Effects of F/G-actin ratio and actin turn-over rate on NADPH oxidase activity in microglia

@inproceedings{Rasmussen2010EffectsOF,
  title={Effects of F/G-actin ratio and actin turn-over rate on NADPH oxidase activity in microglia},
  author={Izabela Rasmussen and L. H\ojlund Pedersen and Luise M Byg and K. Kamiya T. Suzuki and Hideki Sumimoto and Frederik Vilhardt},
  booktitle={BMC Immunology},
  year={2010}
}
Most in vivo studies that have addressed the role of actin dynamics in NADPH oxidase function in phagocytes have used toxins to modulate the polymerization state of actin and mostly effects on actin has been evaluated by end point measurements of filamentous actin, which says little about actin dynamics, and without consideration for the subcellular distribution of the perturbed actin cytoskeleton. Here, we in addition to toxins use conditional expression of the major actin regulatory protein… CONTINUE READING

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ActinsInverse is aG-Actin
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
ActinsNo subtypeG-Actin
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
CytoskeletonIs associated anatomy of gene productActins
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
Our data demonstrate that stimulated NADPH oxidase function was severely impaired only at extreme actin recovery rates and F / G - actin ratios , and surprisingly , that any moderate changes of these parameters of the actin cytoskeleton invariably resulted in an increased NADPH oxidase activity .
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
G-ActinAnatomic structure is physical part ofCytoskeleton
Our data demonstrate that stimulated NADPH oxidase function was severely impaired only at extreme actin recovery rates and F / G - actin ratios , and surprisingly , that any moderate changes of these parameters of the actin cytoskeleton invariably resulted in an increased NADPH oxidase activity .
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
Our data demonstrate that stimulated NADPH oxidase function was severely impaired only at extreme actin recovery rates and F / G - actin ratios , and surprisingly , that any moderate changes of these parameters of the actin cytoskeleton invariably resulted in an increased NADPH oxidase activity .
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
MicrofilamentsIs associated anatomy of gene productActins
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
Our data demonstrate that stimulated NADPH oxidase function was severely impaired only at extreme actin recovery rates and F / G - actin ratios , and surprisingly , that any moderate changes of these parameters of the actin cytoskeleton invariably resulted in an increased NADPH oxidase activity .
Most in vivo studies that have addressed the role of actin dynamics in NADPH oxidase function in phagocytes have used toxins to modulate the polymerization state of actin and mostly effects on actin has been evaluated by end point measurements of filamentous actin , which says little about actin dynamics , and without consideration for the subcellular distribution of the perturbed actin cytoskeleton .
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
Here , we in addition to toxins use conditional expression of the major actin regulatory protein LIM kinase-1 ( LIMK1 ) , and shRNA knock - down of cofilin to modulate the cellular F / G - actin ratio in the Ra2 microglia cell line , and we use Fluorescence Recovery after Photobleaching ( FRAP ) in β-actin - YFP - transduced cells to obtain a dynamic measure of actin recovery rates ( actin turn - over rates ) in different F / G - actin states of the actin cytoskeleton .
F-ActinAnatomic structure is physical part ofCytoskeleton
Most in vivo studies that have addressed the role of actin dynamics in NADPH oxidase function in phagocytes have used toxins to modulate the polymerization state of actin and mostly effects on actin has been evaluated by end point measurements of filamentous actin , which says little about actin dynamics , and without consideration for the subcellular distribution of the perturbed actin cytoskeleton .
Most in vivo studies that have addressed the role of actin dynamics in NADPH oxidase function in phagocytes have used toxins to modulate the polymerization state of actin and mostly effects on actin has been evaluated by end point measurements of filamentous actin , which says little about actin dynamics , and without consideration for the subcellular distribution of the perturbed actin cytoskeleton .
Most in vivo studies that have addressed the role of actin dynamics in NADPH oxidase function in phagocytes have used toxins to modulate the polymerization state of actin and mostly effects on actin has been evaluated by end point measurements of filamentous actin , which says little about actin dynamics , and without consideration for the subcellular distribution of the perturbed actin cytoskeleton .
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