The Experts below are selected from a list of 267 Experts worldwide ranked by ideXlab platform
Peter N. Devreotes - One of the best experts on this subject based on the ideXlab platform.
-
Signaling pathways mediating chemotaxis in the social amoeba, Dictyostelium discoideum
European Journal of Cell Biology, 2006Co-Authors: Stacey S. Willard, Peter N. DevreotesAbstract:Chemotaxis, or cell migration guided by chemical cues, is critical for a multitude of biological processes in a diverse array of organisms. Dictyostelium discoideum amoebae rely on chemotaxis to find food and to survive starvation conditions, and we have taken advantage of this system to study the molecular regulation of this vital cell behavior. Previous work has identified phosphoinositide signaling as one mechanism which may contribute to directional sensing and actin polymerization during chemotaxis; a mechanism which is conserved in mammalian neutrophils. In this review, we will discuss recent data on genes and pathways governing directional sensing and actin polymerization, with a particular emphasis on contributions from our laboratory. © 2006 Elsevier GmbH. All rights reserved.
-
receptor mediated regulation of pi3ks confines pi 3 4 5 p3 to the leading edge of Chemotaxing cells
Molecular Biology of the Cell, 2003Co-Authors: Yi Elaine Huang, Miho Iijima, Carole A Parent, Satoru Funamoto, Richard A Firtel, Peter N. DevreotesAbstract:Recent studies have demonstrated that PH domains specific for PI(3,4,5)P3 accumulate at the leading edge of a number of migrating cells and that PI3Ks and PTEN associate with the membrane at the front and back, respectively, of Chemotaxing Dictyostelium discoideum cells. However, the dependence of chemoattractant induced changes in PI(3,4,5)P3 on PI3K and PTEN activities have not been defined. We find that bulk PI(3,4,5)P3 levels increase transiently upon chemoattractant stimulation, and the changes are greater and more prolonged in pten– cells. PI3K activation increases within 5 s of chemoattractant addition and then declines to a low level of activity identically in wild-type and pten– cells. Reconstitution of the PI3K activation profile can be achieved by mixing membranes from stimulated pi3k1–/pi3k2– cells with cytosolic PI3Ks from unstimulated cells. These studies show that significant control of chemotaxis occurs upstream of the PI3Ks and that regulation of the PI3Ks and PTEN cooperate to shape the temporal and spatial localization of PI(3,4,5)P3.
Gunnar Nilsson - One of the best experts on this subject based on the ideXlab platform.
-
the chemokine receptor cxcr4 is expressed within the mast cell lineage and its ligand stromal cell derived factor 1α acts as a mast cell Chemotaxin
European Journal of Immunology, 2000Co-Authors: Mikael Juremalm, Malin Hjertson, Niclas Olsson, Ilkka T Harvima, Kenneth Nilsson, Gunnar NilssonAbstract:The chemokine receptor CXCR4 is expressed on the mast cell lineage and its ligand SDF-1 acts as a mast cell Chemotaxin
-
The chemokine receptor CXCR4 is expressed within the mast cell lineage and its ligand stromal cell‐derived factor‐1α acts as a mast cell Chemotaxin
European Journal of Immunology, 2000Co-Authors: Mikael Juremalm, Malin Hjertson, Niclas Olsson, Ilkka T Harvima, Kenneth Nilsson, Gunnar NilssonAbstract:The chemokine receptor CXCR4 is expressed on the mast cell lineage and its ligand SDF-1 acts as a mast cell Chemotaxin
-
Demonstration of mast‐cell chemotactic activity in nasal lavage fluid: characterization of one Chemotaxin as c‐kit ligand, stem cell factor
Allergy, 1998Co-Authors: Gunnar Nilsson, Karin Nilsson, Malin Hjertson, M Andersson, L Greiff, Camilla I Svensson, Agneta SiegbahnAbstract:Mast cells are known to accumulate in tissue during allergic inflammation. However, the Chemotaxins responsible are undefined. Using a modified Boyden chamber and Ihe human mast-cell line HMC-1, we first identified mast-cell chemotactic activity in nasal lavage fluid collected before the pollen season after allergen provocation of allergic patients (N=29) (mean migratory response compared to medium control was 121%, range 85-198%). Mast-cell chemotactic activity was also detected in lavage fluid collected after allergen provocation at the end of a Swedish birch-pollen season from three different treatment groups: topical steroid treatment with budesonide; the topical antihistamine, levocabastine; and placebo. There was no significant difference in mast-cell chemotactic activity between nasal lavage fluid collected from the placebo group (mean = 102%), the budesonide-treated group (mean = 1l4%), or the levocabastine group (mean = 125%). Stem cell factor (SCF), a known mast-cell Chemotaxin, was present in the nasal lavage fluids from all three groups, and correlated with the mast-cell chemotactic activity (r = 0.67, P < 0.0l). TTie mast-eell chemotactic activity was inhibited (range 5-tOO%) in some, but not all, nasal lavage fluids by a polyclonal antibody directed against SCF. This report describes the presence of mast-cell chemotactic activity in nasal lavage fluid during an allergic reaction. These findings show that SCF may play a pivotal role in the recruitment of mast cells in allergic rhinitis.
