Adenylate Cyclase Toxin: One of the virulence factors produced by virulent BORDETELLA organisms. It is a bifunctional protein with both ADENYLYL CYCLASES and hemolysin components.Bordetella pertussis: A species of gram-negative, aerobic bacteria that is the causative agent of WHOOPING COUGH. Its cells are minute coccobacilli that are surrounded by a slime sheath.Adenylate Cyclase: An enzyme of the lyase class that catalyzes the formation of CYCLIC AMP and pyrophosphate from ATP. EC 4.6.1.1.Virulence Factors, Bordetella: A set of BACTERIAL ADHESINS and TOXINS, BIOLOGICAL produced by BORDETELLA organisms that determine the pathogenesis of BORDETELLA INFECTIONS, such as WHOOPING COUGH. They include filamentous hemagglutinin; FIMBRIAE PROTEINS; pertactin; PERTUSSIS TOXIN; ADENYLATE CYCLASE TOXIN; dermonecrotic toxin; tracheal cytotoxin; Bordetella LIPOPOLYSACCHARIDES; and tracheal colonization factor.Bordetella bronchiseptica: A species of BORDETELLA that is parasitic and pathogenic. It is found in the respiratory tract of domestic and wild mammalian animals and can be transmitted from animals to man. It is a common cause of bronchopneumonia in lower animals.Bordetella Infections: Infections with bacteria of the genus BORDETELLA.Hemolysis: The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.Whooping Cough: A respiratory infection caused by BORDETELLA PERTUSSIS and characterized by paroxysmal coughing ending in a prolonged crowing intake of breath.Cyclic AMP: An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.Bordetella: A genus of gram-negative, aerobic bacteria whose cells are minute coccobacilli. It consists of both parasitic and pathogenic species.Antigens, CD11b: A CD antigen that contains a conserved I domain which is involved in ligand binding. When combined with CD18 the two subunits form MACROPHAGE-1 ANTIGEN.Pertussis Toxin: One of the virulence factors produced by BORDETELLA PERTUSSIS. It is a multimeric protein composed of five subunits S1 - S5. S1 contains mono ADPribose transferase activity.Sheep: Any of the ruminant mammals with curved horns in the genus Ovis, family Bovidae. They possess lachrymal grooves and interdigital glands, which are absent in GOATS.Hemolysin Proteins: Proteins from BACTERIA and FUNGI that are soluble enough to be secreted to target ERYTHROCYTES and insert into the membrane to form beta-barrel pores. Biosynthesis may be regulated by HEMOLYSIN FACTORS.Antigens, CD18: Cell-surface glycoprotein beta-chains that are non-covalently linked to specific alpha-chains of the CD11 family of leukocyte-adhesion molecules (RECEPTORS, LEUKOCYTE-ADHESION). A defect in the gene encoding CD18 causes LEUKOCYTE-ADHESION DEFICIENCY SYNDROME.Bacterial Toxins: Toxic substances formed in or elaborated by bacteria; they are usually proteins with high molecular weight and antigenicity; some are used as antibiotics and some to skin test for the presence of or susceptibility to certain diseases.Cholera Toxin: An ENTEROTOXIN from VIBRIO CHOLERAE. It consists of two major protomers, the heavy (H) or A subunit and the B protomer which consists of 5 light (L) or B subunits. The catalytic A subunit is proteolytically cleaved into fragments A1 and A2. The A1 fragment is a MONO(ADP-RIBOSE) TRANSFERASE. The B protomer binds cholera toxin to intestinal epithelial cells, and facilitates the uptake of the A1 fragment. The A1 catalyzed transfer of ADP-RIBOSE to the alpha subunits of heterotrimeric G PROTEINS activates the production of CYCLIC AMP. Increased levels of cyclic AMP are thought to modulate release of fluid and electrolytes from intestinal crypt cells.Adenylate Kinase: An enzyme that catalyzes the phosphorylation of AMP to ADP in the presence of ATP or inorganic triphosphate. EC 2.7.4.3.Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2.Guanylyl Imidodiphosphate: A non-hydrolyzable analog of GTP, in which the oxygen atom bridging the beta to the gamma phosphate is replaced by a nitrogen atom. It binds tightly to G-protein in the presence of Mg2+. The nucleotide is a potent stimulator of ADENYLYL CYCLASES.Colforsin: Potent activator of the adenylate cyclase system and the biosynthesis of cyclic AMP. From the plant COLEUS FORSKOHLII. Has antihypertensive, positive inotropic, platelet aggregation inhibitory, and smooth muscle relaxant activities; also lowers intraocular pressure and promotes release of hormones from the pituitary gland.Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.Bacterial Proteins: Proteins found in any species of bacterium.Pituitary Adenylate Cyclase-Activating Polypeptide: A multi-function neuropeptide that acts throughout the body by elevating intracellular cyclic AMP level via its interaction with PACAP RECEPTORS. Although first isolated from hypothalamic extracts and named for its action on the pituitary, it is widely distributed in the central and peripheral nervous systems. PACAP is important in the control of endocrine and homeostatic processes, such as secretion of pituitary and gut hormones and food intake.Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.Phagocytosis: The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).Bacillus anthracis: A species of bacteria that causes ANTHRAX in humans and animals.Guanosine Triphosphate: Guanosine 5'-(tetrahydrogen triphosphate). A guanine nucleotide containing three phosphate groups esterified to the sugar moiety.Fluorides: Inorganic salts of hydrofluoric acid, HF, in which the fluorine atom is in the -1 oxidation state. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed) Sodium and stannous salts are commonly used in dentifrices.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Isoproterenol: Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.Sodium Fluoride: A source of inorganic fluoride which is used topically to prevent dental caries.GTP-Binding Proteins: Regulatory proteins that act as molecular switches. They control a wide range of biological processes including: receptor signaling, intracellular signal transduction pathways, and protein synthesis. Their activity is regulated by factors that control their ability to bind to and hydrolyze GTP to GDP. EC 3.6.1.-.Enzyme Activation: Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.Calmodulin: A heat-stable, low-molecular-weight activator protein found mainly in the brain and heart. The binding of calcium ions to this protein allows this protein to bind to cyclic nucleotide phosphodiesterases and to adenyl cyclase with subsequent activation. Thereby this protein modulates cyclic AMP and cyclic GMP levels.Receptors, Adrenergic, beta: One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.Alprostadil: A potent vasodilator agent that increases peripheral blood flow.Kinetics: The rate dynamics in chemical or physical systems.Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Adenosine Diphosphate Ribose: An ester formed between the aldehydic carbon of RIBOSE and the terminal phosphate of ADENOSINE DIPHOSPHATE. It is produced by the hydrolysis of nicotinamide-adenine dinucleotide (NAD) by a variety of enzymes, some of which transfer an ADP-ribosyl group to target proteins.T-2 Toxin: A potent mycotoxin produced in feedstuffs by several species of the genus FUSARIUM. It elicits a severe inflammatory reaction in animals and has teratogenic effects.Prostaglandins E: (11 alpha,13E,15S)-11,15-Dihydroxy-9-oxoprost-13-en-1-oic acid (PGE(1)); (5Z,11 alpha,13E,15S)-11,15-dihydroxy-9-oxoprosta-5,13-dien-1-oic acid (PGE(2)); and (5Z,11 alpha,13E,15S,17Z)-11,15-dihydroxy-9-oxoprosta-5,13,17-trien-1-oic acid (PGE(3)). Three of the six naturally occurring prostaglandins. They are considered primary in that no one is derived from another in living organisms. Originally isolated from sheep seminal fluid and vesicles, they are found in many organs and tissues and play a major role in mediating various physiological activities.Guanine Nucleotides1-Methyl-3-isobutylxanthine: A potent cyclic nucleotide phosphodiesterase inhibitor; due to this action, the compound increases cyclic AMP and cyclic GMP in tissue and thereby activates CYCLIC NUCLEOTIDE-REGULATED PROTEIN KINASESReceptors, Adrenergic: Cell-surface proteins that bind epinephrine and/or norepinephrine with high affinity and trigger intracellular changes. The two major classes of adrenergic receptors, alpha and beta, were originally discriminated based on their cellular actions but now are distinguished by their relative affinity for characteristic synthetic ligands. Adrenergic receptors may also be classified according to the subtypes of G-proteins with which they bind; this scheme does not respect the alpha-beta distinction.Thionucleotides: Nucleotides in which the base moiety is substituted with one or more sulfur atoms.Dideoxyadenosine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is an inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal side effect is nephrotoxicity. In vivo, dideoxyadenosine is rapidly metabolized to DIDANOSINE (ddI) by enzymatic deamination; ddI is then converted to dideoxyinosine monophosphate and ultimately to dideoxyadenosine triphosphate, the putative active metabolite.
(1/644) Probing the function of Bordetella bronchiseptica adenylate cyclase toxin by manipulating host immunity.

