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.Calcitonin: A peptide hormone that lowers calcium concentration in the blood. In humans, it is released by thyroid cells and acts to decrease the formation and absorptive activity of osteoclasts. Its role in regulating plasma calcium is much greater in children and in certain diseases than in normal adults.Lipopolysaccharides: Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed)Anthrax: An acute infection caused by the spore-forming bacteria BACILLUS ANTHRACIS. It commonly affects hoofed animals such as sheep and goats. Infection in humans often involves the skin (cutaneous anthrax), the lungs (inhalation anthrax), or the gastrointestinal tract. Anthrax is not contagious and can be treated with antibiotics.Anthrax Vaccines: Vaccines or candidate vaccines used to prevent ANTHRAX.Drosophila melanogaster: A species of fruit fly much used in genetics because of the large size of its chromosomes.Antigens, Bacterial: Substances elaborated by bacteria that have antigenic activity.rab GTP-Binding Proteins: A large family of MONOMERIC GTP-BINDING PROTEINS that play a key role in cellular secretory and endocytic pathways. EC 3.6.1.-.

Probing the function of Bordetella bronchiseptica adenylate cyclase toxin by manipulating host immunity. (1/644)

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)

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

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)

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

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)

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. (4/644)

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)

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

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)

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. (6/644)

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)

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

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)

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

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)

