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Robert1bombe

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Ation of stathmin, indicating that LPS activation of Cdk1 kinase is the major contributing factor for rapid stathmin destruction. Our studies focused on early time points of macrophage classical activation when the major morphological and phenotypic events are occurring. We demonstrate that the classically activated macrophages adopt distinct cell morphologies and that stathmin reduction is requir
1
Ation of stathmin, indicating that LPS activation of Cdk1 kinase is the major contributing factor for rapid stathmin destruction. Our studies focused on early time points of macrophage classical activation when the major morphological and phenotypic events are occurring. We demonstrate that the classically activated macrophages adopt distinct cell morphologies and that stathmin reduction is requir
1
Ation of stathmin, indicating that LPS activation of Cdk1 kinase is the major contributing factor for rapid stathmin destruction. Our studies focused on early time points of macrophage classical activation when the major morphological and phenotypic events are occurring. We demonstrate that the classically activated macrophages adopt distinct cell morphologies and that stathmin reduction is requir
1
Ation of stathmin, indicating that LPS activation of Cdk1 kinase is the major contributing factor for rapid stathmin destruction. Our studies focused on early time points of macrophage classical activation when the major morphological and phenotypic events are occurring. We demonstrate that the classically activated macrophages adopt distinct cell morphologies and that stathmin reduction is requir
1
To the cell surface (Fig. 7). Continued signaling through TLR4 is important for NF- B-mediated gene expression and secretion of pro-inflammatory cytokines in macrophages during a pathogenic challenge (9). Here we show that stathmin can modulate this sustained signaling, likely by affecting the stability of MT to enhance intracellular trafficking of receptor-containing vesicles, MMPs, and cytokines
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To the cell surface (Fig. 7). Continued signaling through TLR4 is important for NF- B-mediated gene expression and secretion of pro-inflammatory cytokines in macrophages during a pathogenic challenge (9). Here we show that stathmin can modulate this sustained signaling, likely by affecting the stability of MT to enhance intracellular trafficking of receptor-containing vesicles, MMPs, and cytokines
1
Ation of stathmin, indicating that LPS activation of Cdk1 kinase is the major contributing factor for rapid stathmin destruction. Our studies focused on early time points of macrophage classical activation when the major morphological and phenotypic events are occurring. We demonstrate that the classically activated macrophages adopt distinct cell morphologies and that stathmin reduction is requir
1
Ation of stathmin, indicating that LPS activation of Cdk1 kinase is the major contributing factor for rapid stathmin destruction. Our studies focused on early time points of macrophage classical activation when the major morphological and phenotypic events are occurring. We demonstrate that the classically activated macrophages adopt distinct cell morphologies and that stathmin reduction is requir
1
On observed. We saw reduced degradation of I B in these cells, which likely accounts for less nuclear NF- B. Newly synthesized I B can terminate the inflammatory signal by entering the nucleus and binding to NF- B to cause its export to the cytoplasm (88, 89). Thus the rate of I B recovery determinesJOURNAL OF BIOLOGICAL CHEMISTRYStathmin Reduction in Macrophage Activationthe length of interaction
1
On observed. We saw reduced degradation of I B in these cells, which likely accounts for less nuclear NF- B. Newly synthesized I B can terminate the inflammatory signal by entering the nucleus and binding to NF- B to cause its export to the cytoplasm (88, 89). Thus the rate of I B recovery determinesJOURNAL OF BIOLOGICAL CHEMISTRYStathmin Reduction in Macrophage Activationthe length of interaction