We have examined the role of adenylate cyclase-hemolysin (CyaA) by constructing an in-frame deletion in the Bordetella bronchiseptica cyaA structural gene and comparing wild-type and cyaA deletion strains in natural host infection models. Both the wild-type strain RB50 and its adenylate cyclase toxin deletion (DeltacyaA) derivative efficiently establish persistent infections in rabbits, rats, and mice following low-dose inoculation. In contrast, an inoculation protocol that seeds the lower respiratory tract revealed significant differences in bacterial numbers and in polymorphonuclear neutrophil recruitment in the lungs from days 5 to 12 postinoculation. We next explored the effects of disarming specific aspects of the immune system on the relative phenotypes of wild-type and DeltacyaA bacteria. SCID, SCID-beige, or RAG-1(-/-) mice succumbed to lethal systemic infection following high- or low-dose intranasal inoculation with the wild-type strain but not the DeltacyaA mutant. Mice rendered neutropenic by treatment with cyclophosphamide or by knockout mutation in the granulocyte colony-stimulating factor locus were highly susceptible to lethal infection by either wild-type or DeltacyaA strains. These results reveal the significant role played by neutrophils early in B. bronchiseptica infection and by acquired immunity at later time points and suggest that phagocytic cells are a primary in vivo target of the Bordetella adenylate cyclase toxin.  (+info)

(2/644) Distinct roles for Galphai2, Galphai3, and Gbeta gamma in modulation offorskolin- or Gs-mediated cAMP accumulation and calcium mobilization by dopamine D2S receptors.

Previous studies have shown that a single G protein-coupled receptor can regulate different effector systems by signaling through multiple subtypes of heterotrimeric G proteins. In LD2S fibroblast cells, the dopamine D2S receptor couples to pertussis toxin (PTX)-sensitive Gi/Go proteins to inhibit forskolin- or prostaglandin E1-stimulated cAMP production and to stimulate calcium mobilization. To analyze the role of distinct Galphai/o protein subtypes, LD2S cells were stably transfected with a series of PTX-insensitive Galphai/o protein Cys --> Ser point mutants and assayed for D2S receptor signaling after PTX treatment. The level of expression of the transfected Galpha mutant subunits was similar to the endogenous level of the most abundant Galphai/o proteins (Galphao, Galphai3). D2S receptor-mediated inhibition of forskolin-stimulated cAMP production was retained only in clones expressing mutant Galphai2. In contrast, the D2S receptor utilized Galphai3 to inhibit PGE1-induced (Gs-coupled) enhancement of cAMP production. Following stable or transient transfection, no single or pair set of mutant Galphai/o subtypes rescued the D2S-mediated calcium response following PTX pretreatment. On the other hand, in LD2S cells stably transfected with GRK-CT, a receptor kinase fragment that specifically antagonizes Gbeta gamma subunit activity, D2S receptor-mediated calcium mobilization was blocked. The observed specificity of Galphai2 and Galphai3 for different states of adenylyl cyclase activation suggests a higher level of specificity for interaction of Galphai subunits with forskolin- versus Gs-activated states of adenylyl cyclase than has been previously appreciated.  (+info)

(3/644) GABA(B) receptor-mediated stimulation of adenylyl cyclase activity in membranes of rat olfactory bulb.

Previous studies have shown that GABA(B) receptors facilitate cyclic AMP formation in brain slices likely through an indirect mechanism involving intracellular second messengers. In the present study, we have investigated whether a positive coupling of GABA(B) receptors to adenylyl cyclase could be detected in a cell-free preparation of rat olfactory bulb, a brain region where other Gi/Go-coupled neurotransmitter receptors have been found to stimulate the cyclase activity. The GABA(B) receptor agonist (-)-baclofen significantly increased basal adenylyl cyclase activity in membranes of the granule cell and external plexiform layers, but not in the olfactory nerve-glomerular layer. The adenylyl cyclase stimulation was therefore examined in granule cell layer membranes. The (-)-baclofen stimulation (pD2=4.53) was mimicked by 3-aminopropylphosphinic acid (pD2=4.60) and GABA (pD2=3.56), but not by (+)-baclofen, 3-aminopropylphosphonic acid, muscimol and isoguvacine. The stimulatory effect was counteracted by the GABA(B) receptor antagonists CGP 35348 (pA2=4.31), CGP 55845 A (pA2=7.0) and 2-hydroxysaclofen (pKi=4.22). Phaclofen (1 mM) was inactive. The (-)-baclofen stimulation was not affected by quinacrine, indomethacin, nordihydroguaiaretic acid and staurosporine, but was completely prevented by pertussis toxin and significantly reduced by the alpha subunit of transducin, a betagamma scavenger. The betagamma subunits of transducin stimulated the cyclase activity and this effect was not additive with that produced by (-)-baclofen. In the external plexiform and granule cell layers, but not in the olfactory nerve-glomerular layer, (-)-baclofen enhanced the adenylyl cyclase stimulation elicited by the neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP) 38. Conversely, the adenylyl cyclase activity stimulated by either forskolin or Ca2+/calmodulin-(Ca2+/CaM) was inhibited by (-)-baclofen in all the olfactory bulb layers examined. These data demonstrate that in specific layers of rat olfactory bulb activation of GABA(B) receptors enhances basal and neurotransmitter-stimulated adenylyl cyclase activities by a mechanism involving betagamma subunits of Gi/Go. This positive coupling is associated with a widespread inhibitory effect on forskolin- and Ca2+/CaM-stimulated cyclic AMP formation.  (+info)

(4/644) Signalling by CXC-chemokine receptors 1 and 2 expressed in CHO cells: a comparison of calcium mobilization, inhibition of adenylyl cyclase and stimulation of GTPgammaS binding induced by IL-8 and GROalpha.

