Gotowa bibliografia na temat „CAMP hydrolysis”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Zobacz listy aktualnych artykułów, książek, rozpraw, streszczeń i innych źródeł naukowych na temat „CAMP hydrolysis”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Artykuły w czasopismach na temat "CAMP hydrolysis"
1
Chin, Jik, i Xiang Zou. "Catalytic hydrolysis of cAMP". Canadian Journal of Chemistry 65, nr 8 (1.08.1987): 1882–84. http://dx.doi.org/10.1139/v87-315.
Pełny tekst źródłaStreszczenie:
[Co(trien)(OH2)(OH)]Cl2 is highly efficient in catalyzing the hydrolysis of cAMP to adenosine in neutral water (6 × 10−6 M−1 s−1 at 50 °C). The cobalt complex promoted hydrolysis of cAMP is estimated to be about a hundred million times faster than the uncatalyzed hydrolysis of cAMP. In the time that [Co(trien)(OH2)(OH)]Cl2 produces 50% cleavage of cAMP, [Co(en)2(NH3)(OH)]Cl2 or ZnCl2 has no observable effect on the hydrolysis of cAMP. A detailed mechanism is presented for the cobalt complex promoted hydrolysis of the phosphodiester.
2
Witwicka, Hanna, Marcin Kobiałka i Wojciech A. Gorczyca. "Hydrolysis of cyclic GMP in rat peritoneal macrophages." Acta Biochimica Polonica 49, nr 4 (31.12.2002): 891–97. http://dx.doi.org/10.18388/abp.2002_3748.
Pełny tekst źródłaStreszczenie:
Intact rat peritoneal macrophages (rPM) treated with 3-isobutyl-1-methylxanthine (IBMX), an inhibitor of phosphodiesterases (PDEs), accumulated more cGMP than untreated cells. A PDE activity toward [(3)H]cGMP was detected in the soluble and particulate fractions of rPM. The hydrolysis of cGMP was Ca(2+)/calmodulin-independent but increased in the presence of cGMP excess. Similar results were obtained when [(3)H]cAMP was used as a substrate. The hydrolytic activity towards both nucleotides was inhibited in the presence of IBMX. Therefore, the PDEs of families 2, 5, 10 and 11 are potential candidates for cGMP hydrolysis in the rPM. They may not only regulate the cGMP level in a feedback-controlled way but also link cGMP-dependent pathways with those regulated by cAMP.
3
Alava, M. A., K. E. DeBell, A. Conti, T. Hoffman i E. Bonvini. "Increased intracellular cyclic AMP inhibits inositol phospholipid hydrolysis induced by perturbation of the T cell receptor/CD3 complex but not by G-protein stimulation. Association with protein kinase A-mediated phosphorylation of phospholipase C-γ 1". Biochemical Journal 284, nr 1 (15.05.1992): 189–99. http://dx.doi.org/10.1042/bj2840189.
Pełny tekst źródłaStreszczenie:
Modulation of inositol phospholipid (InsPL) hydrolysis in response to increasing intracellular concentrations of cyclic AMP (cAMP) was studied in a murine T helper type II (Th2) lymphocyte clone, 8-5-5. Intact 8-5-5 cells produced maximal amounts of cAMP in response to prostaglandin E2 (PGE2), cholera toxin (CTx) or 7 beta-deacetyl-7 beta-(gamma-N-methylpiperazino)butyryl forskolin (dmpb-forskolin). cAMP generation reached a plateau after 5 min of treatment with dmpb-forskolin (300 microM) or PGE2 (1 microM), but required 60 min of treatment with CTx (1 microgram/ml). Preincubation of 8-5-5 cells with 1 microM-PGE2 or 300 microM-dmpb-forskolin (10 min at 37 degrees C) or with 1 microgram of CTx/ml (60 min at 37 degrees C) completely inhibited InsPL hydrolysis induced by perturbation of the T cell receptor (TCR)/CD3 complex with the monoclonal antibody 145.2C11. Preincubation with the cAMP analogue 8-bromo-cyclic AMP (8-Br-cAMP) also inhibited InsPL hydrolysis. Tetanolysin-permeabilized 8-5-5 cells produced cAMP in response to PGE2, dmpb-forskolin and guanosine 5′-[gamma-thio]triphosphate (GTP[S]), a non-cell-permeating, non-hydrolysable analogue of GTP that directly activates G-proteins. No inhibition of TCR/CD3-induced InsPL hydrolysis was observed under these conditions. InsPL hydrolysis was also unaffected when permeabilized cells were incubated with up to 10 mM-8-Br-cAMP, suggesting that permeabilized cells lost (a) soluble effector molecule(s) involved in mediating the inhibitory effect observed in intact cells. Treatment of 8-5-5 cells with dmpb-forskolin or CTx prior to permeabilization resulted in inhibition of TCR/CD3-induced InsPL hydrolysis, but did not affect InsPL hydrolysis induced via G-protein stimulation with GTP[S]. Treatment of permeabilized 8-5-5 cells with purified cAMP-dependent protein kinase (PKA) resulted in inhibition of TCR/CD3- but not GTP[S]-induced InsPL hydrolysis. This effect was associated with phosphorylation of phospholipase (PLC)-gamma 1 in the absence of phosphorylation of components of the TCR/CD3 complex. These results suggest that PKA-mediated phosphorylation of PLC may regulate TCR/CD3-induced InsPL hydrolysis.