-
demonstration of mast cell chemotactic activity in nasal lavage fluid characterization of one Chemotaxin as c kit ligand stem cell factor
Allergy, 1998Co-Authors: Gunnar Nilsson, Malin Hjertson, M Andersson, L Greiff, Camilla I Svensson, K Nilsson, Agneta SiegbahnAbstract:Mast cells are known to accumulate in tissue during allergic inflammation. However, the Chemotaxins responsible are undefined. Using a modified Boyden chamber and the human mast-cell line HMC-1, we first identified mast-cell chemotactic activity in nasal lavage fluid collected before the pollen season after allergen provocation of allergic patients (n=29) (mean migratory response compared to medium control was 121%, range 85-198%). Mast-cell chemotactic activity was also detected in lavage fluid collected after allergen provocation at the end of a Swedish birch-pollen season from three different treatment groups: topical steroid treatment with budesonide; the topical antihistamine, levocabastine; and placebo. There was no significant difference in mast-cell chemotactic activity between nasal lavage fluid collected from the placebo group (mean=102%), the budesonide-treated group (mean=114%), or the levocabastine group (mean=125%). Stem cell factor (SCF), a known mast-cell Chemotaxin, was present in the nasal lavage fluids from all three groups, and correlated with the mast-cell chemotactic activity (r=0.67, P<0.01). The mast-cell chemotactic activity was inhibited (range 5-100%) in some, but not all, nasal lavage fluids by a polyclonal antibody directed against SCF. This report describes the presence of mast-cell chemotactic activity in nasal lavage fluid during an allergic reaction. These findings show that SCF may play a pivotal role in the recruitment of mast cells in allergic rhinitis.
-
C3a and C5a are Chemotaxins for human mast cells and act through distinct receptors via a pertussis toxin-sensitive signal transduction pathway.
Journal of Immunology, 1996Co-Authors: Gunnar Nilsson, M Johnell, C H Hammer, H L Tiffany, Karin Nilsson, Dean D. Metcalfe, Agneta Siegbahn, P M MurphyAbstract:Mast cells are known to accumulate at sites of inflammation, however, the Chemotaxins involved are undefined. Since most natural leukocyte secretagogues also induce cell migration, and since the anaphylatoxins C3a and C5a are mast cell secretagogues, we hypothesized that both C3a and C5a are also mast cell Chemotaxins. Here we report that C3a and C5a are, in fact, potent Chemotaxins for the human mast cell line HMC-1. The optimal concentrations, half-maximal effective concentrations (a measure of agonist potency) and the efficacy (response at the optimal concentration) compared with medium control were, for C3a: 10 nM, 0.5 nM, and 256%, respectively; for C5a: 1 nM, 10 pM and 145%. Chemotaxis of HMC-1 cells to both C3a and C5a was blocked by pertussis toxin, suggesting that Gi-coupled receptors are involved in signal transduction. C3a and C5a also induced transient pertussis toxin-inhibitable increases in [Ca2+]i (ED50 = 1 nM for both) that could be homologously but not heterologously desensitized, suggesting that the receptors for C3a and C5a are distinct. These results make C3a the most effective mast cell Chemotaxin identified to date. The chemotactic potency described here for C3a is also 100- to 1000-fold greater than for all of its previously described cellular actions. Direct chemoattraction of mast cells by C3a and C5a may help explain the rapid accumulation of mast cells at sites of inflammation.