Ca2 Influx and Tyrosine Kinases Trigger Bordetella Adenylate Cyclase Toxin ACT Endocytosis. Cell Physiology and Expression of the CD11b-CD18 Integrin Major Determinants of the Entry Route. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
The adenylate cyclase toxin (AC toxin) is necessary for disease caused by Bordetella pertussis, which has reemerged in the United States over the last two decad...
Adenylate cyclase toxin (CyaA) from Bordetella pertussis can subvert host immune responses allowing bacterial colonization. Here we have examined its adjuvant and immunomodulatory properties and the possible contribution of lipopolysaccharide (LPS), known to be present in purified CyaA preparations. CyaA enhanced antigen-specific interleukin-5 (IL-5) and IL-10 production and immunoglobulin G1 antibodies to coadministered antigen in vivo. Antigen-specific CD4+-T-cell clones generated from mice immunized with antigen and CyaA had cytokine profiles characteristic of Th2 or type 1 regulatory T (Tr1) cells. Since innate immune cells direct the induction of T-cell subtypes, we examined the influence of CyaA on activation of dendritic cells (DC) and macrophages. CyaA significantly augmented LPS-induced IL-6 and IL-10 and inhibited LPS-driven tumor necrosis factor alpha and IL-12p70 production from bone marrow-derived DC and macrophages. CyaA also enhanced cell surface expression of CD80, CD86, and ...
Vaccines designed to stimulate CTL should be able to deliver protein antigens to the cytoplasm of host cells for processing and presentation by MHC-I. Many systems have been exploited to accomplish cytoplasmic delivery, including viral and bacterial vectors and DNA vaccines (7, 8, 14, 22, 27, 33, 36). There have also been reports demonstrating that antiviral immunity can be primed in mice vaccinated with a recombinant Bordetella adenylate cyclase toxin incorporating a CTL epitope from LCMV (11, 29, 31); however, the data demonstrated protection only when the recombinant toxin was injected in the presence of an adjuvant, aluminum hydroxide (29). Therefore, it remains unclear whether the antiviral protection was a result of toxin delivery or adjuvant activity. This report describes the use of a nontoxic, truncated form of anthrax toxin as an epitope delivery system without the use of adjuvant.. We demonstrate that protective immunity against a viral pathogen, LCMV, is generated in BALB/c mice ...
Bordetella pertussis adenylate cyclase. Penetration into host cells.: Exposure of Chinese hamster ovary, mouse adrenal cortex tumor (Y-1), THP-1 and U-937 cells
Semantic Scholar extracted view of Spermine inhibition of basal and stimulated adenylate cyclase is mediated by the inhibitory GTP-binding protein (Gi). by Carlo Clô et al.
Pertussis, also known as whooping cough, is an acute respiratory infectious disease caused by a bacteria called Bordetella Pertussis. The characteristic symptoms are paroxysmal cough, inspiratory wheezing and post-tussive vomiting. Following the inhalation of respiratory secretions from an infected individual, bacteria enter the upper respiratory tract and adhere to epithelial cells. Several adhesion factors have been implicated: the filamentous hemagglutinin (FHA), fimbriae, and pertactin (Prn). Pertussis toxin (Ptx) and adenylate cyclase toxin (ACT) have been identified so far as major protein toxins of B. pertussis. PTX is a hexameric AB5-type exotoxin. Catalytic A subunit catalyzes the ADP-ribosylation of the Gi subunits of the heterotrimeric G protein, then inhibits multiple downstream pathways. ACT is able to penetrate the cytoplasmic membrane of host cells and becomes activated through the cleavage and the binding of calmodulin (CaM). Activated ACT converts ATP to cyclic AMP and subverts ...
A factor [the feedback regulator (FR)] formed by adipocytes after the stimulation of a cAMP raising hormone has been found to be a potent inhibitor of membrane-bound adenylate cyclase [EC 4.6.1.1.; ATP pyrophosphate-lyase (cyclizing)]. In a standard assay system using rat adipocyte plasma membrane as the source of adenylate cyclase, the FR inhibited adenylate cyclase by lowering the Vmax without affecting the apparent Km for ATP (0.3-0.6 mM). The apparent Ka for epinephrine (5-6 muM) was also not affected by FR. The inhibitory action of FR was partially countered by Mg2+ ions. An increase in phosphorylation of plasma membrane was observed when FR was present in the incubation system. The concentration required for a 50% inhibition was four times higher when adenosine 5-(beta,gamma-imino) triphosphate [AMP-P(NH)P] replaced ATP as the substrate for adenylate cyclase, implying that adenylate cyclase was inactivated by phosphorylation caused by FR. Increase in FR inhibition obtained by adding low ...
TY - JOUR. T1 - Demonstration and Characterization of Opiate Inhibition of the Striatal Adenylate Cyclase. AU - Law, P. Y.. AU - Wu, J.. AU - Koehler, J. E.. AU - Loh, H. H.. PY - 1981/5. Y1 - 1981/5. N2 - Abstract: The conditions in which Leu5‐enkephalin inhibition of striatal adenylate cyclase was observed were defined. It was determined that enkephalin inhibition was dependent on GTP. The apparent Km for GTP in opiate inhibition was determined to be 0.5 and 2 μM when 0.1 mM‐ and 0.5 mM‐ATP were used as substrate. ITP, but not CTP or UTP, could substitute for GTP in the reaction. Though the addition of monovalent cations-Na+,K+, Li+, Cs+, and choline+-stimulated striatal adenylate cyclase activity, enkephalin inhibition of striatal adenylate cyclase did not require Na+ when theophylline was used as the phosphodiesterase inhibitor. Under optimal conditions, i.e., 20 μM‐GTP and 100 mM‐Na+, Leu5‐enkephalin inhibited the striatal adenylate cyclase activity by 23-27%. When the ...
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Adenylate Cyclase: An enzyme of the lyase class that catalyzes the formation of CYCLIC AMP and pyrophosphate from ATP. EC 4.6.1.1.
The series of molecular signals generated as a consequence of a G-protein coupled receptor binding to its physiological ligand, where the pathway proceeds through inhibition of adenylyl cyclase activity and a subsequent decrease in the concentration of cy…
Visualization for given category : Effector, level : Node and node : ____Cyclases____Adenylate cyclases____Adenylate cyclase 5____Adenylate cyclase 5-Homo sapiens ...
Visualization for given category : Effector, level : Node and node : ____Cyclases____Adenylate cyclases____Adenylate cyclase 4____Adenylate cyclase 4-Homo sapiens ...
The effect of exogenously added adenylate cyclase from Bordetella pertussis (strain 114) has been investigated in Y-1 mouse adrenal tumor, chinese hamster ovary (CHO) and several other cells. A partially purified adenylate cyclase was found not to enter cells but, nevertheless, produced large amounts of cAMP in the medium. We could show that this resulted from release of ATP (and not larger molecules). The ATP released by the cells could be (1) directly measured and was replenished after each change of medium; (2) was reciprocally related to the cAMP produced; and (3) was competed for by ATPases present in added serum or by hexokinase and, less effectively, by exoenzymes on the cell surface. The extent of ATP leakage varied widely between different cell lines, being marked in CHO and Y-1 adrenal cells but negligible in transformed lymphocyte lines. The uncertainty of the origin of cAMP found in media of cultured cells requires separate analysis of cell and medium cAMP and an assessment of ATP ...
The effects of Ca2+-calmodulin on adenylate cyclase activity in EGTA-washed, 27000 g particulate fractions of mouse and rat pancreatic islets were studied. Ca2+ (10 microM)-calmodulin (1 microM) stimulated adenylate cyclase activity 53.1 +/- 5.2 (N = 6)% in the particulate fraction of rat islets. Trifluoperazine (50 microM), a specific inhibitor of calmodulin, inhibited the Ca2+-calmodulin activation of the adenylate cyclase activity of this fraction of rat islets. These results confirm previous reports dealing with Ca2+-Calmodulin and rat islet adenylate cyclase [Valverde, Vandermeers. Anjaneyulu & Malaisse (1979) Science 206, 225-227; Sharp, Wiedenkeller, Kaelin, Siegel & Wollheim (1980) Diabetes 29, 74-77]. In contrast, however, Ca2+ (1-100 microM)-calmodulin (1-10 microM) did not stimulate the adenylate cyclase activity in the EGTA-washed particulate fraction of mouse islets, and trifluoperazine (50 microM) did not inhibit the adenylate cyclase activity of this fraction of mouse islets, ...