4
Mary TANG, K., Elliott K. JANG i Richard J. HASLAM. "Expression and mutagenesis of the catalytic domain of cGMP-inhibited phosphodiesterase (PDE3) cloned from human platelets". Biochemical Journal 323, nr 1 (1.04.1997): 217–24. http://dx.doi.org/10.1042/bj3230217.
Pełny tekst źródłaStreszczenie:
We have used reverse transcriptase PCR, platelet mRNA and degenerate primers based on platelet peptide sequences, to amplify a fragment of platelet cGMP-inhibited phosphodiesterase (cGI-PDE; PDE3). Sequence analysis of this clone established that both the platelet and the cardiac forms of PDE3 were derived from the same gene (PDE3A). A RT-PCR product representing the C-terminal half of platelet PDE3 cDNA and corresponding to amino acid residues 560-1141 of the cardiac enzyme, was cloned and expressed in Escherichia coli cGI-PDEΔ1. Further deletion mutants were constructed by removing either an additional 100 amino acids from the N-terminus (cGI-PDEΔ2) or the 44-amino-acid insert characteristic of the PDE3 family, from the catalytic domain (cGI-PDEΔ1Δi). In addition, site-directed mutagenesis was performed to explore the function of the 44-amino-acid insert. All mutants were evaluated for their ability to hydrolyse cAMP and cGMP, their ability to be photolabelled by [32P]cGMP and for the effects of PDE3 inhibitors. The Km values for hydrolysis of cAMP and cGMP by immunoprecipitates of cGI-PDEΔ1 (182±12 nM and 153±12 nM respectively) and cGI-PDEΔ2 (131±17 nM and 99±1 nM respectively) were significantly lower than those for immunoprecipitates of intact platelet PDE3 (398±50 nM and 252±16 nM respectively). Moreover, N-terminal truncations of platelet enzyme increased the ratio of Vmax for cGMP/Vmax for cAMP from 0.16±0.01 in intact platelet enzyme, to 0.37±0.05 in cGI-PDEΔ1 and to 0.49±0.04 in cGI-PDEΔ2. Thus deletion of the N-terminus enhanced hydrolysis of cGMP relative to cAMP, suggesting that N-terminal sequences may exert selective effects on enzyme activity. Removal of the 44-amino-acid insert generated a mutant with a catalytic domain closely resembling those of other PDE gene families but despite a limited ability to be photolabelled by [32P]cGMP, no cyclic nucleotide hydrolytic activities of the mutant were detectable. Mutation of amino acid residues in putative β-turns at the beginning and end of the 44-amino-acid insert to alanine residues markedly reduced the ability of the enzyme to hydrolyse cyclic nucleotides. The PDE3 inhibitor, lixazinone, retained the ability to inhibit cAMP hydrolysis and [32P]cGMP binding by the N-terminal deletion mutants and the site-directed mutants, suggesting that PDE3 inhibitors may interact exclusively with the catalytic domain of the enzyme.
5
Takahashi, T., S. Kurosawa i C. Owyang. "Regulation of PI hydrolysis and cAMP formation by muscarinic M3 receptor in guinea pig gallbladder". American Journal of Physiology-Gastrointestinal and Liver Physiology 267, nr 4 (1.10.1994): G523—G528. http://dx.doi.org/10.1152/ajpgi.1994.267.4.g523.