Reietsu Itoh - One of the best experts on this subject based on the ideXlab platform.
-
control of cell polarity and motility by the ptdins 3 4 5 p3 phosphatase ship1
Nature Cell Biology, 2007Co-Authors: Miki Nishio, Kenichi Watanabe, Junko Sasaki, Choji Taya, Shunsuke Takasuga, Ryota Iizuka, Tamas Balla, Masakazu Yamazaki, Hiroshi Watanabe, Reietsu ItohAbstract:Proper neutrophil migration into inflammatory sites ensures host defense without tissue damage. Phosphoinositide 3-kinase (PI(3)K) and its lipid product phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P3) regulate cell migration, but the role of PtdIns(3,4,5)P3-degrading enzymes in this process is poorly understood. Here, we show that Src homology 2 (SH2) domain-containing inositol-5-phosphatase 1 (SHIP1), a PtdIns(3,4,5)P3 phosphatase, is a key regulator of neutrophil migration. Genetic inactivation of SHIP1 led to severe defects in neutrophil polarization and motility. In contrast, loss of the PtdIns(3,4,5)P3 phosphatase PTEN had no impact on neutrophil chemotaxis. To study PtdIns(3,4,5)P3 metabolism in living primary cells, we generated a novel transgenic mouse (AktPH–GFP Tg) expressing a bioprobe for PtdIns(3,4,5)P3. Time-lapse footage showed rapid, localized binding of AktPH–GFP to the leading edge membrane of Chemotaxing ship1+/+AktPH–GFP Tg neutrophils, but only diffuse localization in ship1−/−AktPH–GFP Tg neutrophils. By directing where PtdIns(3,4,5)P3 accumulates, SHIP1 governs the formation of the leading edge and polarization required for chemotaxis.
Carolina Alvarezortega - One of the best experts on this subject based on the ideXlab platform.
-
identification of a malate chemoreceptor in pseudomonas aeruginosa by screening for chemotaxis defects in an energy taxis deficient mutant
Applied and Environmental Microbiology, 2007Co-Authors: Carolina Alvarezortega, Caroline S HarwoodAbstract:We found that a robust energy taxis response mediated by the Aer receptor can sometimes mask chemotaxis mediated by other methyl-accepting chemotaxis proteins (MCPs) in Pseudomonas aeruginosa. We identified PA2652 as a chemoreceptor for malate by screening aer mcp double mutants by using swarm plate assays.
Agneta Siegbahn - One of the best experts on this subject based on the ideXlab platform.
-
Demonstration of mast‐cell chemotactic activity in nasal lavage fluid: characterization of one Chemotaxin as c‐kit ligand, stem cell factor
Allergy, 1998Co-Authors: Gunnar Nilsson, Karin Nilsson, Malin Hjertson, M Andersson, L Greiff, Camilla I Svensson, Agneta SiegbahnAbstract:Mast cells are known to accumulate in tissue during allergic inflammation. However, the Chemotaxins responsible are undefined. Using a modified Boyden chamber and Ihe human mast-cell line HMC-1, we first identified mast-cell chemotactic activity in nasal lavage fluid collected before the pollen season after allergen provocation of allergic patients (N=29) (mean migratory response compared to medium control was 121%, range 85-198%). Mast-cell chemotactic activity was also detected in lavage fluid collected after allergen provocation at the end of a Swedish birch-pollen season from three different treatment groups: topical steroid treatment with budesonide; the topical antihistamine, levocabastine; and placebo. There was no significant difference in mast-cell chemotactic activity between nasal lavage fluid collected from the placebo group (mean = 102%), the budesonide-treated group (mean = 1l4%), or the levocabastine group (mean = 125%). Stem cell factor (SCF), a known mast-cell Chemotaxin, was present in the nasal lavage fluids from all three groups, and correlated with the mast-cell chemotactic activity (r = 0.67, P < 0.0l). TTie mast-eell chemotactic activity was inhibited (range 5-tOO%) in some, but not all, nasal lavage fluids by a polyclonal antibody directed against SCF. This report describes the presence of mast-cell chemotactic activity in nasal lavage fluid during an allergic reaction. These findings show that SCF may play a pivotal role in the recruitment of mast cells in allergic rhinitis.
