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1.
Figure 6.

Figure 6.Regulation of macrophage polarity and motility.. From: Macrophage motility requires distinct ?5?1/FAK and ?4?1/paxillin signaling events.

We propose a model in which α5β1 couples with FAK and α4β1 with paxillin to regulate macrophage polarity and motility through modulation of Rac and Rho activity.

Michelle Y. Abshire, et al. J Leukoc Biol. 2011 February;89(2):251-257.
2.
Figure 1.

Figure 1.α5β1 and α4β1 control distinct haptotactic invasion pathways in macrophages.. From: Macrophage motility requires distinct ?5?1/FAK and ?4?1/paxillin signaling events.

Invasion of WT and FAK−/− BMMs toward FN was measured in matrigel-coated, modified Boyden chambers following pretreatment with the indicated GST proteins. Bars represent the average number of invaded cells divided by the number of WT BMMs that migrated under control (untreated) conditions. *Values significantly different from WT GST treatment conditions; ∧values significantly different from WT cells under the same treatment conditions; n = 8.

Michelle Y. Abshire, et al. J Leukoc Biol. 2011 February;89(2):251-257.
3.
Figure 3.

Figure 3.FAK and paxillin regulate CSF-1-dependent macrophage invasion through separate signaling pathways.. From: Macrophage motility requires distinct ?5?1/FAK and ?4?1/paxillin signaling events.

(A) Immunoblot analysis showing paxillin knockdown under control (Lanes 1 and 2) and siPaxillin-treated conditions (lanes 3 and 4) in WT and FAK−/− BMMs. (B) Relative invasion toward CSF-1 of WT and FAK−/− BMMs treated with vehicle or siRNAs targeting paxillin. *Values that are significantly different from vehicle-treated WT cells; ^values that are significantly different from WT cells under the same treatment conditions; n = 6.

Michelle Y. Abshire, et al. J Leukoc Biol. 2011 February;89(2):251-257.
4.
Figure 4.

Figure 4.FAK and paxillin regulate CSF-1-dependent macrophage polarization through separate signaling pathways.. From: Macrophage motility requires distinct ?5?1/FAK and ?4?1/paxillin signaling events.

(A) Representative fields of CSF-1-starved WT and FAK−/− BMMs treated with siControl or siPaxillin and stained with phalloidin. (b, c, e, and f). Cells were stimulated with CSF-1 for 6 h. Arrows indicate areas of actin accumulation at the front of polarized cells. (B) Quantification of cell polarization. *Values that are significantly different from WT siControl-treated BMMs stimulated with CSF-1; ^values that are significantly different from WT cells under the same treatment conditions; n = 7.

Michelle Y. Abshire, et al. J Leukoc Biol. 2011 February;89(2):251-257.
5.
Figure 2.

Figure 2.Stimulation of α4β1 and α5β1 integrins leads to FAK-dependent changes in macrophage morphology.. From: Macrophage motility requires distinct ?5?1/FAK and ?4?1/paxillin signaling events.

(A) Representative fields of CSF-1-starved WT and FAK−/− BMMs following 5 min stimulation with the indicated GST proteins. Cells were fixed and stained for phalloidin. Cell elongation (B) and polarization (C) were determined as described in Materials and Methods. *Values significantly different from WT cells treated with GST; ^values significantly different from WT cells under the same treatment conditions; n = 3–4.

Michelle Y. Abshire, et al. J Leukoc Biol. 2011 February;89(2):251-257.
6.
Figure 5.

Figure 5.Chemotaxis of macrophages toward CSF-1 requires separate α5β1/FAK and α4β1/paxillin signaling pathways.. From: Macrophage motility requires distinct ?5?1/FAK and ?4?1/paxillin signaling events.

(A) Invasion of WT and FAK−/− BMMs toward CSF-1 was measured in the presence of the indicated function-blocking antibodies. Bars represent the average number of migrated cells divided by the number of WT BMMs that migrated under control (IgG-treated) conditions. (B) Invasion was measured as above in control (Vehicle, black bars) or siPaxillin-treated (gray bars) WT and FAK−/− BMMs. *Values significantly different from WT IgG control-treated cells; ^values significantly different from WT cells under the same conditions; n = 3–8.

Michelle Y. Abshire, et al. J Leukoc Biol. 2011 February;89(2):251-257.

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