Pełny tekst źródłaStreszczenie:
Carbachol (10(-8)-10(-3) M) produced two distinct biochemical responses in the guinea pig gallbladder smooth muscle: simulation of phosphoinositide (PI) hydrolysis and inhibition of forskolin-mediated adenosine 3',5'-cyclic monophosphate (cAMP) formation in a dose-dependent manner. The mean effective dose (ED50) concentration (1.6 x 10(-5) M) of carbachol-mediated stimulation of PI hydrolysis was 145 times greater than the ED50 concentration (1.1 x 10(-7) M) of carbachol mediated inhibition of cAMP formation. The inhibitory effect of carbachol on cAMP formation was antagonized by the pretreatment of pertussis toxin. To determine whether these two biochemical responses were mediated by the same or different subtypes of muscarinic receptors, the relative potencies of muscarinic receptor antagonists were calculated by Schild analysis. The M3 muscarinic antagonist 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) exhibited inhibitory constant (Ki) values at 0.3 and 1.2 nM in antagonizing the stimulation of PI hydrolysis and the inhibition of cAMP formation, respectively. The corresponding Ki values for pirenzepine, a muscarinic M1 antagonist, were 11 and 130 nM. The corresponding Ki values for AF-DX 116, a muscarinic M2 antagonist, were 34 and 450 nM. Thus 4-DAMP was 37x and 108x more potent than pirenzepine in antagonizing the stimulation of PI hydrolysis and the inhibition of cAMP formation, respectively. In addition, compared with AF-DX 116, 4-DAMP was 113x and 375x more potent in reducing stimulation of PI hydrolysis and inhibition of cAMP formation. Cholecystokinin (CCK) octapeptide (10(-10)-(10-6) M) caused a significant increase of PI hydrolysis but had no inhibitory effects on cAMP formation evoked by forskolin (10(-5) M).(ABSTRACT TRUNCATED AT 250 WORDS)
6
Bosgraaf, Leonard, Henk Russcher, Helena Snippe, Sonya Bader, Joyce Wind i Peter J. M. Van Haastert. "Identification and Characterization of Two Unusual cGMP-stimulated Phoshodiesterases in Dictyostelium". Molecular Biology of the Cell 13, nr 11 (listopad 2002): 3878–89. http://dx.doi.org/10.1091/mbc.e02-05-0302.
Pełny tekst źródłaStreszczenie:
Recently, we recognized two genes, gbpA andgbpB, encoding putative cGMP-binding proteins with a Zn2+-hydrolase domain and two cyclic nucleotide binding domains. The Zn2+-hydrolase domains belong to the superfamily of β-lactamases, also harboring a small family of class II phosphodiesterases from bacteria and lower eukaryotes. Gene inactivation and overexpression studies demonstrate thatgbpA encodes the cGMP-stimulated cGMP-phosphodiesterase that was characterized biochemically previously and was shown to be involved in chemotaxis. cAMP neither activates nor is a substrate of GbpA. The gbpB gene is expressed mainly in the multicellular stage and seems to encode a dual specificity phosphodiesterase with preference for cAMP. The enzyme hydrolyses cAMP ∼9-fold faster than cGMP and is activated by cAMP and cGMP with aK A value of ∼0.7 and 2.3 μM, respectively. Cells with a deletion of the gbpB gene have increased basal and receptor stimulated cAMP levels and are sporogeneous. We propose that GbpA and GbpB hydrolyze the substrate in the Zn2+-hydrolase domain, whereas the cyclic nucleotide binding domains mediate activation. The human cGMP-stimulated cAMP/cGMP phosphodiesterase has similar biochemical properties, but a completely different topology: hydrolysis takes place by a class I catalytic domain and GAF domains mediate cGMP activation.
7
Weijer, Cornelis J., i Antony J. Durston. "Influence of cyclic AMP and hydrolysis products on cell type regulation in Dictyostelium discoideum". Development 86, nr 1 (1.04.1985): 19–37. http://dx.doi.org/10.1242/dev.86.1.19.
Pełny tekst źródłaStreszczenie:
We describe the effect of cyclic AMP on regulation of the proportion of prespore and prestalk cells in Dictyostelium discoideum. Prespore and prestalk cells from slugs were enriched on Percoll density gradients and allowed to regulate in suspension culture under 100% oxygen. The transition of prespore to prestalk cells is blocked by cAMP, while cAMP phosphodiesterase and caffeine cause a decrease in the number of prespore cells. This suggests that extracellular cAMP plays a role in cell type proportioning by inhibiting the conversion of prespore to prestalk cells. Low concentrations of cAMP prevent the conversion of prestalk to prespore cells; the same effect is seen with hydrolysis products of cAMP, 5 AMP, adenosine and also adenine. We suggest that, when low concentrations of cAMP are added to regulating cells, the cAMP itself is quickly broken down and the breakdown products thereafter inhibit the prestalk-to-prespore conversion. The relevance of these findings is discussed in the context of an non-positional double-negative feedback model for cell type homeostasis.
8
Tulsian, Nikhil K., Abhijeet Ghode i Ganesh S. Anand. "Adenylate control in cAMP signaling: implications for adaptation in signalosomes". Biochemical Journal 477, nr 16 (21.08.2020): 2981–98. http://dx.doi.org/10.1042/bcj20200435.