The effect of interleukin-8 (IL-8) and growth-related oncogene alpha (GROalpha) on [35S]-guanosine 5'-O-(3-thiotriphosphate) ([35S]GTPgammaS) binding, forskolin-stimulated cyclic AMP accumulation and cytosolic calcium concentration were determined in recombinant CHO cells expressing HA-tagged CXC-chemokine receptors 1 and 2 (CXCR1 and CXCR2). Radioligand binding assays confirmed that the binding profiles of the recombinant receptors were similar to those of the native proteins. IL-8 displaced [125I]-IL-8 binding to CXCR1 and CXCR2 with pKi values of 8.89+/-0.05 and 9.27+/-0.03, respectively. GROalpha, a selective CXCR2 ligand, had a pKi value of 9.66+/-0.39 at CXCR2 but a pKi>8 at CXCR1. Calcium mobilization experiments were also consistent with previous reports on native receptors. Activation of both receptors resulted in stimulation of [35S]GTPgammaS binding and inhibition of adenylyl cyclase. A comparison of the functional data at CXCRI showed that a similar potency order (IL-8> >GROalpha) was obtained in all three assays. However, at CXCR2 whilst the potency orders for calcium mobilization and inhibition of adenylyl cyclase were similar (IL-8 > or = GROalpha), the order was reversed for stimulation of [35S]GTPgammaS binding (GROalpha > IL-8). All of the functional responses at both receptors were inhibited by pertussis toxin (PTX), suggesting coupling to a Gi/Go protein. However, the calcium mobilization induced by IL-8 at CXCR1 was not fully inhibited by PTX, suggesting an interaction with a G-protein of the Gq family. Our results with pertussis toxin also suggested that, in the [35S]GTPgammaS binding assay, CXCR1 displays some constitutive activity. Thus, we have characterized the binding and several functional responses at HA-tagged CXCRs 1 and 2 and have shown that their pharmacology agrees well with that of the native receptors. We also have preliminary evidence that CXCR1 displays constitutive activity in our cell line and that CXCR2 may traffic between different PTX sensitive G-proteins.  (+info)

(5/644) Cell-specific coupling of PGE2 to different transduction pathways in arginine vasopressin- and glucagon-sensitive segments of the rat renal tubule.

1. The aim of the present study was to investigate the transduction pathways elicited by prostaglandin E2 (PGE2) to inhibit hormone-stimulated adenosine 3':5'-cyclic monophosphate (cyclic AMP) accumulation in the outer medullary collecting duct (OMCD) and medullary thick ascending limb (MTAL) microdissected from the rat nephron. 2. In the OMCD, 0.3 microM PGE2 and low concentrations of Ca2+ ionophores (10 nM ionomycin or 50 nM A23187) inhibited by about 50% a same pool of arginine vasopressin (AVP)-stimulated cyclic AMP content through a same process insensitive to Bordetella pertussis toxin (PTX). 3. Sulprostone, an agonist of the EP1/EP3 subtypes of the PGE2 receptor, decreased AVP-dependent cyclic AMP accumulation in OMCD and MTAL samples. The concentration eliciting half-maximal inhibition was of about 50 nM in OMCD and 0.1 nM in MTAL. 4. In MTAL, 1 nM sulprostone and PGE2 inhibited by about 90% a same pool of AVP-dependent cyclic AMP content through a PTX-sensitive, Ca2+ -independent pathway. 5. In the OMCD, PGE2 decreased by about 50% glucagon-dependent cyclic AMP synthesis by a process sensitive to PTX and Ca2+ -independent. Sulprostone 1 nM induced the same level of inhibition. 6. These results demonstrate that PGE2 decrease hormone-dependent cyclic AMP accumulation through a G(alpha)i-mediated inhibition of adenylyl cyclase activity in MTAL cells and glucagon-sensitive cells of the OMCD or through a PTX-insensitive increase of intracellular Ca2+ concentration in AVP-sensitive cells of the OMCD.  (+info)

(6/644) The conserved lysine 860 in the additional fatty-acylation site of Bordetella pertussis adenylate cyclase is crucial for toxin function independently of its acylation status.

The Bordetella pertussis RTX (repeat in toxin family protein) adenylate cyclase toxin-hemolysin (ACT) acquires biological activity upon a single amide-linked palmitoylation of the epsilon-amino group of lysine 983 (Lys983) by the accessory fatty-acyltransferase CyaC. However, an additional conserved RTX acylation site can be identified in ACT at lysine 860 (Lys860), and this residue becomes palmitoylated when recombinant ACT (r-Ec-ACT) is produced together with CyaC in Escherichia coli K12. We have eliminated this additional acylation site by replacing Lys860 of ACT with arginine, leucine, and cysteine residues. Two-dimensional gel electrophoresis and microcapillary high performance liquid chromatography/tandem mass spectrometric analyses of mutant proteins confirmed that the two sites are acylated independently in vivo and that mutations of Lys860 did not affect the quantitative acylation of Lys983 by palmitoyl (C16:0) and palmitoleil (cis Delta9 C16:1) fatty-acyl groups. Nevertheless, even the most conservative substitution of lysine 860 by an arginine residue caused a 10-fold decrease of toxin activity. This resulted from a 5-fold reduction of cell association capacity and a further 2-fold reduction in cell penetration efficiency of the membrane-bound K860R toxin. These results suggest that lysine 860 plays by itself a crucial structural role in membrane insertion and translocation of the toxin, independently of its acylation status.  (+info)

(7/644) Therapy of murine tumors with recombinant Bordetella pertussis adenylate cyclase carrying a cytotoxic T cell epitope.

Bordetella pertussis secretes an invasive adenylate cyclase toxin, CyaA, that is able to deliver its N-terminal catalytic domain into the cytosol of eukaryotic target cells directly through the cytoplasmic membrane. We have shown previously that recombinant CyaA can be used to deliver viral CD8+ T cell epitopes to the MHC-class I presentation pathway to trigger specific CTL responses in vivo. In the present study, we show that mice immunized with a detoxified but still invasive CyaA carrying a CD8+ T cell epitope of OVA developed strong epitope-specific CTL responses, which kill tumor cells expressing this Ag. Treating mice with this recombinant molecule after the graft of melanoma cells expressing OVA induced a strong survival advantage compared with control animals. To our knowledge, this study represents the first demonstration that a nonreplicative and nontoxic vector carrying a single CTL epitope can stimulate efficient protective and therapeutic antitumor immunity.  (+info)

(8/644) Activation of adenylate cyclase by human recombinant sst5 receptors expressed in CHO-K1 cells and involvement of Galphas proteins.

1. The coupling of the human somatostatin sst5 receptor recombinantly expressed in Chinese hamster ovary (CHO-K1) cells to adenylate cyclase was investigated using receptor selective ligands. 2. Forskolin (10 microM)-stimulated adenosine 3': 5'-cyclic monophosphate (cyclic AMP) accumulation was inhibited by somatostatin-14 and a number of receptor-selective agonists with a rank order of agonist potency typical of the sst5 receptor. L-362,855 and BIM-23056 behaved as full agonists. At higher somatostatin-14 concentrations there was sub-maximal inhibition resulting in a bell-shaped concentration-effect relationship. Pertussis toxin (PTx; 100 ng ml(-1), 18 h) pre-treatment abolished agonist-mediated inhibition of cyclic AMP accumulation and markedly enhanced stimulation of cyclic AMP at higher agonist concentrations. 3. The concentration of prostaglandin E2 (PGE2) in the incubation media was raised 14 fold by 1 microM somatostatin-14 but was insufficient to stimulate adenylate cyclase activity via endogenous prostanoid receptors. 4. Pre-treatment with cholera toxin (ChTx; 20 microg ml(-1), 18 h) markedly inhibited sst5 receptor-mediated increases in cyclic AMP formation in intact cells. Somatostatin-14-stimulated cyclic AMP accumulation was also observed in sst5 receptor containing CHO-K1 membranes and was inhibited by the synthetic peptide Galphasacetyl-354-372-amide (100 microM) by 65.9+/-3.5%, implicating a Galphas protein involvement in this response. 5. Activation of Galphas proteins by somatostatin-14 could be demonstrated with [35S]-guanosine 5'-[gamma-thio]triphosphate ([35S]-GTPgammaS) binding and subsequent immunoprecipitation of 35S labelled Galphas proteins with anti-Galphas serum. 6. These data show that the sst5 receptor is very efficiently coupled in a negative manner to adenylate cyclase. However, at higher agonist concentrations the receptor can also mediate activation of adenylate cyclase by a mechanism apparently involving Galphas protein activation.  (+info)

