Mice deficient in plasminogen activator inhibitor-1 have improved skeletal muscle regeneration.
about
Functional characterization of mouse urea transporters UT-A2 and UT-A3 expressed in purified Xenopus laevis oocyte plasma membranesGenetically determined proteolytic cleavage modulates alpha7beta1 integrin function.Requirement of plasminogen binding to its cell-surface receptor α-enolase for efficient regeneration of normal and dystrophic skeletal muscleCOX-2 inhibitor reduces skeletal muscle hypertrophy in mice.The plasminogen activation system modulates differently adipogenesis and myogenesis of embryonic stem cells.Impaired macrophage and satellite cell infiltration occurs in a muscle-specific fashion following injury in diabetic skeletal muscle.Inhibition of plasminogen activator inhibitor-1 restores skeletal muscle regeneration in untreated type 1 diabetic mice.Macrophage-specific expression of urokinase-type plasminogen activator promotes skeletal muscle regenerationThe Development of Macrophage-Mediated Cell Therapy to Improve Skeletal Muscle Function after Injury.The effect of acute and long-term physical activity on extracellular matrix and serglycin in human skeletal muscleuPA deficiency exacerbates muscular dystrophy in MDX mice.Human FXYD2 G41R mutation responsible for renal hypomagnesemia behaves as an inward-rectifying cation channelOpposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency.Smad3 induces atrogin-1, inhibits mTOR and protein synthesis, and promotes muscle atrophy in vivo.Diabetic myopathy: impact of diabetes mellitus on skeletal muscle progenitor cells.Urokinase-type plasminogen activator increases hepatocyte growth factor activity required for skeletal muscle regeneration.Plasminogen activator inhibitor-1 deficiency augments visceral mesothelial organization, intrapleural coagulation, and lung restriction in mice with carbon black/bleomycin-induced pleural injury.Effects of type 1 diabetes mellitus on skeletal muscle: clinical observations and physiological mechanisms.Phenotypic transitions of macrophages orchestrate tissue repair.Macrophage activation and skeletal muscle healing following traumatic injury.Endogenous interferon-gamma is required for efficient skeletal muscle regeneration.Mycobacterium ulcerans infections cause progressive muscle atrophy and dysfunction, and mycolactone impairs satellite cell proliferation.Reduced monocyte adhesion to aortae of diabetic plasminogen activator inhibitor-1 knockout mice.Signalling pathways regulating muscle mass in ageing skeletal muscle: the role of the IGF1-Akt-mTOR-FoxO pathway.Adipose Tissue-Derived Plasminogen Activator Inhibitor-1 Function and Regulation.Characterization and utilization of the flexor digitorum brevis for assessing skeletal muscle function.
P2860
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P2860
Mice deficient in plasminogen activator inhibitor-1 have improved skeletal muscle regeneration.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年学术文章
@wuu
2005年学术文章
@zh
2005年学术文章
@zh-cn
2005年学术文章
@zh-hans
2005年学术文章
@zh-my
2005年学术文章
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2005年學術文章
@yue
2005年學術文章
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name
Mice deficient in plasminogen ...... skeletal muscle regeneration.
@en
Mice deficient in plasminogen ...... skeletal muscle regeneration.
@nl
type
label
Mice deficient in plasminogen ...... skeletal muscle regeneration.
@en
Mice deficient in plasminogen ...... skeletal muscle regeneration.
@nl
prefLabel
Mice deficient in plasminogen ...... skeletal muscle regeneration.
@en
Mice deficient in plasminogen ...... skeletal muscle regeneration.
@nl
P2093
P2860
P1476
Mice deficient in plasminogen ...... skeletal muscle regeneration.
@en
P2093
Augustina M Pucci
Scott C Bryer
Thomas H Sisson
Timothy J Koh
P2860
P304
P356
10.1152/AJPCELL.00555.2004
P577
2005-02-16T00:00:00Z