Pełny tekst źródłaStreszczenie:
In cAMP-Protein Kinase A (PKA) signaling, A-kinase anchoring protein scaffolds assemble PKA in close proximity to phosphodiesterases (PDE), kinase-substrates to form signaling islands or ‘signalosomes’. In its basal state, inactive PKA holoenzyme (R2:C2) is activated by binding of cAMP to regulatory (R)-subunits leading to dissociation of active catalytic (C)-subunits. PDEs hydrolyze cAMP-bound to the R-subunits to generate 5′-AMP for termination and resetting the cAMP signaling. Mechanistic basis for cAMP signaling has been derived primarily by focusing on the proteins in isolation. Here, we set out to simulate cAMP signaling activation-termination cycles in a signalosome-like environment with PDEs and PKA subunits in close proximity to each other. Using a combination of fluorescence polarization and amide hydrogen exchange mass spectrometry with regulatory (RIα), C-subunit (Cα) and PDE8 catalytic domain, we have tracked movement of cAMP through activation-termination cycles. cAMP signaling operates as a continuum of four phases: (1) Activation and dissociation of PKA into R- and C-subunits by cAMP and facilitated by substrate (2) PDE recruitment to R-subunits (3) Hydrolysis of cAMP to 5′-AMP (4) Reassociation of C-subunit to 5′-AMP-bound-RIα in the presence of excess ATP to reset cAMP signaling to form the inactive PKA holoenzyme. Our results demonstrate that 5′-AMP is not merely a passive hydrolysis end-product of PDE action. A ‘ligand-free’ state R subunit does not exist in signalosomes as previously assumed. Instead the R-subunit toggles between cAMP- or 5′-AMP bound forms. This highlights, for the first time, the importance of 5′-AMP in promoting adaptation and uncovers adenylate control in cAMP signaling.
9
Takasu, N., T. Yamada i Y. Shimizu. "Thyrotrophin and prostaglandin E2 increase calmodulin levels and cyclic AMP phosphodiesterase activity in cultured porcine thyroid cells". Journal of Endocrinology 117, nr 1 (kwiecień 1988): 109–14. http://dx.doi.org/10.1677/joe.0.1170109.
Pełny tekst źródłaStreszczenie:
ABSTRACT Thyrotrophin (TSH) and prostaglandin E2 (PGE2) increased cellular cyclic AMP (cAMP), calmodulin levels and cAMP phosphodiesterase activity in cultured porcine thyroid cells. Dibutyryl cAMP (dbcAMP), a stable analogue of cAMP, increased calmodulin levels and cAMP phosphodiesterase activity. These results indicate that TSH- and PGE2-stimulated increases in calmodulin are mediated by cAMP. This increased concentration of calmodulin in turn stimulates cAMP phosphodiesterase. Double reciprocal plots of cAMP hydrolysis yielded two apparent Michaelis constants (Km); the lower in the 1 μmol/l and the higher in the 10 μmol/l range. Thyrotrophin, PGE2 and dbcAMP increased the values of maximal velocity without changing the Km values. J. Endocr. (1988) 117, 109–114
10
Artman, M., P. A. Kithas, J. S. Wike i S. J. Strada. "Inotropic responses change during postnatal maturation in rabbit". American Journal of Physiology-Heart and Circulatory Physiology 255, nr 2 (1.08.1988): H335—H342. http://dx.doi.org/10.1152/ajpheart.1988.255.2.h335.
Pełny tekst źródłaStreszczenie:
Inotropic response to four different types of pharmacological stimuli were compared in isolated right ventricular papillary muscles from newborn (24–48 h of age), immature (14–16 days), and adult (6–7 mo) rabbits. Forskolin, a direct activator of adenylate cyclase, produced a 12.5-fold increase in the maximal rate of tension development in the newborn group. The maximum response to isoproterenol was only 45% of the maximum forskolin response, suggesting incomplete physiological coupling of myocardial beta-adrenergic receptors to adenylate cyclase at birth. In contrast to the substantial inotropic response to agents that stimulate adenosine 3',5'-cyclic monophosphate (cAMP) generation (forskolin and isoproterenol), a selective inhibitor of cAMP hydrolysis (milrinone) was relatively ineffective in the newborn group. Sulmazole, a drug that enhances calcium sensitivity of the contractile proteins, produced its greatest inotropic effect in immature myocardium. Cytosolic high-affinity cAMP phosphodiesterase activity was partially purified from ventricular homogenates by anion-exchange chromatography. The kinetics of cAMP hydrolysis (Km and Vmax) and inhibitory potency of milrinone were comparable in each age group. Thus the age-related differences in inotropic responsiveness may not be attributable to postnatal changes in myocardial cytosolic high-affinity cAMP phosphodiesterase activity.
Rozprawy doktorskie na temat "CAMP hydrolysis"
1
D’Oliveira, Elisabete Castro. "Origem da acidez da nascente do rio Campo Belo, maciço do Itatiaia - R.J". Niterói, 2017. https://app.uff.br/riuff/handle/1/5382.