*  Pertussis toxin
Bagley K, Abdelwahab S, Tuskan R, Fouts T, Lewis G (2002). "Pertussis toxin and the adenylate cyclase toxin from Bordetella ... Carbonetti NH (2010). "Pertussis toxin and adenylate cyclase toxin: key virulence factors of Bordetella pertussis and cell ... The Gi subunits remain locked in their GDP-bound, inactive state, thus unable to inhibit adenylate cyclase activity, leading to ... Pertussis toxin is an exotoxin with six subunits (named S1 through S5-each complex contains two copies of S4). The subunits are ...
*  Bordetella
One of the most important of the regulated toxins is adenylate cyclase toxin, which aids in the evasion of innate immunity. The ... Gray MC, Donato GM, Jones FR, Kim T, Hewlett EL (2004). "Newly secreted adenylate cyclase toxin is responsible for intoxication ... Hewlett EL, Donato GM, Gray MC (2006). "Macrophage cytotoxicity produced by adenylate cyclase toxin from Bordetella pertussis: ... Recently discovered activities of adenylate cyclase toxin, including transmembrane pore formation and stimulation of calcium ...
*  CyaA
Carbonetti NH, Artamonova GV, Andreasen C, Bushar N (May 2005). "Pertussis toxin and adenylate cyclase toxin provide a one-two ... Ladant D, Ullmann A (April 1999). "Bordatella pertussis adenylate cyclase: a toxin with multiple talents". Trends Microbiol. 7 ... "The adenylate cyclase toxin of Bordetella pertussis binds to target cells via the alpha(M)beta(2) integrin (CD11b/CD18)". J. ... Bifunctional hemolysin/adenylate cyclase is a protein that in B. pertussis (the bacteria that causes whooping cough) is encoded ...
*  RTX toxin
"Membrane restructuring by Bordetella pertussis adenylate cyclase toxin, a member of the RTX toxin family". Journal of ... Adenylate cyclase toxin (ACT or CyaA), is a primary virulence factor in Bordetella pertussis. CyaA is a multifunctional RTX ... The C-terminal domain of the adenylate cyclase toxin (ACT or CyaA; TC# 1.C.11.1.4) of Bordetella pertussis forms a small cation ... Bumba, Ladislav; Jiri Masin; Radovan Fiser; Peter Sebo (2010). "Bordetella Adenylate Cyclase Toxin Mobilizes Its b2 Integrin ...
*  List of MeSH codes (D08)
... adenylate cyclase MeSH D08.811.520.650.200.040 --- adenylate cyclase toxin MeSH D08.811.520.650.600 --- guanylate cyclase MeSH ... adp-ribosyl cyclase MeSH D08.811.913.400.725.115.680 --- pertussis toxin MeSH D08.811.913.400.725.115.690 --- poly(adp-ribose) ... cholera toxin MeSH D08.811.913.400.725.115.220 --- diphtheria toxin MeSH D08.811.913.400.725.115.660 --- nad+ nucleosidase MeSH ... adp-ribosyl cyclase MeSH D08.811.277.450.737.400.060.500 --- antigens, cd38 MeSH D08.811.277.450.770 --- oligo-1,6-glucosidase ...
*  AB5 toxin
Carbonetti, N. H. (2010). "Pertussis toxin and adenylate cyclase toxin: Key virulence factors of Bordetella pertussis and cell ... AB5 Toxins Biochemistry Cholera toxin Pertussis toxin Shiga toxin Subtilase Le Nours, J.; Paton, A. W.; Byres, E.; Troy, S.; ... Cholera toxin, pertussis toxin, and shiga toxin all have their targets in the cytosol of the cell. After their B subunit binds ... Cholera toxin, shiga toxin, and SubAB toxin all have B subunits that are made up of five identical protein components, meaning ...
*  List of MeSH codes (D23)
... tetanus toxin MeSH D23.946.123.946 --- virulence factors, bordetella MeSH D23.946.123.946.040 --- adenylate cyclase toxin MeSH ... adenylate cyclase toxin MeSH D23.946.896.980.690 --- pertussis toxin. ... shiga toxins MeSH D23.946.123.794.100 --- shiga-like toxin i MeSH D23.946.123.794.124 --- shiga-like toxin ii MeSH D23.946. ... shiga toxins MeSH D23.946.330.575.120 --- shiga-like toxin i MeSH D23.946.330.575.124 --- shiga-like toxin ii MeSH D23.946. ...
*  Alfred G. Gilman
"Requirements for cholera toxin-dependent ADP-ribosylation of the purified regulatory component of adenylate cyclase". The ... Haga, T; Ross, EM; Anderson, HJ; Gilman, AG (1977). "Adenylate cyclase permanently uncoupled from hormone receptors in a novel ... Haga, T; Haga, K; Gilman, AG (1977). "Hydrodynamic properties of the beta-adrenergic receptor and adenylate cyclase from wild ... Gilman, AG (1984). "G proteins and dual control of adenylate cyclase". Cell. 36 (3): 577-9. doi:10.1016/0092-8674(84)90336-2. ...
*  Cholera toxin
Subunit B binds while subunit A activates the G protein which activates adenylate cyclase. The three-dimensional structure of ... Cholera toxin acts by the following mechanism: First, the B subunit ring of the cholera toxin binds to GM1 gangliosides on the ... The toxin then most likely binds to other types of glycans attached to proteins instead of lipids. Once bound, the entire toxin ... Cholera toxin was discovered in 1959 by Late Prof. Sambhu Nath De at Kolkata (India) The cholera toxin is an oligomeric complex ...
*  Anthrax toxin
EF acts as a Ca2+ and calmodulin dependent adenylate cyclase that greatly increases the level of cAMP in the cell. This ... the tripartite protein toxin, called anthrax toxin. Anthrax toxin is a mixture of three protein components: (i) protective ... The toxin was first discovered by Harry Smith in 1954. Anthrax toxin is composed of a cell-binding protein, known as protective ... The toxin may even induce cell lysis, as is observed for macrophage cells. Anthrax toxin allows the bacteria to evade the ...
*  Bordetella pertussis
The toxin, known as pertussis toxin (or PTx), inhibits G protein coupling that regulates an adenylate cyclase-mediated ... Its virulence factors include pertussis toxin, filamentous hæmagglutinin, pertactin, fimbria, and tracheal cytotoxin. The ...
*  Killer yeast
The mechanism of action appears to be the inhibition of adenylate cyclase in sensitive cells. Affected cells are arrested in G1 ... Breinig, Sendzik, Eisfeld and Schmitt (2006) showed that K28 toxin is neutralized in toxin-expressing cells by the α chain in ... The methods were not effective at reducing toxin production in other yeast species. Many toxins are sensitive to pH levels; for ... based on their sensitivity to each toxin. This was extended by Morace et al. (1989) to use toxins to differentiate between 58 ...
*  Antoine Danchin
... of adenylate cyclases after his laboratory successfully cloned and sequenced the genes of adenylyl cyclase toxins from the ... 27:109-162 Glaser P, Ladant D, Sezer O, Pichot F, Ullmann A, Danchin A. (1988) The calmodulin-sensitive adenylate cyclase of ... from the structure and function of adenylate cyclase, to modelisation of learning in the nervous system and the early ... Structural homology between virulence-associated bacterial adenylate cyclases. Gene. 71:293-298 Danchin A. (2002) Not every ...
*  Bacillus anthracis
The organism also produces three plasmid-coded exotoxins: edema factor, a calmodulin-dependent adenylate cyclase, causes ... The lethal toxin is a combination of PA with LF and the edema toxin is a combination of PA with EF. The PAI also contains genes ... it forms a calmodulin-dependent adenylate cyclase exotoxin known as anthrax edema factor, along with anthrax lethal factor. It ... The enterotoxins and virulence factors are encoded on the chromosome, while the emetic toxin is encoded on a 270-kb plasmid, ...