Inositol phosphate accumulation and adenylate cyclase activity were investigated in the cortex of young and aged ethanol-treated rats. Three months of ethanol treatment of young rats decreased maximal stimulation of inositol phosphate accumulation by carbachol by 26%, from 494 ± 76% of basal turnover in control animals to 396 ± 54% in ethanol-treated animals (mean ± SD). In aged rats ethanol-related changes were no longer observed but age-related changes were evident. EC50 was significantly higher than in young animals and maximal stimulation was significantly lower. Basal adenylate cyclase activity in cortical membranes of all groups of animals was not different. Forskolin-stimulated adenylate cyclase activity was not affected by ethanol treatment, but was higher in aged animals. The activity of forskolin-stimulated adenylate cyclase in the presence of carbachol was higher in both young and aged ethanol-treated animals, when compared to young controls. These results suggest that both ethanol ...
B pertussis produces numerous virulence factors, including toxins and attachment agents, many of which are antigenic and included in the acellular vaccine. The link of each virulence factor to clinical illness has been difficult to elucidate due to lack of an animal model for experimentation. However, a recently developed model in infant baboons has the potential to address unanswered questions. The bacteria attach to ciliated epithelial cells of the respiratory tract, induce ciliary paralysis and local inflammation, and thicken and decrease clearance of secretions. B pertussis is not invasive. Pertussis toxin, necessary but not sufficient to cause clinical pertussis, is secreted by the bacteria and affects G-protein function, which prevents migration of lymphocytes to the area of infection, and inhibits the function of neutrophils, macrophages, monocytes, and lymphocytes. Adenylate cyclase toxin invades phagocytes and induces high levels of cyclic adenosine monophosphate (AMP), which impairs ...
Adipocytes of hypothyroid rats display an increased responsiveness to agents which function by inhibiting the production of cyclic AMP. Anti-peptide antisera which selectively recognise the alpha subunit of the inhibitory guanine nucleotide binding protein (Gi) detected a 40 kDa polypeptide in adipocyte plasma membranes of both euthyroid and hypothyroid rats. Amounts of the alpha subunit of Gi were elevated some 2-fold in the hypothyroid preparations in comparison with the euthyroid controls, when equal amounts of membrane protein of the two treatments were examined. As cells from the hypothyroid animals contained 2.7 times as much membrane protein as those from the control animals, the amounts of alpha subunit of Gi are elevated some 5.6-fold per cell in adipocytes of the hypothyroid animals compared with the euthyroid controls. Amounts of the 36 kDa beta subunit of G-proteins were also elevated in plasma membranes of adipocytes of hypothyroid animals, in this case by some 50% when compared on ...
This study investigates the hypothesis that inflammatory cytokines, interleukin (IL)-1alpha IL-1beta, and tumor necrosis factor (TNF), influence cardiac function by affecting calcium homeostasis and that this effect is mediated by the beta-adrenergic-adenylate cyclase system. After 4 days in culture, neonatal rat ventricular myocytes were treated with cytokines (10 ng/ml) for short (2 h) or longer (18 h) times. Myocyte calcium, contractility, and adenylate cyclase were measured under each condition. Anticipated stepwise increases in adenylate cyclase and intracellular calcium were found in controls (non-cytokine-treated) with 10(-7) M isoproterenol, 10(-7) M isoproterenol + 0.1 mM guanosine triphosphate, and 10(-9) M forskolin. Cells in the presence of cytokine for 2 h show increased basal calcium levels but no changes in adenylate cyclase activities, and isoproterenol fails to elevate adenylate cyclase levels or affect contractile shortening. After long-term treatment with IL-1beta or TNF, but ...
TY - JOUR. T1 - Multiple forms of brain adenylate cyclase. T2 - Stimulation by Mn2+. AU - Malamuda, Daniel F.. AU - DiRusso, Concetta C.. AU - Aprille, June R.. PY - 1977/11/23. Y1 - 1977/11/23. N2 - Mn2+-stimulated adenylate cyclase (ATP pyrophosphate-lyase-(cyclizing), EC 4.6.1.1) activity in detergent solubilized preparations from mouse brain. While NaF-stimulated activity was decreased by both solubilization and storage at 0-4°C, the ability of the enzyme to be stimulated by Mn2+ was maintained for up to one week. By including Mn+ in the assay of adenylate cyclase in gel fractions after isoelectric focusing, two distinct peaks of enzyme activity (pI1 = 5.8, pI2 = 6.4) were detected, suggesting the existence of more than one type of catalytic subunit in mouse brain cell membranes.. AB - Mn2+-stimulated adenylate cyclase (ATP pyrophosphate-lyase-(cyclizing), EC 4.6.1.1) activity in detergent solubilized preparations from mouse brain. While NaF-stimulated activity was decreased by both ...
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TY - JOUR. T1 - Differential unmasking of adenylate cyclase activity (AC) in cardiac membrane sheets and vesicles. AU - Fleming, J. W.. AU - Besch, H. R.. AU - Jones, L. R.. AU - Watanabe, A. M.. PY - 1978/1/1. Y1 - 1978/1/1. UR - http://www.scopus.com/inward/record.url?scp=0017841068&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0017841068&partnerID=8YFLogxK. M3 - Article. AN - SCOPUS:0017841068. VL - 20. JO - Pharmacologist. JF - Pharmacologist. SN - 0031-7004. IS - 3. ER - ...
Decreased activity of the guanine nucleotide regulatory protein (N) of the adenylate cyclase system is present in cell membranes of some patients with pseudohypoparathyrodism (PHP-Ia) whereas others have normal activity ...
Decreased activity of the guanine nucleotide regulatory protein (N) of the adenylate cyclase system is present in cell membranes of some patients with pseudohypoparathyrodism (PHP-Ia) whereas others have normal activity ...
|br| |br| The plan has a unique method which helps you reach a specific weight healthy measures will increase your ability to lose weight in a short span of time. Adverse Effects of the Diet While you may notice that you have lost weight or can help you lose weight without a balanced diet and regular exercise. This condition is termed as ketosis...
Fingerprint Dive into the research topics of Effect of membrane phospholipid composition changes on adenylate cyclase activity in normal and rous-sarcoma-transformed chicken embryo fibroblasts. Together they form a unique fingerprint. ...
TY - JOUR. T1 - Hormone-sensitive adenylate cyclase in glomerular cells. Possible role for inflammatory diseases of the glomerulus. AU - Paietta, Elisabeth M.. AU - Schwarzmeier, J. D.. AU - Simbruner, G.. AU - Latzka, U.. AU - Lubec, G.. PY - 1981. Y1 - 1981. N2 - Using the adenylate cyclase assay after Ross the authors examined hormone sensitivity of isolated glomerular cells. cAMP production was increased 1.3-1.6-fold by stimulation with isoproterenol, 1.5-1.8 times by prostaglandin E 1 and 1.4-1.5 times by histamine. The isoproterenol reaction could be completely inhibited by propranolol, the histamine effect was abolished by the H2-blocking agent cimetidine. As a control the authors applied sodium fluoride, which directly activates the catalytic adenylate cyclase unit, increasing the activity 1.8-2.7 times (depending on the method of homogenization). These findings could reflect some physiological or pathophysiological implications, which are discussed.. AB - Using the adenylate cyclase ...
Previous studies on immortalized B lymphoblasts from patients with EH and enhanced Na+-H+ exchanger activity have revealed an enhanced activation of PTX-sensitive G proteins.7 This conclusion was mainly based on two findings. First, HT lymphoblasts displayed enhanced [Ca2+]i signals upon stimulation with platelet-activating factor and somatostatin. Pretreatment with PTX strongly reduced these agonist-evoked Ca2+ signals, and the residual Ca2+ responses were no longer different between NT and HT cell lines. Second, both receptor-mediated stimulation and direct (by mastoparan-7) stimulation of GTPγS binding to PTX-sensitive G proteins were significantly increased in HT lymphoblasts.7 Unfortunately, B lymphoblasts apparently do not express functional receptors that are selectively coupled to PTX-insensitive G proteins, eg, Gq or Gs. Therefore, our proposal of a selective enhancement of signal transduction via PTX-sensitive G proteins in HT cell lines was based on circumstantial evidence but could ...
Hudson, T H. and Johnson, G L., "Peptide mapping of adenylate cyclase regulatory proteins that are cholera toxin substrates." (1980). Subject Strain Bibliography 1980. 3108 ...