Pełny tekst źródłaStreszczenie:
Submitted by Biblioteca de Pós-Graduação em Geoquímica BGQ (bgq@ndc.uff.br) on 2017-12-18T14:58:25Z
No. of bitstreams: 1
Dissertação realmente corrigida.pdf: 2600370 bytes, checksum: f6dfd5312d899b3cc7513282683ff5be (MD5)Made available in DSpace on 2017-12-18T14:58:25Z (GMT). No. of bitstreams: 1 Dissertação realmente corrigida.pdf: 2600370 bytes, checksum: f6dfd5312d899b3cc7513282683ff5be (MD5)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
Universidade Federal Fluminense. Instituto de Química. Programa de Pós-Graduação em Geoquímica, Niterói, RJ
Pode-se considerar a química das águas naturais dividida em duas categorias de reações mais comuns: as reações ácido-base e as de oxidação-redução. Os fenômenos ácidobase e de solubilidade controlam o pH e as concentrações de íons inorgânicos, resultando em composição química variada de acordo com as condições bioclimáticas. A origem da acidez de uma água natural pode estar relacionada à geoquímica e ao aporte de matéria orgânica e nutrientes, fenômeno frequente em ambientes que apresentam drenagem sob turfeira. As turfeiras são ambientes especiais para estudos relacionados com a dinâmica da matéria orgânica, elas contribuem para o sequestro global de carbono, além de funcionarem como reservatórios de água. Nesse contexto, o objetivo desse trabalho foi analisar a correlação da matéria orgânica e da interação água-rocha com a acidez observada na nascente do rio Campo Belo, situada à 2419 m de altitude, no Maciço do Itatiaia. Para isso, foram coletadas amostras de água e solo, submetidas à analise dos parâmetros físico-químicos in situ e análise dos íons maiores e elementos traço em laboratório. Os resultados encontrados foram utilizados para a realização da modelagem para especiação de íons em água e tratamento estatístico multivariado, que mostraram que a disponibilidade do alumínio no solo está correlacionada com as variações do pH ao longo do perfil. A liberação do alumínio aumenta a acidez do sistema através da hidrólise ácida da água, o que por sua vez, favorece o aumento da desmineralização e lixiviação de bases, favorecendo a concentração e retenção do alumínio no solo. Embora a matéria orgânica não seja responsável pela acidez, a presença da turfa é fator imprescindível para a manutenção da acidez, pois atua como sequestrador de bases ao formar complexos com as substâncias húmicas, além de exercer papel tamponante no sistema.
The chemistry of natural waters can be divided in two more common reaction categories: acid-base reactions, and oxidation-reduction reactions. Acid-base and solubility phenomena control the pH and the inorganic ions concentrations, which result in diverse chemical composition, according to bioclimatic conditions. Acidity origin of natural waters can be related to its geochemistry and to organic matter and nutrient supplies, which are frequent phenomena in environments that present drainage underneath turf. Turfs are special environments for studies related to organic matter dynamic, they contribute to carbon global sequestration, besides functioning as water reservoirs. In that context, the aim of this work was to analyse the correlation between organic matter and water-rock interaction with the acidity observed at the Campo Belo river spring, located at 2419 m of altitude, at the Itatiaia massif. For that, water and soil samples were collected, and analised in terms of their physical-chemical parameters, in situ, and also analysis of the major ions and trace elements in laboratory. The observed results were used in an ion speciation modeling in water, and multivariate statistical analysis, that showed that the availability of aluminum in the soil is correlated to the pH variations along the soil profile. The liberation of aluminum increases the system acidity through acidic hydrolysis of water, which, in turn, promotes the increase of the demineralization and leaching of basis, favoring the concentration and retention of the aluminum of the soil. Despite the organic matter is not responsible for the acidity, the presence of turf is an indispensable factor for the maintenance of the acidity, since it acts as basis sequestrant as it forms complexes with humic substances, besides playing a role in buffering the system.
2
Biswas, Priyanka. "Rv0805, a novel regulator of central carbon metabolism and cell envelope properties in mycobacteria". Thesis, 2020. https://etd.iisc.ac.in/handle/2005/4617.
Pełny tekst źródłaStreszczenie:
Metabolic flexibility is one of the key factors that underpin mycobacterial physiology and pathogenesis. During infection, mycobacteria shift towards utilising host-derived fatty acids, lipids, cholesterol and cholesterol-esters. This, coupled with elevation in virulence polyketide lipid synthesis, induces critical changes in host-pathogen interaction that affect key signalling events inside macrophages that favour intracellular survival of mycobacteria. However, assimilation of cholesterol leads to elevated levels of propionyl-CoA, which can result in extreme metabolic toxicity unless utilised efficiently. In a high throughout analysis, the gene encoding Rv0805, present in slow-growing, pathogenic mycobacterial species and characterized as a cAMP phosphodiesterase, was identified as one of the genes essential for cholesterol utilisation in mycobacteria.