*  Exotoxin
For example, Cholera toxin ADP-ribosylates, thereby activating tissue adenylate cyclase to increase the concentration of cAMP, ... Toxins of this type include cholera toxin, pertussis toxin, Shiga toxin and heat-liable enterotoxin from E. coli. Once in the ... AB5 toxin) By domain architecture of the toxin (for example, polymorphic toxins) By the ability of the toxin to endure in ... Membrane-damaging toxins can be divided into two categories, the channel-forming toxins and toxins that function as enzymes ...
*  GTPase
They always use the activation of adenylate cyclase as the next step in the signal chain. The s stands for stimulation. Their ... Most Gi protein family members can be inhibited by the pertussis toxin of Bordetella pertussis. Gq family. These proteins ... Among the target molecules of the active GTPase are adenylate cyclase and ion channels. The heterotrimeric G proteins can be ... The i stands for inhibition of the adenylate cyclase; another effector molecule for this protein family is phospholipase C. ...
*  Heat-labile enterotoxin
... through ADP-ribosylation of the alpha-subunit of a Gs protein leading to the constitutive activation of adenylate cyclase. ... In addition to its effects on chloride secretion, which involve the same steps as the effects of cholera toxin, heat-labile ... Heat-labile enterotoxin is a type of labile toxin found in Escherichia coli and Bacillus cereus. The heat-labile enterotoxin is ... Mudrak B and Kuehn MJ (2010). "Heat-labile enterotoxin: Beyond GM1 binding". Toxins. 2 (6): 1445-1470. doi:10.3390/ ...
*  Acetylcholine receptor
The alpha subunit of the G-protein deactivates adenylate cyclase while the beta-gamma subunit activates the K-channels and ... Nicotinic acetylcholine receptors can be blocked by curare, hexamethonium and toxins present in the venoms of snakes and ...
*  GM1
This will lock it in the active state and it will continuously stimulate adenylate cyclase. The sustained adenylate cyclase ... The bacteria Vibrio cholerae produces a multimeric toxin called the cholera toxin. The secreted toxin attaches to the surface ... Besides its function in the physiology of the brain, GM1 acts as the site of binding for both Cholera toxin and E. coli heat- ... The A1 subunit of this toxin will gain entry to intestinal epithelial cells with the assistance of the B subunit via the GM1 ...
*  Ira Pastan
... showed that antibodies from the serum of patients with hyperthyroidism specifically activated thyroid gland adenylate cyclase, ... is attached to a potent bacterial toxin. Pastan, with his colleague Jesse Roth, was the first to clearly demonstrate the ... Nature 228: 864-866, 1970 Levey, G.S. and Pastan, I.: Activation of thyroid adenyl cyclase by long-acting thyroid stimulator. ... Specific binding of ACTH-125I and its relation to adenyl cyclase. Proc. Natl. Acad. Sci. USA 65: 745-752, 1970 Lefkowitz, R., ...
*  Anthrax
Edema factor is a calmodulin-dependent adenylate cyclase. Adenylate cyclase catalyzes the conversion of ATP into cyclic AMP ( ... Protective antigen combines with these other two factors to form lethal toxin and edema toxin, respectively. These toxins are ... PA plus LF produces lethal toxin, and PA plus EF produces edema toxin. These toxins cause death and tissue swelling (edema), ... and the tripartite protein toxin, called anthrax toxin. Anthrax toxin is a mixture of three protein components: protective ...
*  Cannabinoid receptor type 1
Alternatively, in some rare cases CB1 receptor activation may be coupled to Gs proteins, which stimulate adenylate cyclase. ... stereoselective and pertussis toxin-sensitive manner. The CB1 receptor is activated by cannabinoids, generated naturally inside ... adenylate cyclase, and increases mitogen-activated protein kinase (MAP kinase) concentration. ...
*  Neurotrophic factors
... pituitary adenylate cyclase-activating peptide (PACAP), interleukin-1 (IL-1), interleukin-2 (IL-2), interleukin-3 (IL-3), ... Specifically, studies have shown GDNF plays a protective role against MPTP toxins for DA neurons. It has also been detected in ...
*  Psychosis
The increased adenylate cyclase activity affects genetic expression in the nerve cell, which takes time. Hence antipsychotic ... Testing may be done to check for central nervous system diseases, toxins, or other health problems as a cause. Treatment may ... While dopamine receptor D2 suppresses adenylate cyclase activity, the D1 receptor increases it. If D2-blocking drugs are ... Tests may be done to exclude substance use, medication, toxins, surgical complications, or other medical illnesses. Delirium ...
*  Formyl peptide receptor 2
Pituitary adenylate cyclase-activating polypeptide 27 (pro-inflammatory). Eicosanoid receptor Formyl peptide receptor Lipoxin ... "The formylpeptide chemoattractant receptor copurifies with a GTP-binding protein containing a distinct 40-kDa pertussis toxin ...
*  Κ-opioid receptor
... and kappa-opioid receptor-mediated inhibition of neurotransmitter release and adenylate cyclase activity in rat brain slices: ... kappa opioid receptor expressed on the mouse R1.1 thymoma cell line is coupled to adenylyl cyclase through a pertussis toxin- ... "Relationship between kappa 1 opioid receptor binding and inhibition of adenylyl cyclase in guinea pig brain membranes". ...
Adenylate cyclase toxin from Bordetella pertussis synergises with lipopolysaccharide to promote innate IL-10 production and...  Adenylate cyclase toxin from Bordetella pertussis synergises with lipopolysaccharide to promote innate IL-10 production and...
Ross, P.J., Lavelle, E.C., Mills, K.H.G. and A.P. Boyd `Adenylate cyclase toxin from Bordetella pertussis synergises with ... Adenylate cyclase toxin from Bordetella pertussis synergises with lipopolysaccharide to promote innate IL-10 production and ... Adenylate cyclase toxin (CyaA) from Bordetella pertussis can subvert host immune responses allowing bacterial colonization. ... Adenylate Cyclase Toxin from Bordetella pertussis Synergizes with Lipopolysaccharide To Promote Innate Interleukin-10 ...
more infohttp://www.tara.tcd.ie/handle/2262/33327
Bordetella adenylate cyclase toxin: the role of cell interaction in toxin functio - Joshua Eby  Bordetella adenylate cyclase toxin: the role of cell interaction in toxin functio - Joshua Eby
AC toxin) is necessary for disease caused by Bordetella pertussis, which has reemerged in the United States over the last two ... Bordetella adenylate cyclase toxin: the role of cell interaction in toxin functio Eby, Joshua Clark University of Virginia, ... The toxin molecule is a unique hybrid of an adenylate cyclase enzyme and a binding domain homologous to the repeats-in-toxin ( ... Bordetella adenylate cyclase toxin: the role of cell interaction in toxin functio. Eby, Joshua Clark / University of Virginia. ...
