Cytosolic Free Calcium and the Cytoskeleton in the Control of Leukocyte Chemotaxis

1998 ◽  
Vol 78 (4) ◽  
pp. 949-967 ◽  
Author(s):  
ELIZABETH J. PETTIT ◽  
FREDRIC S. FAY†
Keyword(s):  
Rational Design ◽  
Free Calcium ◽  
Molecular Signaling ◽  
Cytosolic Free Calcium ◽  
Kinase Activation ◽  
Pathogen Invasion ◽  
Kinase C ◽  
Leukocyte Chemotaxis ◽  
Essential Function

Pettit, Elizabeth J., and Frederic S. Fay. Cytosolic Free Calcium and the Cytoskeleton in the Control of Leukocyte Chemotaxis. Physiol. Rev. 78: 949–967, 1998. — In response to a chemotactic gradient, leukocytes extravasate and chemotax toward the site of pathogen invasion. Although fundamental in the control of many leukocyte functions, the role of cytosolic free Ca2+in chemotaxis is unclear and has been the subject of debate. Before becoming motile, the cell assumes a polarized morphology, as a result of modulation of the cytoskeleton by G protein and kinase activation. This morphology may be reinforced during chemotaxis by the intracellular redistribution of Ca2+stores, cytoskeletal constituents, and chemoattractant receptors. Restricted subcellular distributions of signaling molecules, such as Ca2+, Ca2+/calmodulin, diacylglycerol, and protein kinase C, may also play a role in some types of leukocyte. Chemotaxis is an essential function of most cells at some stage during their development, and a deeper understanding of the molecular signaling and structural components involved will enable rational design of therapeutic strategies in a wide variety of diseases.

scholarly journals Role of the kinase activation loop on protein kinase C θ activity and intracellular localisation

FEBS Letters ◽  
2003 ◽  
Vol 554 (1-2) ◽  
pp. 35-40 ◽  
Author(s):  
Bianca Sparatore ◽  
Mario Passalacqua ◽  
Marco Pedrazzi ◽  
Sabina Ledda ◽  
Mauro Patrone ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Activation Loop ◽  
Kinase Activation ◽  
Kinase C ◽  
Intracellular Localisation

scholarly journals Regulation of cytosolic free calcium concentration by intrasynaptic mitochondria.

1992 ◽  
Vol 3 (2) ◽  
pp. 235-248 ◽  
Author(s):  
A Martínez-Serrano ◽  
J Satrústegui
Keyword(s):  
Calcium Concentration ◽  
Adenine Nucleotides ◽  
Free Calcium ◽  
Nerve Terminals ◽  
Cytosolic Free Calcium ◽  
Free Calcium Concentration ◽  
Cytosolic Free Calcium Concentration ◽  
Presynaptic Nerve Terminals

By the use of digitonin permeabilized presynaptic nerve terminals (synaptosomes), we have found that intrasynaptic mitochondria, when studied "in situ," i.e., surrounded by their cytosolic environment, are able to buffer calcium in a range of calcium concentrations close to those usually present in the cytosol of resting synaptosomes. Adenine nucleotides and polyamines, which are usually lost during isolation of mitochondria, greatly improve the calcium-sequestering activity of mitochondria in permeabilized synaptosomes. The hypothesis that the mitochondria contributes to calcium homeostasis at low resting cytosolic free calcium concentration ([Ca2+]i) in synaptosomes has been tested; it has been found that in fact this is the case. Intrasynaptic mitochondria actively accumulates calcium at [Ca2+]i around 10(-7) M, and this activity is necessary for the regulation of [Ca2+]i. When compared with other membrane-limited calcium pools, it was found that depending on external concentration the calcium pool mobilized from mitochondria is similar or even greater than the IP3- or caffeine-sensitive calcium pools. In summary, the results presented argue in favor of a more prominent role of mitochondria in regulating [Ca2+]i in presynaptic nerve terminals, a role that should be reconsidered for other cellular types in light of the present evidence.

The role of cytosolic free calcium in the regulation of pyruvate dehydrogenase in synaptosomes

1994 ◽  
Vol 19 (1) ◽  
pp. 89-95 ◽  
Author(s):  
H. M. Huang ◽  
L. Toral-Barza ◽  
K. F. R. Sheu ◽  
G. E. Gibson
Keyword(s):  
Pyruvate Dehydrogenase ◽  
Free Calcium ◽  
Cytosolic Free Calcium

Carbachol inhibits stimulant-induced increases in fundic D-cell cytosolic Ca2+ concentration

1989 ◽  
Vol 257 (2) ◽  
pp. G308-G312 ◽  
Author(s):  
T. Chiba ◽  
T. Fujita ◽  
T. Yamada
Keyword(s):  
Pertussis Toxin ◽  
Gastric Fundus ◽  
Free Calcium ◽  
Guanine Nucleotide ◽  
Cytosolic Free Calcium ◽  
Guanine Nucleotide Binding Protein ◽  
Kinase C ◽  
D Cell ◽  
Guanine Nucleotide Binding ◽  
D Cells

We undertook these studies to examine the mechanisms by which carbachol inhibits somatostatin release. For these studies, we utilized cultured D-cells isolated from the canine gastric fundus. Carbachol inhibited somatostatin release induced by both pentagastrin and 12-O-tetradecanoyl-phorbol-13-acetate but did not alter the redistribution of protein kinase C induced by these agents. In contrast, carbachol diminished the increase in D-cell cytosolic free calcium levels ([Ca2+]i) induced by pentagastrin, and this effect was no longer evident after pretreatment of D-cells with pertussis toxin. Although carbachol by itself had no effect on [Ca2+]i, after pretreatment of D-cells with pertussis toxin, carbachol both enhanced [Ca2+]i and stimulated somatostatin release. These data indicate that carbachol activates signals in D-cells that result in both increase and decrease in [Ca2+]i. The latter effect, which appears to be mediated via a pertussis toxin-sensitive guanine nucleotide binding protein, may be one mechanism responsible for cholinergic inhibition of somatostatin release.

Role of cytosolic free calcium in the reorientation of pollen tube growth

1994 ◽  
Vol 5 (3) ◽  
pp. 331-341 ◽  
Author(s):  
Rui Malho ◽  
Nick D. Read ◽  
M. Salome Pais ◽  
Anthony J. Trewavas
Keyword(s):  
Pollen Tube ◽  
Pollen Tube Growth ◽  
Tube Growth ◽  
Free Calcium ◽  
Cytosolic Free Calcium
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