Temporary disruption of the plasma membrane is required for c-fos expression in response to mechanical stress.
about
Spatiotemporal dynamics of actin remodeling and endomembrane trafficking in alveolar epithelial type I cell wound healing.Response network analysis of differential gene expression in human epithelial lung cells during avian influenza infectionsAutophagy in pulmonary macrophages mediates lung inflammatory injury via NLRP3 inflammasome activation during mechanical ventilation.The role of purinergic signaling on deformation induced injury and repair responses of alveolar epithelial cellsInvited review: plasma membrane stress failure in alveolar epithelial cells.Cell membrane disruption stimulates NO/PKG signaling and potentiates cell membrane repair in neighboring cells.Hypercapnia: a nonpermissive environment for the lung.Cellular stress failure in ventilator-injured lungsPresentation of exogenous antigens on major histocompatibility complex (MHC) class I and MHC class II molecules is differentially regulated during dendritic cell maturation.Understanding the mechanisms of lung mechanical stress.Wound repair: toward understanding and integration of single-cell and multicellular wound responses.Initial pulmonary respiration causes massive diaphragm damage and hyper-CKemia in Duchenne muscular dystrophy dog.Cell wounding and repair in ventilator injured lungs.Biophysical determinants of alveolar epithelial plasma membrane wounding associated with mechanical ventilation.Spinal cord injury modulates the lung inflammatory response in mechanically ventilated rats: a comparative animal study.Cytoskeleton and mechanotransduction in the pathophysiology of ventilator-induced lung injury.Endothelium under stress: local and systemic messages.The pathway of cross-presentation is influenced by the particle size of phagocytosed antigen.Mechanisms of surface-tension-induced epithelial cell damage in a model of pulmonary airway reopening.Deformation-induced lipid trafficking in alveolar epithelial cells.Hypercapnic acidosis impairs plasma membrane wound resealing in ventilator-injured lungs.Endocytic response of type I alveolar epithelial cells to hypertonic stress.Long-term potentiation of wound-induced exocytosis and plasma membrane repair is dependent on cAMP-response element-mediated transcription via a protein kinase C- and p38 MAPK-dependent pathway.Stretch-activated ion channels and c-fos expression remain active after repeated eccentric bouts.Temporary loss of plasma membrane integrity in orthodontic tooth movement.Cell membrane disruption stimulates cAMP and Ca2+ signaling to potentiate cell membrane resealing in neighboring cells.Mechanical loading disrupts osteocyte plasma membranes which initiates mechanosensation events in bone.Cell suffering and its prevention in lung.
P2860
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P2860
Temporary disruption of the plasma membrane is required for c-fos expression in response to mechanical stress.
description
1999 nî lūn-bûn
@nan
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
1999年论文
@zh
1999年论文
@zh-cn
name
Temporary disruption of the pl ...... response to mechanical stress.
@en
type
label
Temporary disruption of the pl ...... response to mechanical stress.
@en
prefLabel
Temporary disruption of the pl ...... response to mechanical stress.
@en
P2093
P2860
P356
P1476
Temporary disruption of the pl ...... response to mechanical stress.
@en
P2093
K P Grembowicz
P L McNeil
P2860
P304
P356
10.1091/MBC.10.4.1247
P577
1999-04-01T00:00:00Z