Adenylate cyclase type 5 (EC 4.6.1.1) (ATP pyrophosphate-lyase 5) (Adenylate cyclase type V) (Adenylyl cyclase 5) (Ca(2+)-inhibitable adenylyl cyclase ...
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P-ARs are coupled by Gs to adenylate cyclase and produce alterations in cellular activity by raising intracellular levels of cyclic AMP (Fig. 3).
An important eukaryotic signal transduction pathway involves the regulation of the effector enzyme adenylate cyclase, which produces the second messenger, cAMP. Previous genetic analyses demonstrated that glucose repression of transcription of the Schizosaccharomyces pombe fbp1 gene requires the function of adenylate cyclase, encoded by the git2 gene. As mutations in git2 and in six additional git genes are suppressed by exogenous cAMP, these upstream git genes were proposed to act to produce a glucose-induced cAMP signal. We report here that assays of cAMP levels in wild-type and various mutant S. pombe cells, before and after exposure to glucose, show that this is the case. The data suggest that the cAMP signal results from the activation of adenylate cyclase. Therefore these upstream git genes appear to encode a glucose-induced adenylate cyclase activation pathway. Assays of cAMP on a strain carrying a mutation in the git6 gene, which acts downstream of adenylate cyclase, indicate that ...
The time course of cAMP production by S49 cell membranes in the presence of forskolin and a nonhydrolyzable GTP analog can yield information about the regulation of adenylate cyclase by both the inhibitory and stimulatory GTP-binding proteins (Gi and Gs). The time courses are complex and interpretation in terms of the activities of G1 and Gs requires a quantitative hypothesis. We present a general quantitative hypothesis that defines adenylate cyclase as existing in a distribution of two states, active and inactive. Gi and Gs, in their active states, alter the equilibrium of this distribution. Two distinct models are derived based on this hypothesis to accommodate two different proposed mechanisms for the action of Gi to inhibit adenylate cyclase: 1) a direct interaction between Gi and the catalytic subunit of adenylate cyclase and 2) a direct interaction between Gi and Gs. Perturbations of the regulation of adenylate cyclase by pertussis toxin and phorbol ester are simulated and interpreted ...
PST receptors were purified and characterized in the liver, hepatoma membranes, as well as the signal transduction (55, 62, 63). This receptor appears to mediate the dual signaling mechanism in liver (57). PST stimulation activates pertussis toxin-insensitive G protein (Gαq/11), leading to the activation of phospholipase C b3 isoform (PLC-b3) (69), and therefore mediates the glycogenolytic effect in the liver by increasing cytoplasmic free calcium and stimulating PKC, while the pertussis toxin-sensitive G protein (Gai1,2) leads to the activation of guanylatecyclase (51). In the signaling pathway, hydrolysis of phosphatidylinositol 4,5-bisphosphate by Ca2+-mobilizing hormones leads to the formation of two second messengers i.e., inositol-1,4,5-triphosphate (InsP3) and diacylglycerol (DAG). The primary function of InsP3 is to mobilize Ca2+ from intracellular stores (60), whereas DAG stimulates PKC (58).. Active PST receptors were solubilized from rat liver membranes, and these results support the ...
Separation of the catalytic and stimulatory regulatory subunits of rat brain adenylate cyclase.: The catalytic subunit of rat brain adenylate cyclase was separa
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The primary mode of action of forskolin is by increasing the cellular concentrations of cyclic AMP (cAMP) and cAMP-mediated functions, via activation of the enzyme adenylate cyclase. For details visit our online portal
11/2017 There have been some unexpected changes to the OpenWetWare platform, affecting the formatting of the Banta Lab Website. We are currently working on addressing these issues. A new website is under development and should be launched soon. 10/2017 The Banta Lab is pleased to welcome another new graduate student into the lab group. Nadim Massad has joined the research group this semester. 9/2017 A paper entitled "Block V RTX domain of adenylate cyclase from Bordetella pertussis: A conformationally dynamic scaffold for protein engineering applications" by Bulutoglu and Banta was published in Toxins as an Invited Review for the Special Issue: Adenylate Cyclase (CyaA) Toxin 9/2017 A paper entitled "Catch and release: Engineered allosterically-regulated β-roll peptides enable on/off biomolecular recognition" by Bulutoglu, Dooley, Szilvay, Blenner and Banta was published in ACS Synthetic Biology. 9/2017 A paper entitled "Block V RTX domain of adenylate cyclase from Bordetella pertussis: A ...
11/2017 There have been some unexpected changes to the OpenWetWare platform, affecting the formatting of the Banta Lab Website. We are currently working on addressing these issues. A new website is under development and should be launched soon. 10/2017 The Banta Lab is pleased to welcome another new graduate student into the lab group. Nadim Massad has joined the research group this semester. 9/2017 A paper entitled "Block V RTX domain of adenylate cyclase from Bordetella pertussis: A conformationally dynamic scaffold for protein engineering applications" by Bulutoglu and Banta was published in Toxins as an Invited Review for the Special Issue: Adenylate Cyclase (CyaA) Toxin 9/2017 A paper entitled "Catch and release: Engineered allosterically-regulated β-roll peptides enable on/off biomolecular recognition" by Bulutoglu, Dooley, Szilvay, Blenner and Banta was published in ACS Synthetic Biology. 9/2017 A paper entitled "Block V RTX domain of adenylate cyclase from Bordetella pertussis: A ...
G-protein coupled receptor that functions as receptor for endogenous enkephalins and for a subset of other opioids. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase. Signaling leads to the inhibition of adenylate cyclase activity. Inhibits neurotransmitter release by reducing calcium ion currents and increasing potassium ion conductance. Plays a role in the perception of pain and in opiate-mediated analgesia. Plays a role in developing analgesic tolerance to morphine. ...
Increases of cAMP are controlled by the enzyme adenylate cyclase (sAC). This enzyme produces cAMP molecules from the cellular energy reservoir adenosyne triphosphate (ATP). In order for the enzyme to assume this catalytic function, it itself has to be activated, e.g. by bicarbonate.. • The opposite process, e.g. the reduction of cAMP levels, is initiated by another enzyme. The protein involved here originates from the family of phosphodiesterases (PDE); to be precise, an isoform of PDE2A. This enzyme must also be activated so that it may reduce the amount of cAMP contained in the mitochondria. This process is performed by molecules which aggregate along an area at the end of the protein, the N-terminus of the PDE2A molecules.. In this manner, the messenger cAMP acts as an enzyme controlled switch which strengthens or weakens the energy metabolism. The "position" of the switch is determined by which of the two enzymes dominates: Adenylate cyclase (sAC) increases the amount of cAMP, ...
Cyclic AMP is 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. cAMP is synthesized from ATP by adenylate cyclase. Adenylate cyclase is located at the cell membranes. Adenylate cyclase is activated by the hormones glucagon and adrenaline and by G protein. Liver adenylate cyclase responds more strongly to glucagon, and muscle adenylate cyclase responds more strongly to adrenaline. cAMP decomposition into AMP is catalyzed by the enzyme phosphodiesterase ...
Withdrawal of mice from chronic ethanol treatment results in a decreased responsiveness of striatal (but not mesolimbic) dopamine-sensitive adenylate cyclase activity to stimulation by dopamine. This subsensitivity is not apparent at the time of withdrawal from chronic feeding of ethanol, when animals are still intoxicated, but becomes evident as ethanol is eliminated from the animals. Addition of ethanol in vitro to tissue homogenates from ethanol-withdrawn animals, at concentrations similar to those found in brain at the time of withdrawal, normalizes the response of the adenylate cyclase to dopamine. No difference is evident between control and ethanol-withdrawn animals in stimulation of adenylate cyclase by sodium fluoride. The specificity of the response of striatal adenylate cyclase to stimulation by dopamine, as compared to other transmitters, is unaltered by chronic ethanol feeding. Chronic treatment with ethanol and withdrawal also does not affect the specific binding of spiroperidol in ...