more infohttp://grantome.com/grant/NIH/K08-AI081900-05
Ca2 Influx and Tyrosine Kinases Trigger Bordetella Adenylate Cyclase Toxin ACT Endocytosis. Cell Physiology and Expression of...  Ca2 Influx and Tyrosine Kinases Trigger Bordetella Adenylate Cyclase Toxin ACT Endocytosis. Cell Physiology and Expression of...
Ca2 Influx and Tyrosine Kinases Trigger Bordetella Adenylate Cyclase Toxin ACT Endocytosis. Cell Physiology and Expression of ... Ca2 Influx and Tyrosine Kinases Trigger Bordetella Adenylate Cyclase Toxin ACT Endocytosis. Cell Physiology and Expression of ... Ca2 Influx and Tyrosine Kinases Trigger Bordetella Adenylate Cyclase Toxin ACT Endocytosis. Cell Physiology and Expression of ... This pathogenic bacterium produces a unique adenylate cyclase toxin ACT which enters human phagocytes and catalyzes the ...
more infohttp://libros.duhnnae.com/2017/jun8/149829571451-Ca2-Influx-and-Tyrosine-Kinases-Trigger-Bordetella-Adenylate-Cyclase-Toxin-ACT-Endocytosis-Cell-Physiology-and-Expression-of-the-CD11b-CD18-Integrin.php
Effects of pertussis toxin on adenylate cyclase responses to prostaglandin E2 and calcitonin in human breast cancer cells |...  Effects of pertussis toxin on adenylate cyclase responses to prostaglandin E2 and calcitonin in human breast cancer cells |...
Effects of pertussis toxin on adenylate cyclase responses to prostaglandin E2 and calcitonin in human breast cancer cells. V P ... of adenylate cyclase, there was no change in basal or calcitonin-responsive adenylate cyclase in intact cells. However, the ... Effects of pertussis toxin on adenylate cyclase responses to prostaglandin E2 and calcitonin in human breast cancer cells ... Effects of pertussis toxin on adenylate cyclase responses to prostaglandin E2 and calcitonin in human breast cancer cells ...
more infohttp://www.biochemj.org/content/224/2/371
Bordetella - Wikipedia  Bordetella - Wikipedia
One of the most important of the regulated toxins is adenylate cyclase toxin, which aids in the evasion of innate immunity. The ... Gray MC, Donato GM, Jones FR, Kim T, Hewlett EL (2004). "Newly secreted adenylate cyclase toxin is responsible for intoxication ... Hewlett EL, Donato GM, Gray MC (2006). "Macrophage cytotoxicity produced by adenylate cyclase toxin from Bordetella pertussis: ... Recently discovered activities of adenylate cyclase toxin, including transmembrane pore formation and stimulation of calcium ...
more infohttps://en.wikipedia.org/wiki/Bordetella
5-hydroxytryptamine release into human jejunum by cholera toxin. | Gut  5-hydroxytryptamine release into human jejunum by cholera toxin. | Gut
BACKGROUND: Cholera toxin produces intestinal secretion by activation of the adenylate cyclase complex. However animal studies ... METHODS: A closed 10 cm segment of upper jejunum was exposed to 15 micrograms of cholera toxin for two hours prior to closed ... RESULTS: In contrast with controls, all subjects secreted fluid in response to cholera toxin, median-2.1 ml/cm/h (interquartile ... After exposure to cholera toxin median urinary 5-hydroxyindoleacetic acid was 5.7 (4.1 to 6.3), which was similar to controls ...
more infohttp://gut.bmj.com/content/39/4/528
Pituitary adenylate cyclase-activating polypeptide (PACAP) has neuroprotective function in dopamine-based neurodegeneration...  Pituitary adenylate cyclase-activating polypeptide (PACAP) has neuroprotective function in dopamine-based neurodegeneration...
Following the toxin treatments a significant increase in the MB-COMT level was observed in both models and the increased MB- ... Pituitary adenylate cyclase-activating polypeptide (PACAP) has neuroprotective function in dopamine-based neurodegeneration ... Pituitary adenylate cyclase-activating polypeptide (PACAP) has neuroprotective function in dopamine-based neurodegeneration ... Pituitary adenylate cyclase-activating polypeptide (PACAP) has neuroprotective function in dopamine-based neurodegeneration ...
more infohttp://dmm.biologists.org/content/early/2016/12/14/dmm.027185
Bordetella pertussis adenylate cyclase. Penetration into host...  Bordetella pertussis adenylate cyclase. Penetration into host...
Bordetella pertussis adenylate cyclase. Penetration into host cells.: Exposure of Chinese hamster ovary, mouse adrenal cortex ... Inhibitors of the effect of diphtheria toxin, such as NH4Cl, methylamine, chloroquine or monensin, have no inhibitory effect on ... In Y-1 adrenal cells the urea-extract adenylate cyclase stimulates steroidogenesis. Anti-(B. pertussis) antibodies inhibit ... THP-1 and U-937 cells and human erythrocytes to adenylate-cyclase-containing urea extracts of Bordetella pertussis (strain 114 ...
more infohttps://www.mysciencework.com/publication/show/bordetella-pertussis-adenylate-cyclase-penetration-host-cells-b9d90363
adenocarcinoma of pituitary gland 2005:2010[pubdate] *count=100 - BioMedLib™ search engine  adenocarcinoma of pituitary gland 2005:2010[pubdate] *count=100 - BioMedLib™ search engine
Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide. Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, ... Chemical-registry-number] 0 / Neuromuscular Agents; EC 3.4.24.69 / Botulinum Toxins, Type A ... Pituitary Adenylate Cyclase-Activating Polypeptide; 0 / Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I; ...
more infohttp://www.bmlsearch.com/?kwr=adenocarcinoma+of+pituitary+gland+2005:2010%5Bpubdate%5D&cxts=100&stmp=b0
Plus it  Plus it
... pituitary adenylyl cyclase-activating polypeptide; AC, adenylate cyclase; PLC, phospholipase C; PLA2, phospholipase A2; 5-HT, 5 ... a calcium response mediated by a promiscuous Gα15 protein and a pertussis toxin-resistant [35S]GTPγS binding response mediated ... The agonists (PACAP-27 and -38) stimulated adenylate cyclase (AC) with equal potencies, but only PACAP-38 could invoke the ... A ternary complex model explains the agonist-specific binding properties of the adenylate cyclase-coupled β-adrenergic receptor ...
more infohttp://pharmrev.aspetjournals.org/content/57/2/147
Mechanism of action of adenylate cyclase toxin on immune function of dendritic cells  Mechanism of action of adenylate cyclase toxin on immune function of dendritic cells
Abstract The adenylate cyclase toxin (CyaA) is a key virulence factor of the whooping cough agent Bordetella pertussis. CyaA ... Mechanism of action of adenylate cyclase toxin on immune function of dendritic cells. *Detail práce ... Mechanism of action of adenylate cyclase toxin on immune function of dendritic cells ... An enzymatically inactive adenylate cyclase toxoid (CyaA-AC-) has then been abundantly used as an efficient antigen delivery ...
more infohttps://is.cuni.cz/webapps/zzp/detail/90017/?lang=cs
Effect of Different Forms of Adenylate Cyclase Toxin of Bordetella pertussis on Protection Afforded by an Acellular Pertussis...  Effect of Different Forms of Adenylate Cyclase Toxin of Bordetella pertussis on Protection Afforded by an Acellular Pertussis...