Previous reports from our laboratory suggested that cAMP hydrolysis is not the main function of Rv0805. Therefore, to elucidate the biological role of Rv0805 in mycobacteria, M. bovis BCG was chosen as a model system, and the effects of deletion of the orthologue of rv0805 (bcg_0857) were analysed. Analysis of growth and measurement of metabolites and their turnover using 13C flux approaches showed that BCG_0857 is crucial for growth in media containing cholesterol and propionate. BCGΔ0857 showed impaired propionate assimilation and depletion of CCM metabolites, when propionate was provided as the sole carbon source. Based on gene expression analysis of enzymes involved in the metabolism of propionate, it appeared that the BCGΔ0857 strain experienced a depletion in its carbon reservoir because of increased lipid synthesis. Supporting this, analysis of polar and apolar lipids from the cell envelope of BCGΔ0857 showed anomalies in the levels of PDIMs, PGL and AC2PIM2. Changes in cell envelope composition rendered BCGΔ0857 susceptible to cell wall perturbants, lipophilic antibiotics and led to perturbation of intrabacterial pH homeostasis. Induction of sigE and clgR further supported the presence of a stressed cell envelope in BCGΔ0857. Induction of sigE was attributed to the abberrant accumulation of an unkown phosphodiester substrate of BCG_0857, as evidenced by the fact that the catalytic activity of BCG_0857 was critical for rescuing growth and cell wall-related defects. To conclude, the findings show how a cell envelope localised metallophosphoesterase plays an important regulatory function in central carbon metabolism and generation of an optimum cell envelope in slow growing mycobacteria. Based on this knowledge, we suggest that MtbΔrv0805 would be compromised in intracellular survival during infection and future anti-mycobacterial strategies could be designed that target Rv0805.
Części książek na temat "CAMP hydrolysis"
1
Chornet, Esteban, i Ralph P. Overend. "How the Severity Factor in Biomass Hydrolysis Came About". W Hydrothermal Processing in Biorefineries, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56457-9_1.
Pełny tekst źródła
2
Benjamin Kaupp, U., Claudia Dzeja, Stephan Frings, Jürgen Bendig i Volker Hagen. "[23] Applications of caged compounds of hydrolysis-resistant analogs of cAMP and cGMP". W Methods in Enzymology, 415–30. Elsevier, 1998. http://dx.doi.org/10.1016/s0076-6879(98)91026-6.
Pełny tekst źródła
3
Freitas, Izabela Silva, Aryane Maria de Oliveira Lima, Edson de Paiva Alves, Luiz Antônio Magalhães Pontes i Guilherme João Musse Neto. "Simulation of tubular reactor for production of methacrylic acid via hydrolysis of methacrylamide sulfate". W Engenharia, Gestão e Inovação – Volume 3. Editora Poisson, 2022. http://dx.doi.org/10.36229/978-65-5866-179-5.cap.14.
Pełny tekst źródła
4
Brown, Andrew. "Revolutions in Physiology and Power". W Bound by Muscle, 104—C8.N60. Oxford University PressNew York, 2022. http://dx.doi.org/10.1093/oso/9780197582633.003.0008.
Pełny tekst źródłaStreszczenie:
Abstract In 1930, Lundsgaard from Copenhagen showed poisoned muscle fibers could still contract but generate no lactic acid. He explained to Hill, “the lactic acid formation only plays quite a secondary role for the liberation of energy during the contraction.” Meyerhof invited Lundsgaard to his new lab in Heidelberg and their subsequent work prompted Hill to proclaim “a revolution in muscle physiology.” Lohmann continued to study the high-energy phosphate molecule, ATP. Meyerhof came to the realization that hydrolysis of ATP, with the release of a burst of energy, is the primary event leading to contraction. Meyerhof’s group also continued to unravel the multiple steps of glycolysis and identified a large proportion of the coenzymes that facilitate the process. Hitler’s ascent early in 1933 cast a pall over German universities. Meyerhof was acutely aware but thought it would be short-lived. Hill helped to create the Academic Assistance Council in the United Kingdom.
Streszczenia konferencji na temat "CAMP hydrolysis"
1
Brass, L. F., D. R. Manning i M. J. Woolkalis. "G PROTEIN REGULATORS OF PHOSPHOLIPASE C AND ADENYLATE CYCLASE IN PLATELETS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644630.