A novel neuropeptide which stimulates adenylate cyclase in rat anterior pituitary cell cultures was isolated from ovine hypothalamic tissues. Its amino acid sequence was revealed as: His-Ser-Asp-Gly-Ile-Phe-Thr-Asp-Ser-Tyr-Ser-Arg-Tyr-Arg-Lys-Gln- Met-Ala- Val-Lys-Lys-Tyr-Leu-Ala-Ala-Val-Leu-Gly-Lys …
To synchronize a network of pacemakers in the Drosophila brain, a neuropeptide receptor specifically associates with adenylate cyclase 3 to create a
Several natural or synthetic chemicals have been indicated as potential thyroid disruptors. The development of in vitroassays has been recommended to comprehensively assess the potential thyroid...
Complete information for ADCY10 gene (Protein Coding), Adenylate Cyclase 10, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Cat.No.AD00697ZDescriptionAdenovirus with ORF of adenylate cyclase 9 (ADCY9) with C terminal Flag and His tag.InsertADCY9Product TypeAdenoviral particleShippingDry iceSize/Form1
MTSQEKTEEYPFADIFDEDETERNFLLSKPVCFVVFGKPGVGKTTLARYITQAWKCIRVEALPILEEQIA 1 - 70 AETESGVMLQSMLISGQSIPDELVIKLMLEKLNSPEVCHFGYIITEIPSLSQDAMTTLQQIELIKNLNLK 71 - 140 PDVIINIKCPDYDLCQRISGQRQHNNTGYIYSRDQWDPEVIENHRKKKKEAQKDGKGEEEEEEEEQEEEE 141 - 210 AFIAEMQMVAEILHHLVQRPEDYLENVENIVKLYKETILQTLEEVMAEHNPQYLIELNGNKPAEELFMIV 211 - 280 MDRLKYLNLKRAAILTKLQGAEEEINDTMENDELFRTLASYKLIAPRYRWQRSKWGRTCPVNLKDGNIYS 281 - 350 GLPDYSVSFLGKIYCLSSEEALKPFLLNPRPYLLPPMPGPPCKVFILGPQYSGKTTLCNMLAENYKGKVV 351 - 420 DYAQLVQPRFDKARETLVENTIAEATAAAIKVVKEKLLRELQARKQAETALREFQRQYEKMEFGVFPMEA 421 - 490 THSSIDEEGYIQGSQRDRGSSLVDTEEAKTKSENVLHDQAAKVDKDDGKETGETFTFKRHSQDASQDVKL 491 - 560 YSDTAPTEDLIEEVTADHPEVVTMIEETIKMSQDINFEQPYEKHAEILQEVLGEVMEENKDRFPGAPKYG 561 - 630 GWIVDNCPIVKELWMALIKKGIIPDLVIYLSDTENNGKCLFNRIYLQKKSEIDSKILERLLEELQKKKKE 631 - 700 EEEARKATEEELRLEEENRRLLELMKVKAKEAEETDNEDEEEIEGDELEVHEEPEASHDTRGSWLPEEFE 701 - 770 ASEVPETEPEAVSEPIEETTVETEIPKGSKEGLEIEKLSETVVLPEFPEDSYPDVPEMEPFKEKIGSFII 771 - 840 ...
TY - JOUR. T1 - The effect of pertussis toxin on the growth of vascular smooth muscle cells stimulated by serum or platelet-derived growth factor. AU - Zhang, L. M.. AU - Newman, W. H.. AU - Castresana, Manuel R. AU - Hildebrandt, J. D.. PY - 1994/1/1. Y1 - 1994/1/1. N2 - The involvement of a G(i)- or G(o)-related G-protein as a regulator of the growth of guinea pig thoracic aorta smooth muscle (TASM) cells was studied by investigating the effects of pertussis toxin (PTX) on the growth of these cells. PTX treatment decreased the growth rate of TASM cells by 70-100%. This effect was apparent within 24 h after exposure in the toxin and persisted for at least 10 days after starting the treatment. The effect of the toxin appeared to be the result of the inactivation of a G-protein because 1) TASM cell membranes contained a 40-kilodalton substrate for the toxin in in vitro assays that was absent in membranes prepared from cells pretreated with toxin; and 2) the effect required both the enzymatic ...
This study was performed to investigate the regulatory mechanism of cerebral blood flow of adenosine A $_{2B}$ receptor agonist in the rats, and to define whether its mechanism is mediated by adenylate cyclase, guanylate cyclase and potassium channel. In pentobarbital-anesthetized, pancuronium-par...
Guanine nucleotide-binding proteins (G proteins) are involved as modulators or transducers in various transmembrane signaling systems.
Catalyzes the formation of the signaling molecule cAMP in response to G-protein signaling (PubMed:15385642). Down-stream signaling cascades mediate changes in gene expression patterns and lead to increased IL6 production. Functions in signaling cascades downstream of the muscarinic acetylcholine receptors (By similarity).
Reactivity: Cow, Human, Mouse and more. Compare 8 different ADCYAP1R1 ELISA Kits & buy the right one directly at antibodies-online.com!
Complete information for ADCY6 gene (Protein Coding), Adenylate Cyclase 6, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Looking for online definition of guanine nucleotide-binding protein subunit beta-5 in the Medical Dictionary? guanine nucleotide-binding protein subunit beta-5 explanation free. What is guanine nucleotide-binding protein subunit beta-5? Meaning of guanine nucleotide-binding protein subunit beta-5 medical term. What does guanine nucleotide-binding protein subunit beta-5 mean?
Periodical: McGee, Richard, Paul Simpson, Clifford Christian, Marina Mata, Phillip Nelson, and Marshall W. Nirenberg. Regulation of Acetylcholine Release from Neuroblastoma x Glioma Hybrid Cells. Proceedings of the National Academy of Sciences of the United States of America 75, 3 (March 1978): 1314-1318. Article. 5 Images ...
In cultured intact LLC-PK1 renal epithelial cells, a nonhydrolyzable ATP analogue, ATP gamma S, inhibits AVP-stimulated cAMP formation. In LLC-PK1 membranes, several ATP analogues inhibit basal, GTP-, forskolin-, and AVP-stimulated adenylate cyclase activity in a dose-dependent manner. The rank order potency of inhibition by ATP analogues suggests that a P2y type of ATP receptor is involved in this inhibition. The compound ATP gamma S inhibits agonist-stimulated adenylate cyclase activity in solubilized and in isobutylmethylxanthine (IBMX) and quinacrine pretreated membranes, suggesting that ATP gamma S inhibition occurs independent of AVP and A1 adenosine receptors and of phospholipase A2 activity. The ATP gamma S inhibition of AVP-stimulated adenylate cyclase activity is not affected by pertussis toxin but is attenuated by GDP beta S, suggesting a possible role for a pertussis toxin insensitive G protein in the inhibition. Exposure of intact LLC-PK cells to ATP gamma S results in a significant ...
The lipoglycoproteins of the WNT family act on seven transmembrane-spanning Class Frizzled receptors. Here, we show that WNT-5A evokes a proliferative response in a mouse microglia-like cell line (N13), which is sensitive to pertussis toxin, thus implicating the involvement of heterotrimeric G proteins of the G(i/o) family. We continue to show that WNT-5A stimulation of N13 membranes and permeabilized cells evokes the exchange of GDP for GTP of pertussis toxin-sensitive G proteins employing [gamma-(35)S]GTP assay and activity state-specific antibodies to GTP-bound G(i) proteins. Our functional analysis of the PTX-sensitivity of WNT-induced G protein activation and PCR analysis of G protein and FZD expression patterns suggest that WNT-5A stimulation leads to the activation of G(i2/3) proteins in N13 cells possibly mediated by FZD(5), the predominant FZD expressed ...
This study was undertaken to determine whether receptor and non-receptor components of the adenylate cyclase (AC) cascade were altered in brown adipose tissue (BAT) of 14-day-old pre-obese (fa/fa) rats, before endocrine status is strongly modified by fa gene expression. Activity of the AC catalytic subunit did not differ between the two genotypes. In fa/fa rats compared with control Fa/fa rats, there was a 50% decrease in the activity of alpha Gs (stimulated by NaF or guanosine 5′-[gamma-thio]triphosphate) but no change in protein content (Western blotting). alpha Gi function, assessed by the inhibitory action of low concentrations of guanosine 5′-[beta gamma-imido]triphosphate upon 10(-4) M forskolin-stimulated AC activity, was equally low in both genotypes. Analysis of dose-response curves for different beta-agonists revealed that (i) both the basal and the maximally stimulated activity of AC were 2-fold lower in fa/fa rats than in Fa/fa rats; (ii) BRL37344 and CGP12177 (beta 3 agonists) ...
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Amphetamine has complex behavioral actions in the rat that depend upon the release of dopamine in striatal and mesolimbic brain regions. To explore a possible role of the dopamine-sensitive cAMP second-messenger system in mediating these effects, we examined the effects of in vivo amphetamine treatments on the D1 receptor-coupled adenylate cyclase system in membranes from striatal and mesolimbic rat brain regions. The results show that amphetamine produces a regional, dose- and time- dependent down-regulation of adenylate cyclase activity. Intermediate and high doses of amphetamine (2.5 and 7.5 mg/kg, respectively), but not a low dose (1.0 mg/kg), resulted in a decrease in the apparent Vmax and/or an increase in the apparent Ka for the selective D1 partial agonist, SKF38393, in striatal membranes 30 min after amphetamine treatment. Treatment of rats with 7.5 mg/kg amphetamine for 30 and 60 min, but not 10 min, similarly resulted in a down-regulation of D1- mediated adenylate cyclase activity in ...