-
demonstration of mast cell chemotactic activity in nasal lavage fluid characterization of one Chemotaxin as c kit ligand stem cell factor
Allergy, 1998Co-Authors: Gunnar Nilsson, Malin Hjertson, M Andersson, L Greiff, Camilla I Svensson, K Nilsson, Agneta SiegbahnAbstract:Mast cells are known to accumulate in tissue during allergic inflammation. However, the Chemotaxins responsible are undefined. Using a modified Boyden chamber and the human mast-cell line HMC-1, we first identified mast-cell chemotactic activity in nasal lavage fluid collected before the pollen season after allergen provocation of allergic patients (n=29) (mean migratory response compared to medium control was 121%, range 85-198%). Mast-cell chemotactic activity was also detected in lavage fluid collected after allergen provocation at the end of a Swedish birch-pollen season from three different treatment groups: topical steroid treatment with budesonide; the topical antihistamine, levocabastine; and placebo. There was no significant difference in mast-cell chemotactic activity between nasal lavage fluid collected from the placebo group (mean=102%), the budesonide-treated group (mean=114%), or the levocabastine group (mean=125%). Stem cell factor (SCF), a known mast-cell Chemotaxin, was present in the nasal lavage fluids from all three groups, and correlated with the mast-cell chemotactic activity (r=0.67, P<0.01). The mast-cell chemotactic activity was inhibited (range 5-100%) in some, but not all, nasal lavage fluids by a polyclonal antibody directed against SCF. This report describes the presence of mast-cell chemotactic activity in nasal lavage fluid during an allergic reaction. These findings show that SCF may play a pivotal role in the recruitment of mast cells in allergic rhinitis.
-
C3a and C5a are Chemotaxins for human mast cells and act through distinct receptors via a pertussis toxin-sensitive signal transduction pathway.
Journal of Immunology, 1996Co-Authors: Gunnar Nilsson, M Johnell, C H Hammer, H L Tiffany, Karin Nilsson, Dean D. Metcalfe, Agneta Siegbahn, P M MurphyAbstract:Mast cells are known to accumulate at sites of inflammation, however, the Chemotaxins involved are undefined. Since most natural leukocyte secretagogues also induce cell migration, and since the anaphylatoxins C3a and C5a are mast cell secretagogues, we hypothesized that both C3a and C5a are also mast cell Chemotaxins. Here we report that C3a and C5a are, in fact, potent Chemotaxins for the human mast cell line HMC-1. The optimal concentrations, half-maximal effective concentrations (a measure of agonist potency) and the efficacy (response at the optimal concentration) compared with medium control were, for C3a: 10 nM, 0.5 nM, and 256%, respectively; for C5a: 1 nM, 10 pM and 145%. Chemotaxis of HMC-1 cells to both C3a and C5a was blocked by pertussis toxin, suggesting that Gi-coupled receptors are involved in signal transduction. C3a and C5a also induced transient pertussis toxin-inhibitable increases in [Ca2+]i (ED50 = 1 nM for both) that could be homologously but not heterologously desensitized, suggesting that the receptors for C3a and C5a are distinct. These results make C3a the most effective mast cell Chemotaxin identified to date. The chemotactic potency described here for C3a is also 100- to 1000-fold greater than for all of its previously described cellular actions. Direct chemoattraction of mast cells by C3a and C5a may help explain the rapid accumulation of mast cells at sites of inflammation.