Pełny tekst źródłaStreszczenie:
The hydrolysis of polyphosphoinositides (PI) by phospholipase C during platelet activation produces two key intracellular messengers, inositol triphosphate and diacylglycerol. This process is thought to be regulated by a guanine nucleotide binding protein referred to as Gp. Although the evidence that Gp exists is compelling, to date it has not been isolated. Uncertainty about its identity has been compounded by variations between tissues in the susceptibility of Gp to pertussis toxin and by reconstitution studies which show that pertussis toxin-inhibited PI hydrolysis can be restored by purified Gi, the pertussis toxin-sensitive G protein which inhibits adenylate cyclase. Therefore, it remains unclear whether Gp represents a new G protein or a second role for Gj. When platelets permeabilized with saponin were incubated with pertussis toxin and 32P-NAD, a single 42 kDa protein was 32P-ADP-ribosylated which co-migrated with the purified a subunit of Gi. Preincubating the platelets with an agonist inhibited labeling of this protein by dissociating the G protein into subunits. The extent of inhibition correlated with the number of toxin-sensitive functions caused by the agonist. Labeling was abolished by thrombin, which inhibited cAMP formation and caused toxin-inhibitable PI hydrolysis. Labeling was partially inhibited by vasopressin and platelet activating factor, which caused toxin-inhibitable PI hydrolysis, but had no effect on cAMP formation and by epinephrine, which inhibited cAMP formation, but did not cause PI hydrolysis. Labeling was unaffected by the TxA2 analog U46619, which neither caused toxin-sensitive PI hydrolysis nor inhibited cAMP formation. These observations suggest that the 42 kDa band may contain a subunits from both Gp and Gi and, in fact, 2D electrophoresis resolved the 42 kDa protein band into two proteins with distinct pi. However, those agonists linked functionally only to Gp or only to Gi decreased the labeling of both proteins. Therefore, our data suggest (1) that Gj and Gp are the same protein and (2) that whether a aiven platelet agonist affects adenylate cyclase or phospholipase C or both depends upon factors extrinsic to the G protein.
2
Grant, P. G., A. F. Mannarino i R. W. Colman. "REGULATION OF CYCLIC NUCLEOTIDE PHOSPHODIESTERASE ACTIVITY IN PLATELETS BY PHOSPHORYLATION". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642820.
Pełny tekst źródłaStreszczenie:
Cyclic nucleotide phosphodiesterases (PDE) provide the only known pathway for the hydrolysis of cyclic nucleotides in cells and thus have the potential for modulating the effects of cAMP and cGMP on cells. In platelets a rise in intracellular cAMP levels inhibits platelet aggregation and secretion. Since cAMP exerts many of its effects through a cAMP-dependent kinase we questioned whether phosphorylation of cAMP PDE might be a mode for regulation of PDE activity in platelets. When platelets were incubated for 10 min with forskolin (100 μM) the level of cAMP rose at least 10-fold.When the low Km cyclic nucleotide PDE was isolated from freeze-thaw lysates of forskolin treated platelets by chromatography on blue dextran-Sepharose, the specific activity of this enzyme was increased 3 to 13-fold over similarly processed control platelets. The specific activity of a second PDE, the cGMP-stimulated cAMP PDE, was increased 1.5 to 3-fold by forskolin treatment of platelets. Forskolin had no direct effect on either purified PDE. The stimulation of the low Km cAMP PDE activity by exposure of platelets to forskolin was blocked when the platelets were simultaneously treated with the protein kinase inhibitor H-8 (100 μM) which is most potent toward cAMP dependent protein kinase indicating that this kinase may be responsible for the stimulation. When platelets which had been prelabeled with 32P inorganic phosphate were treated with forskolin and the low Km cAMP PDE isolated by blue dextran-Sepharose chromatography, a protein migrating in SDS gels at Mr=110,000, the molecular weight of the low Km cAMP PDE, was labeled indicating that phosphorylation of the PDE occurred coincident with stimulation of activity. These results suggest that phosphorylation of the low Km cAMP PDE by protein kinase may be an important regulatory mechanism for cAMP PDE activity and cyclic nucleotide levels in platelets.
3
Asaji, T., E. Murakami, N. Takekoshi, S. Matsui i T. Imaoka. "EFFECT OF ATRIAL NATRIURETIC POLYPEPTIDES ON PLATELET FUNCTION". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644872.