Bordetella pertussis toxin IgG for suspected cases over 12 months of age with cough ,14 days duration and who have not been immunised against pertussis in the past year. The IgG test can not be used to determine immunity as there are currently no agreed correlated of protection. Bordetella pertussis DNA for suspected cases with cough ,21 days duration and within 48 hours of antibiotic therapy.. ...
TY - JOUR. T1 - 5 Hydroxytryptamine-induced tachyphylaxis of the molluscan heart and concomitant desensitization of adenylate cyclase. AU - Higgins, W. J.. PY - 1977/12/1. Y1 - 1977/12/1. UR - http://www.scopus.com/inward/record.url?scp=0017707535&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0017707535&partnerID=8YFLogxK. M3 - Article. C2 - 915059. AN - SCOPUS:0017707535. VL - 3. SP - 293. EP - 302. JO - Journal of Receptors and Signal Transduction. JF - Journal of Receptors and Signal Transduction. SN - 1079-9893. IS - 4. ER - ...
View Notes - D103 clicker+questions_lecture+16-18 from BIOL 05400 at UC Irvine. A. expression level of AKAPs B. level of adenylyl cyclase activity C. increased cytosolic concentration of cAMP D.
Chi, Alice Sut, "Calcium-gonadotropin interaction and their regulation of adenylate cyclase in rat luteal membranes" (1985). Yale Medicine Thesis Digital Library. 2459 ...
Forskolin acts primarily by activating the enzyme adenylate cyclase, which results in increased cyclic adenosine monophosphate (cAMP) in cells. Thus, Forskolin can increase cyclic AMP without the assistance of neurotransmitters or hormones. Get a risk-free trial of the #1 Forskolin… Continue Reading →. ...
P2Y11 is a receptor binding to ATP and ADP. It mediates both mobilization of intracellular calcium and stimulation of adenylate cyclase. The P2Y11-receptor may play a role in the differentiation of immunocytes and maturation of human monocyte-derived dendritic cells.
p,Individuals from a Greenlandic Inuit population with homozygous loss-of-function variants in ,i,ADCY3,/i, (adenylate cyclase 3) have increased risk for obesity and type 2 diabetes. Carriers of rare ,i,ADCY3,/i, variants in trans-ancestry ...
View Notes - Slides3 011911(1) from BIOL 212 at UPenn. Today: 1) Short discussion of ATP and other carrier molecules 2) Protein folding 3) Exploration of adenylate kinase structure and
Pertussis (Whooping Cough) | Definition | Treatment | Management of Disease | Diagnosis | Symptoms | Etiology | Pathophysiology | Procedure
Whooping cough (pertussis) is dangerous in babies and young children. This article looks at the symptoms, treatment and prevention of the illness...
GTP-binding regulatory proteins (G proteins) regulate various biological functions, but their participation in controlling coronary microvascular tone has not been established yet. The goal of the present study was to elucidate the role of pertussis toxin (PTX)-sensitive G protein in regulating coronary microvascular tone during autoregulation and ischemia. In 42 open-chest dogs, coronary arterial microvessels on the surface of the left ventricle were directly observed by epi-illuminated fluorescence microangiography using a floating objective system. PTX (300 ng/mL) was superfused onto the surface of the left ventricle for 2 hours to block Gi and G(o) protein in epimyocardial coronary microvessels in vivo. PTX superfusion caused no change in the resting diameters of microvessels and significantly blocked the vasoconstriction induced by BHT 920 (a selective alpha 2-agonist). After pretreatment with PTX or its vehicle, the left anterior descending coronary artery (LAD) was occluded by a hydraulic ...
In vivo administration of pertussis toxin is often used to study the involvement of guanine nucleotide binding proteins in signal transduction. Especially when it is administered in the brain the effect is often poor. This could be due to the fact that pertussis toxin does not reach the area of interest. To evaluate the extent to which pertussis toxin is distributed in rat brain after intraventricular injection, different techniques were used. Immunohistochemical studies with an antibody against pertussis toxin showed that immunoreactivity was limited to periventricular brain structures less than 0.5 mm from the lumen. The highest immunoreactivity was seen 16-24 h after injection. After 96 h the labeling was very weak. The proportion of guanine nucleotide binding proteins that were ADP-ribosylated by in vivo injection of pertussis toxin into the ventricles as assessed by in vitro [32P]-back-ADP-ribosylation was very low 48 h after the injection, in all regions studied. Direct injection of pertussis
The parasite Trypanosoma brucei possesses a large family of transmembrane receptor-like adenylate cyclases. Activation of these enzymes requires the dimerization of the catalytic domain and typically occurs under stress. Using a dominant-negative strategy, we found that reducing adenylate cyclase activity by about 50% allowed trypanosome growth but reduced the parasites ability to control the early innate immune defense of the host. Specifically, activation of trypanosome adenylate cyclase resulting from parasite phagocytosis by liver myeloid cells inhibited the synthesis of the trypanosome-controlling cytokine tumor necrosis factor-α through activation of protein kinase A in these cells. Thus, adenylate cyclase activity of lyzed trypanosomes favors early host colonization by live parasites. The role of adenylate cyclases at the host-parasite interface could explain the expansion and polymorphism of this gene family.. ...
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Pertussis toxin (PT) is a protein-based AB5-type exotoxin produced by the bacterium Bordetella pertussis, which causes whooping cough. PT is involved in the colonization of the respiratory tract and the establishment of infection. Research suggests PT may have a therapeutic role in treating a number of common human ailments, including hypertension, viral inhibition, and autoimmune inhibition. PT clearly plays a central role in the pathogenesis of pertussis although this was discovered only in the early 1980s. The appearance of pertussis is quite recent, compared with other epidemic infectious diseases. The earliest mention of pertussis, or whooping cough, is of an outbreak in Paris in 1414. This was published in Moultons The Mirror of Health, in 1640. Another epidemic of pertussis took place in Paris in 1578 and was described by a contemporary observer, Guillaume de Baillou. Pertussis was well known throughout Europe by the middle of the 18th century. Jules Bordet and Octave Gengou described in ...
What is pertussis (whooping cough)? Pertussis (also called whooping cough) is a disease caused by the bacteria Bordetella pertussis that spreads from person-to-person with close contact. It may cause severe coughing fits which can affect breathing. Pertussis is often milder in older children and adults, but can cause serious problems in infants. Pertussis can lead to pneumonia, convulsions, inflammation of the brain and sometimes death. Most of these serious problems occur in infants who are less than one year old. Who can get pertussis? Pertussis can occur in any age group; however, pertussis is more common among infants since they are too young to have full protection from the vaccine. Pertussis is also more common in adolescents and adults who have lost the protection they got from vaccination or illness in childhood. How is pertussis spread? Pertussis is spread from one person to another through respiratory droplets from the nose or throat of an infected person by coughing or sneezing, and ...
We have recently described a procedure to produce a monomeric, stable, soluble and functional state of the full-length CyaA toxin. We are now investigating the physico-chemical properties of CyaA in solution and upon its insertion into membranes.. The characterization of CyaA in solution should be instrumental for the development of a new generation of vacines against whooping cough. Biophysical approaches will be coined to follow the translocation process both in vitro on lipid membranes and in vivo on eukaryotic cells. These studies should provide a better understanding of the mechanisms of toxin translocation across biological membranes, and in addition, will allow to further develop CyaA-based vaccines (two of them are currently in phase I/II clinical trials). Indeed, Daniel Ladant, in collaboration with C. Leclercs team at Institut Pasteur, previously showed that CyaA is a potent vehicle able to deliver vaccine antigens into dendritic cells thus triggering specific cell-mediated immune ...
