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