Effect of Different Forms of Adenylate Cyclase Toxin of Bordetella pertussis on Protection Afforded by an Acellular Pertussis ... Effect of Different Forms of Adenylate Cyclase Toxin of Bordetella pertussis on Protection Afforded by an Acellular Pertussis ... Effect of Different Forms of Adenylate Cyclase Toxin of Bordetella pertussis on Protection Afforded by an Acellular Pertussis ... Effect of Different Forms of Adenylate Cyclase Toxin of Bordetella pertussis on Protection Afforded by an Acellular Pertussis ...
more infohttps://iai.asm.org/content/74/12/6797/figures-only
Adenylate Cyclase Toxin Mobilizes Its β Integrin Receptor into Lipid Rafts to Accomplish Translocation across Target Cell...  Adenylate Cyclase Toxin Mobilizes Its β Integrin Receptor into Lipid Rafts to Accomplish Translocation across Target Cell...
... block the entry of Bacillus anthracis adenylate cyclase toxin but not that of Bordetella pertussis adenylate cyclase toxin. ... 1990 Adenylate cyclase toxin is critical for colonization and pertussis toxin is critical for lethal infection by Bordetella ... 2004 Membrane restructuring by Bordetella pertussis adenylate cyclase toxin, a member of the RTX toxin family. J Bacteriol 186 ... 2001 Translocation-specific conformation of adenylate cyclase toxin from Bordetella pertussis inhibits toxin-mediated hemolysis ...
more infohttps://www.prolekare.cz/casopisy/plos-pathogens/2010-5/adenylate-cyclase-toxin-mobilizes-its-b-integrin-receptor-into-lipid-rafts-to-accomplish-translocation-across-target-cell-membrane-in-two-steps-46190
Bordetella pertussis adenylate cyclase toxin modulates innate and adaptive immune responses: distinct roles for acylation and...  Bordetella pertussis adenylate cyclase toxin modulates innate and adaptive immune responses: distinct roles for acylation and...
Adenylate cyclase toxin (CyaA) of Bordetella pertussis belongs to the repeat in toxin family of pore-forming toxins, which ... Boyd, A.P., Ross, P.J., Conroy, H., Mahon, N Lavelle, E.C.and Mills, K.H.G. `Bordetella pertussis adenylate cyclase toxin ... Bordetella pertussis adenylate cyclase toxin modulates innate and adaptive immune responses: distinct roles for acylation and ... Bordetella pertussis adenylate cyclase toxin modulates innate and adaptive immune responses - distinct roles for acylation and ...
more infohttp://www.tara.tcd.ie/handle/2262/33228
Purification and characterization of adenylate cyclase toxin from Bordetella pertussis.  Purification and characterization of adenylate cyclase toxin from Bordetella pertussis.
One of these factors, adenylate cyclase toxin (ACT), has been implicated to penetrate human neutrophils and macrophages and ... In order to adequately study the nature of ACT and its role in pathogenesis, it is necessary to isolate the toxin from other ...
more infohttps://repository.arizona.edu/handle/10150/184998
Alexandre Chenal - Biophysical characterization of the translocation process of Bordetella pertussis adenylate cyclase toxin...  Alexandre Chenal - Biophysical characterization of the translocation process of Bordetella pertussis adenylate cyclase toxin...
Biophysical characterization of the translocation process of Bordetella pertussis adenylate cyclase toxin CyaA. ... Originally, we principally focused on the Repeat Domain (RD) of CyaA, composed of about 40 Repeat in Toxin (RTX) motifs in ... Sotomayor-Pérez AC, Ladant D, Chenal A, Calcium-induced folding of intrinsically disordered repeat-in-toxin (RTX) motifs via ... This project aims to describe the hydrodynamic and thermodynamic properties of the CyaA toxin and the conformational changes it ...
more infohttps://research.pasteur.fr/en/project/biophysical-characterization-of-the-translocation-process-of-bordetella-pertussis-adenylate-cyclase-toxin-cyaa/
Ca2+ Influx and Tyrosine Kinases Trigger Bordetella Adenylate Cyclase Toxin (ACT) Endocytosis. Cell Physiology and Expression...  Ca2+ Influx and Tyrosine Kinases Trigger Bordetella Adenylate Cyclase Toxin (ACT) Endocytosis. Cell Physiology and Expression...
This pathogenic bacterium produces a unique adenylate cyclase toxin (ACT) which enters human phagocytes and catalyzes the ... Ca2+ Influx and Tyrosine Kinases Trigger Bordetella Adenylate Cyclase Toxin (ACT) Endocytosis. Cell Physiology and Expression ... which suggests the mounting of an anti-toxin cell repair-response, very likely involving the toxin elimination from the cell ... into the target cell appear to be common master denominators in the different endocytic strategies activated by this toxin. ...
more infohttps://addi.ehu.es/handle/10810/11378
PNAS Plus Significance Statements | PNAS  PNAS Plus Significance Statements | PNAS
Phospholipase A activity of adenylate cyclase toxin mediates translocation of its adenylate cyclase domain. David González- ... Phospholipase A activity of adenylate cyclase toxin mediates translocation of its adenylate cyclase domain ... Bordetella pertussis adenylate cyclase toxin (ACT) delivers its catalytic domain directly across the cell membrane by an ... Numerous bacterial toxins can cross cell membranes, penetrating the cytosol of their target cells, but to do so exploits ...
more infohttps://www.pnas.org/content/114/33/8683
The Comprehensive Sourcebook of Bacterial Protein Toxins - 4th Edition  The Comprehensive Sourcebook of Bacterial Protein Toxins - 4th Edition
Purchase The Comprehensive Sourcebook of Bacterial Protein Toxins - 4th Edition. Print Book & E-Book. ISBN 9780128001882, ... His other research interests include the other class II bacterial adenylate cyclase toxins, such as Edema Factor (EF) from ... Descriptions of relevant toxins as well as representative toxins of the main bacterial toxin families to allow for a better ... using as a model system a bacterial toxin, the adenylate cyclase (CyaA) produced by Bordetella pertussis, the causative agent ...
more infohttps://www.elsevier.com/books/the-comprehensive-sourcebook-of-bacterial-protein-toxins/alouf/978-0-12-800188-2
nature.com search  nature.com search
Phosphoproteomics of cAMP signaling of Bordetella adenylate cyclase toxin in mouse dendritic cells *Jakub Novák ... Rights & permissionsfor article Phosphoproteomics of cAMP signaling of ,i,Bordetella,/i, adenylate cyclase toxin in mouse ... Human CD45 is an F-component-specific receptor for the staphylococcal toxin Panton-Valentine leukocidin *Angelino T. Tromp ... Rights & permissionsfor article Human CD45 is an F-component-specific receptor for the staphylococcal toxin Panton-Valentine ...
more infohttp://www.nature.com/search?article_type=protocols,research,reviews&subject=immune-evasion&error=cookies_not_supported&code=177de14e-0c2d-4c93-bca0-e61972d90171
Reconstruction of Long Noncircumferential Tracheal or Carinal Resections with Bronchial Flaps.  Reconstruction of Long Noncircumferential Tracheal or Carinal Resections with Bronchial Flaps.
They include filamentous hemagglutinin; FIMBRIAE PROTEINS; pertactin; PERTUSSIS TOXIN; ADENYLATE CYCLASE TOXIN; dermonecrotic ... A set of BACTERIAL ADHESINS and TOXINS, BIOLOGICAL produced by BORDETELLA organisms that determine the pathogenesis of ...