What is pertussis?. Pertussis (also called "whooping cough") is a respiratory illness caused by bacteria that is easily spread from person to person. A person with pertussis can have severe coughing spasms that last for weeks. Is pertussis dangerous?. Pertussis is usually mild in older children and adults, but can be dangerous for infants and young children. Although rare, pertussis can cause serious health and breathing problems such as pneumonia, seizures, and swelling of the brain (encephalopathy), especially among infants less than six months of age. How is it spread?. The bacteria that causes pertussis lives in the nose, mouth and throat and is sprayed into the air when an infected person sneezes, cough or talks. People nearby can then breathe in the germs. Spread of pertussis occurs by droplets or direct contact with mucus or saliva from an infected person. People with pertussis can spread the disease starting two weeks before until three weeks after their cough starts. However, treatment ...
Mooi FR; van Loo IHM; van Gent M; He Q; Bart MJ; Heuvelman KJ; de Greeff SC; Diavatopoulos D; Teunis P; Nagelkerke N; Mertsola J (2009 ...
We next investigated whether beta gamma subunits play a role in the sensitization of type VI adenylyl cyclase activity; using expression of alpha tau to inhibit beta gamma-mediated effects, we found that the quinpirole-induced sensitization of type VI adenylyl cyclase was abolished ...
Minocherhomjee M. , Selfe S. , Flowers N.J. , Storm D.R. Direct interaction between the catalytic subunit of the calmodulinsensitive adenylate cyclase from bovine brain with 1251-labeled wheat germ agglutinin and 1251-labeled calmodulin // Biochemistry. 1987. Vol. 26. P. 4444-4448. Biochemistry. 1987 ...
Description: Pertussis (Whooping Cough) Pipeline Review, H1 2017, provides an overview of the Pertussis (Whooping Cough) (Infectious Disease) pipeline land
The drug brand named Pentact-HIB contains generic salt-Bordetella Pertussis inactivated and is manufactured by Sanofi-Aventis ...
Do you feel your body is running under par? Maybe your toxic load is too high. Read 11 signs of an overly toxic body, and what to do to reduce the load.
بیوگاز یکی از منابع تجدید پذیر انرژی است که توسط باکتری-هایی که موجب تجزیه مواد آلی در شرایط بی-هوازی می‌گردند، تولید می-شود. به منظور تصمیم‌گیری در مورد انتخاب مکان-های مناسب راه اندازی واحد-های بیوگاز، سهولت دسترسی به ضایعات آلی و تخمین مقدار آن-ها حائز اهمیت است. در پژوهش حاضر با بهره گیری از اطلاعاتی نظیر تراکم جمعیت روستایی و جمعیت دام در منطقه و نقشه-های کاربری اراضی، مدلی برای تعیین پتانسیل تولید بیوگاز از فضولات دامی و پسماند-های روستایی، پراکنش آن در سطح استان کردستان و تعیین نقاط مستعد برای احداث واحدهای بیوگاز با استفاده از سیستم اطلاعات
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 ...
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 ...
Requirements for cholera toxin-dependent ADP-ribosylation of the purified regulatory component of adenylate cyclase. J Biol ... The regulatory component of adenylate cyclase. Purification and properties. J Biol Chem. 1981 Nov 25;256(22):11517-26. PMID ... Molecular cloning of complementary DNA for the alpha subunit of the G protein that stimulates adenylate cyclase. Science. 1985 ... The regulatory component of adenylate cyclase. Purification and properties of the turkey erythrocyte protein. J Biol Chem. 1981 ...
"Requirements for cholera toxin-dependent ADP-ribosylation of the purified regulatory component of adenylate cyclase". 》The ... Gilman, AG (1984). "G proteins and dual control of adenylate cyclase". 》Cell》 36 (3): 577-9. doi:10.1016/0092-8674(84)90336-2. ... Sternweis, PC; Northup, JK; Smigel, MD; Gilman, AG (1981). "The regulatory component of adenylate cyclase. Purification and ... Hanski, E; Sternweis, PC; Northup, JK; Dromerick, AW; Gilman, AG (1981). "The regulatory component of adenylate cyclase. ...
"Pertussis toxin and adenylate cyclase toxin: key virulence factors of Bordetella pertussis and cell biology tools". Future ... "cough toxin".[33] Pertussis toxin causes lymphocytosis by an unknown mechanism. The elevated number of white blood cells leads ... The bacteria secrete a number of toxins. Tracheal cytotoxin, a fragment of peptidoglycan, kills ciliated epithelial cells and ... adults and adolescents who have already been infected for several weeks to determine whether antibody against pertussis toxin ...
"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. ...
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 ...
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 ...
Increased Gαs activation leads to increased adenylate cyclase activity, which increases the intracellular concentration of 3',5 ... Cholera toxin acts by the following mechanism: First, the B subunit ring of the cholera toxin binds to GM1 gangliosides on the ... Subunit B binds while subunit A activates the G protein which activates adenylate cyclase. The three-dimensional structure of ... the entire toxin complex is endocytosed by the cell and the cholera toxin A1 (CTA1) chain is released by the reduction of a ...
... 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 ...
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 ...
"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 ...
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 ...
... 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. ...
Extracellular adenylate cyclase. Mechanisms. *type I *Superantigen. *type II *Pore-forming toxin ... "toxin" at Dorland's Medical Dictionary *^ "toxin - Definition from the Merriam-Webster Online Dictionary". Retrieved 13 ... For other uses, see Toxin (disambiguation).. A toxin (from Ancient Greek: τοξικόν, translit. toxikon) is a poisonous substance ... 3 Environmental toxins *3.1 Finding information about toxins. *3.2 Computational resources for prediction of toxic peptides and ...
Cholera toxin/Heat-labile enterotoxin. *Pertussis toxin. *Pseudomonas exotoxin. *Extracellular adenylate cyclase ... Microbial toxins. References[edit]. *^ a b c d e f g Montecucco C, Molgó J (June 2005). "Botulinal neurotoxins: revival of an ... Toxin production[edit]. Botulism toxins are produced by bacteria of the genus Clostridium, namely Clostridium botulinum, C. ... Botulinum toxin produced by Clostridium botulinum is the cause of botulism.[17] Humans most commonly ingest the toxin from ...
Extracellular adenylate cyclase. Mechanisms. *type I *Superantigen. *type II *Pore-forming toxin ... Microbial toxins. References[edit]. *^ a b c d e f g Montecucco C, Molgó J (June 2005). "Botulinal neurotoxins: revival of an ... Toxin production[edit]. Botulism toxins are produced by bacteria of the genus Clostridium, namely Clostridium botulinum, C. ... Botulinum toxin is used to treat a number of problems. Muscle spasticity[edit]. Botulinum toxin is used to treat a number of ...
... 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 ...
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 ...
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, ...
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 ...
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. ...
... 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/ ...
Cholera toxin · Pertussis toxin · Pseudomonas exotoxin · Extracellular adenylate cyclase ... "toxin" tại Từ điển Y học Dorland *^ "toxin - Definition from the Merriam-Webster Online Dictionary". Truy cập ngày 13 tháng 12 ... type I (Superantigen) · type II (Pore forming toxins) · type III (AB toxin/AB5) ... Shiga toxin · Verotoxin/shiga-like toxin (E. coli) · E. coli heat-stable enterotoxin/enterotoxin · ...
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 ...
Glucagon activates adenylate cyclase through a seven transmembrane receptor coupled to Gs which, in turn, activates adenylate ... cyclase to increase intracellular concentrations of cAMP. cAMP binds to and releases an active form of protein kinase A (PKA). ... Diphtheria toxin. *NAD(P)+:arginine ADP-ribosyltransferase *Pertussis toxin. *Cholera toxin. *Poly ADP ribose polymerase ...
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. ...
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 ...
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 ...
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 ...
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; ...
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 ...
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 ...
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 ...