more infohttps://www.bioportfolio.com/resources/pmarticle/2331910/Reconstruction-of-Long-Noncircumferential-Tracheal-or-Carinal-Resections-with-Bronchial-Flaps.html
McGrath videolaryngoscope versus Macintosh laryngoscope for tracheal intubation: A systematic review and meta-analysis with...  McGrath videolaryngoscope versus Macintosh laryngoscope for tracheal intubation: A systematic review and meta-analysis with...
They include filamentous hemagglutinin; FIMBRIAE PROTEINS; pertactin; PERTUSSIS TOXIN; ADENYLATE CYCLASE TOXIN; dermonecrotic ... A set of BACTERIAL ADHESINS and TOXINS, BIOLOGICAL produced by BORDETELLA organisms that determine the pathogenesis of ...
more infohttps://www.bioportfolio.com/resources/pmarticle/1960683/McGrath-videolaryngoscope-versus-Macintosh-laryngoscope-for-tracheal-intubation-A-systematic-review-and.html
Table of Contents - March 13, 2018, 115 (11) | PNAS  Table of Contents - March 13, 2018, 115 (11) | PNAS
Phospholipase A activity of adenylate cyclase toxin? Jiri Masin, Radim Osicka, Ladislav Bumba, and Peter Sebo ...
more infohttp://www.pnas.org/content/115/11
Gordon VM[au] - PubMed - NCBI  Gordon VM[au] - PubMed - NCBI
... block the entry of Bacillus anthracis adenylate cyclase toxin but not that of Bordetella pertussis adenylate cyclase toxin. ... Adenylate cyclase toxin from Bordetella pertussis. Conformational change associated with toxin activity. ... Hemolytic activity of adenylate cyclase toxin from Bordetella pertussis.. Ehrmann IE, Gray MC, Gordon VM, Gray LS, Hewlett EL. ... Adenylate cyclase toxins from Bacillus anthracis and Bordetella pertussis. Different processes for interaction with and entry ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed?cmd=search&term=Gordon+VM%5Bau%5D&dispmax=50
Cell proliferation, tumorogenicity, and apoptosis sub-cluster 17  Cell proliferation, tumorogenicity, and apoptosis sub-cluster 17
The adenylate cyclase toxins. Ahuja Nidhi - - 2004 Cyclic AMP is a ubiquitous messenger that integrates many processes of the ... The Clostridium botulinum C2 toxin is the prototype of the family of binary actin-ADP-ribosylating toxins. C2 toxin is composed ... Toxin binding to its receptor, guanylyl cyclase C (GC-C), results in receptor activation and the production of high ... Diverse families of adenylate cyclases and phosphodiesterases stringently regulate the intracellular concentration of cAMP. Any ...
more infohttp://www.biomedsearch.com/cluster/2/Cell-proliferation-tumorogenicity-and-apoptosis/sub-17-p7.html
  • Thereafter, the bacteria proliferate and spread further into the respiratory tract, where the secretion of toxins causes ciliostasis and facilitates the entry of bacteria to tracheal/bronchial ciliated cells. (wikipedia.org)
  • One of the first toxins to be expressed is tracheal cytotoxin, which is a disaccharide-tetrapeptide derived from peptidoglycan. (wikipedia.org)
  • The name RTX (repeats in toxin) refers to the glycine and aspartate-rich repeats located at the C-terminus of the toxin proteins, which facilitate export by a dedicated T1SS encoded within the rtx operon. (wikipedia.org)
  • The magnitude of intoxication correlates with the relative surface expression of the (32 integrin, CD11b/CD18, a receptor expressed most abundantly on neutrophils and macrophages;however, the relationship between AC toxin and CD11b/CD18 is not well defined. (grantome.com)
  • ACT-induced Ca2+ influx and activation of non-receptor Tyr kinases into the target cell appear to be common master denominators in the different endocytic strategies activated by this toxin. (duhnnae.com)
  • These studies will shed light upon the mechanism of pore formation by bacterial toxins, and the pathogenesis of disease caused by all Bordetellae. (grantome.com)
  • Here, we will characterize the basic mechanisms of cell binding by AC toxin and show that these mechanisms affect the function of the toxin and determine its role as a virulence factor. (grantome.com)
  • A major virulence factor of H. pylori is VacA, a toxin that causes massive vacuolization of epithelial cell lines in vitro and gastric epithelial erosion in vivo. (biomedsearch.com)
  • Shiga toxin is an infectious disease caused by the rod shaped Shigella dysenteriae as well as Escherichia coli (STEC), and is also known as Stx. (wikipedia.org)
  • The toxin is inactive until post-translational modification by the cis-encoded RTX toxin activator, which typically occurs within the target cell. (wikipedia.org)
  • Recently discovered activities of adenylate cyclase toxin, including transmembrane pore formation and stimulation of calcium influx, may also contribute to the intoxication of phagocytes. (wikipedia.org)
  • However, evidence has shown leukotoxic activity in the hemolysins, leading to reclassification of RTX toxin subgroups into two families: pore-forming leukotoxins (RTX-toxin family, 1.C.11.1.1) and the MARTX toxins (CCT family, 1.C.57.3.4) (multifunctional autoprocessing RTX toxins). (wikipedia.org)
  • The RTX-toxin family (TC# 1.C.11) (subfamily of RTX-toxin superfamily) is a large family of multidomain Gram-negative bacterial pore-forming exotoxins. (wikipedia.org)
  • Prior induction of an endoplasmic reticulum stress response has been associated with an increased tolerance to cellular toxins in in vitro systems, primarily involving renal and neuronal cells. (biomedsearch.com)
  • Membrane-damaging toxins exhibit hemolysin or cytolysin activity in vitro. (wikipedia.org)
  • This provides molecular details of how two structurally homologous bacterial toxins evolved divergently to bind calmodulin, an evolutionarily conserved calcium sensor. (wikipedia.org)
  • The halotolerant yeast P. membranifaciens CYC 1106 produces a unique 18 kDa killer toxin that exerts its killer activity against C. boidinii IGC 3430 only in the presence of NaCl. (biomedsearch.com)
  • Considerable progress has been made in understanding the structure, function, interaction and trafficking into cells, as well as mechanism of action of toxins. (elsevier.com)
  • Since no structural information on the RTX cytolysin moiety is available, the mechanistic details of toxin translocation across the lipid bilayer of cell membrane remain poorly understood. (prolekare.cz)
  • 2:19-30 Glaser P, Ladant D, Sezer O, Pichot F, Ullmann A, Danchin A. (1988) Structural homology between virulence-associated bacterial adenylate cyclases. (wikipedia.org)
  • Vaccination with genetically modified Shiga-like toxin IIe prevents edema disease in swine. (nih.gov)
  • Proteolytic activation of bacterial toxins by eukaryotic cells is performed by furin and by additional cellular proteases. (nih.gov)
  • Prevention of translocation by an antibody to the catalytic domain or by certain mutations will enhance the other major function of the toxin, formation of oligomeric pores which cause lysis of erythrocytes and contribute to non-apoptotic cell death of macrophages. (grantome.com)