... 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 ...
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 ...
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 ...
Bordetella adenylate cyclase toxin-hemolysin (CyaA) penetrates the cytoplasmic membrane of phagocytes and employs two distinct ... Calcium influx rescues adenylate cyclase-hemolysin from rapid cell membrane removal and enables phagocyte permeabilization by ... translocates the adenylate cyclase enzyme (AC) domain into cells and converts cytosolic ATP to cAMP. We show that the calcium- ... Hence, by mediating calcium influx into cells, the translocating conformer of CyaA controls the removal of bystander 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 ...
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 ...
This coordinated disruption of the Rab11/Sec15 exocyst by anthrax toxins may contribute to toxin-dependent barrier disruption ... Tests in human endothelial cells indicate that the toxins have a similar effect on Rab11/Sec15 activity and Notch signalling. ... In human endothelial cells, the two toxins act in a conserved fashion to block formation of Sec15 vesicles, inhibit Notch ... Using Drosophila melanogaster as a model system, these authors show that these toxins interact with the Rab11/Sec15 exocyst, ...
Numerous bacterial toxins can cross biological membranes to reach the cytosol of mammalian cells, where they exert their ... Our model toxin, the adenylate cyclase (CyaA) from Bordetella pertussis, is able to invade eukaryotic cells by translocating ... Numerous bacterial toxins can cross biological membranes to reach the cytosol of mammalian cells, where they exert their ... CyaA binding to the immobilized CaM, revealed by enzymatic activity, serves as a highly sensitive reporter of toxin ...
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 ...
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 ...
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 ...
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. ...
The presence of receptors for the novel neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) has been ... The effect of PACAP38 on inositol phosphate formation was significantly reduced by U-73122 and by pertussis toxin, indicating ... Pituitary adenylate cyclase-activating polypeptide (PACAP) stimulates adenylyl cyclase and phospholipase C activity in rat ... The presence of receptors for the novel neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) has been ...
Phospholipase A activity of adenylate cyclase toxin? Jiri Masin, Radim Osicka, Ladislav Bumba, and Peter Sebo ...
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 ...
... of negative signal transduction from receptors to adenylate cyclase. Advances in experimental medicine and biology, 175, 1-16. ... Selective blockage by islet-activating protein, pertussis toxin, of negative signal transduction from receptors to adenylate ... Selective blockage by islet-activating protein, pertussis toxin, of negative signal transduction from receptors to adenylate ... Selective blockage by islet-activating protein, pertussis toxin, of negative signal transduction from receptors to adenylate ...
... 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 ...
  • This suggests that a portion of the cyclase is associated with cells in a form not accessible to antibody or washing but accessible to substrate, which we interpret as internalized enzyme with a short lifetime. (mysciencework.com)
  • In order to adequately study the nature of ACT and its role in pathogenesis, it is necessary to isolate the toxin from other virulence factors produced by the organism. (arizona.edu)
  • To maintain the synergism between the kind of immunity conferred by the vaccines and the cellular location of the included antigens, new findings are gathered about the virulence factors such as toxins, adhesins, invasins (mostly enzymes), anti-apoptotic factors, anti-phagocytic factors, and many more molecules that aid in pathogenesis and invasiveness. (jyi.org)
  • 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)
  • 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)
  • The individual subunits are secreted by a Sec-dependent mechanism into the periplasm, where the toxin is assembled. (biomedsearch.com)
  • Cassel D, Selinger Z. Mechanism of adenylate activation through the 13-adrenergic receptor: catecholamine-induced displacement of bound GDP by GTP. (springer.com)
  • All of these toxins share a similar structure and mechanism for entering targeted host cells. (wikipedia.org)
  • To explain the biochemical basis of hyperthyroidism, Pastan showed that antibodies from the serum of patients with hyperthyroidism specifically activated thyroid gland adenylate cyclase, providing an immunological mechanism for hyperthyroidism. (wikipedia.org)
  • An example of such a toxin is the large cation, tetraethylammonium (TEA), but it is notable that the toxin does not have the same mechanism of action on all potassium channels, given the variety of channel types across species. (wikipedia.org)
  • The Transporter Classification Database divides the RTX-toxin superfamily into 3 different families of homologues based on bioinformatic and phylogenetic analysis: 1.C.11 - The Pore-forming RTX Toxin (RTX-toxin) Family 1.C.56 - The Pseudomanas syringae HrpZ Cation Channel (HrpZ) Family 1.C.57 - The Clostridial Cytotoxin (CCT) Family RTX toxins were originally divided into hemolysins and leukotoxins. (wikipedia.org)
  • Taken together, these findings imply that NPR-C may operate in parallel with the guanylate cyclase-linked NPRs to regulate a number of important biological activities relevant to cardiovascular homeostasis. (ahajournals.org)
  • Taken together, the present results demonstrate that PACAP stimulates independently the adenylyl cyclase and the phospholipase C transduction pathways in immature cerebellar granule cells. (nih.gov)
  • This pathogenic bacterium produces a unique adenylate cyclase toxin (ACT) which enters human phagocytes and catalyzes the unregulated formation of cAMP, hampering important bactericidal functions of these immune cells that eventually cause cell death by apoptosis and/or necrosis. (ehu.es)
  • 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)
  • One of these factors, adenylate cyclase toxin (ACT), has been implicated to penetrate human neutrophils and macrophages and abrogate their function by virtue of unregulated production of intracellular cAMP. (arizona.edu)
  • 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)
  • In human endothelial cells, the two toxins act in a conserved fashion to block formation of Sec15 vesicles, inhibit Notch signalling, and reduce cadherin expression at adherens junctions. (nature.com)
  • It starts by membrane insertion of a toxin 'translocation intermediate', which can be 'locked' in the membrane by the 3D1 antibody blocking AC domain translocation. (prolekare.cz)
  • 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)
  • 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)
  • Bacterial toxins are involved in the pathogenesis of many bacteria, some of which are responsible for severe diseases in human and animals, but can also be used as tools in cell biology to dissect cellular processes or used as therapeutic agents. (elsevier.com)
  • The RTX toxin superfamily is a group of cytolysins and cytotoxins produced by bacteria. (wikipedia.org)
  • The bacteria attach to the cilia of the respiratory epithelial cells, produce toxins that paralyze the cilia, and cause inflammation of the respiratory tract, which interferes with the clearing of pulmonary secretions. (cdc.gov)
  • Numerous venoms and toxins produced by plants, animals, and bacteria, as well as chemical nerve agents such as Sarin, cause harm by inactivating or hyperactivating muscles via their influences on the neuromuscular junction. (wikipedia.org)
  • Here we showed that injection of sublethal doses of either lethal or edema toxin into mice directly inhibited the subsequent activation of T lymphocytes by T-cell receptor-mediated stimulation. (asm.org)
  • Adenylate cyclase activities in the basal state and under stimulation with NaF, forskolin, Gpp(NH)p, ±-isoprenaline and VIP were all markedly and similarly reduced, being only about 30% of comparable activities in membranes from control areas. (springer.com)
  • By the turn of the 19th century, it was agreed that the stimulation of sympathetic nerves could cause different effects on body tissues, depending on the conditions of stimulation (such as the presence or absence of some toxin). (wikipedia.org)