Pełny tekst źródłaStreszczenie:
Atrial natriuretic polypeptides (ANP) have been shown to possess a potent diuretic and natriuretic activity, and medicated to patients with heart insufficiency as a drug to be mediated by cGMPaccumulation in glomeruli. A existence of receptors for ANP have recently beenreported in human platelet. But, whether ANP has a direct effect on platelet function remains to be known.Single stimulation of ANP in any concentration did not induce aggregation in neither platelet rich plasma, nor washed platelets. Also no effect of pretreatment with ANP was observed against aggregation triggered by known mediators of platelet activation (Thrombin, ADP, Epinephrine, Collagen) using platelet rich plasma and washed platelets.Therefore, biochemical parameters such as cyclic nucleotides (cAMP, cGMP), phosphatidylinositol hydrolysis and protein phosphorylation, leading to the early stage of platelet activation were examined to investigate the effect of ANP in receptor linked transducing mechanism. Neither cyclic nucleotides accumulation nor [32 P] phosphatidic acid production were detected in platelets treated with ANP. ANP caused a small increase of 32P incorporation into M 30K protein, but no change on the level of phosphorylation of 47K, 20K protein (Imaoka, T. and Haslam, R.J., J.Biol.Chem.258,11404, 1983) was observed.These results clearly suggested thatANP binding with membrane receptor was not linked with adenylate cyclase, ganulate cyclase and phosphatidylinositol phosphate turnover in human platelet, maybe because of too few numbers of ANP receptor. Mechanism of 30K protein phosphorylation and Ca++ mobilization are important subjects for future study, (supported by MESC of Japan)
4
Kumrungsee, Thanutchaporn, Norihisa Kato, Toshiro Matsui i Yongshou Yang. "Plant and gut microbiota-derived protein metabolites and potential health functions". W 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/envt3719.
Pełny tekst źródłaStreszczenie:
Bioactive peptides can be obtained from protein hydrolysates through in vitro enzymatic hydrolysis, gastrointestinal digestion, and microbial fermentation. Recent emerging research suggests that prebiotic-stimulated gut microbiota also plays a role in generating bioactive peptides and amino acids in gut. In this study, we examined if enzymatic hydrolysis of soybean and wheat germ, plant materials often used in oil industry, can generate antihypertensive peptides and determined if prebiotic digestive enzymes can induce the production of gut microbiota-derived amino acids. In the first experiment, soybean and wheat germ were hydrolyzed by protease enzymes. Then, their hydrolysates were subjected to peptide isolation and identification. Identified peptides were subjected to test for their potential antihypertensive activities. For the second experiment, rodents were fed an Aspergillus-derived protease- or lipase-mixed diet for 2 weeks. Then, cecum contents were collected for bacteria and metabolite analyses. As a result, we found that His-Gly-Lys from soybean hydrolysate strongly inhibited angiotensin II-induced elevated intracellular Ca2+ concentration in vascular smooth muscle cells (VSMCs). Trp-Val and Trp-Ile from wheat germ hydrolysate were found to inhibit Ca2+-calmodulin (CaM)-dependent protein kinase II (CaMK II), a protein kinase promoting hypertension by inducing Ca2+ influx into VSMCs, in rat thoracic aorta rings. These findings suggest the potential of the plant-derived peptides in preventing hypertension and vascular-related diseases. In the second experiment, we found that the dietary protease and lipase increased Bifidobacterium and Lactobacillus probiotics and induced the production of probiotic-derived amino acids, taurine, ornithine, and γ-aminobutyric acid. Since these amino acids have versatile functions including in gut health modulation and brain functions, it can be hypothesized that the dietary prebiotic-digestive enzymes may be beneficial for gut health and brain functions. This study suggests the possibility of applying oil processing by-products in the production of functional food ingredients including bioactive peptides and amino acids.
Raporty organizacyjne na temat "CAMP hydrolysis"
1
Gent, David B., Jared L. Johnson i Ian T. Osgerby. Characterization of Firing Range Soil from Camp Edwards, MA, and the Efficacy of Acid and Alkaline Hydrolysis for the Remediation of M1 105mm M67 Propellant. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2013. http://dx.doi.org/10.21236/ada583085.
Pełny tekst źródła
2
Philosoph-Hadas, Sonia, Richard Crain, Shimon Meir, Nehemia Aharoni i Susan Lurie. Calcium-Mediated Signal Transduction during Leaf Senescence. United States Department of Agriculture, listopad 1995. http://dx.doi.org/10.32747/1995.7604925.bard.
Pełny tekst źródłaStreszczenie:
We have examined the possibility that modulation of [Ca2+]cyt may represent a signal which induces senescence processes in leaves, through triggering of lipid hydrolysis leading to the cascade of detriorative events. Characterization of the signal transduction components operating during leaf senescence was gained by studying various Ca2+-dependent activities of parsley and chrysanthemum leaves, in relation to several senescence functions, and in response to senescence-modulating hormones (ethylene,ABA, BA and IAA). Some innovative findings regarding the control of senescence processes by [Ca2+]cyt were established: Several Ca2+-or CaM-related compounds were shown to modulate [Ca2+]cyt and action, thereby affecting whole leaf senescence. The involvement of [Ca2+]cyt in mediating the effects of senescence-modulating hormones has been demonstrated. Loss of energized Ca2+-transport capability of PM was found to an early event in leaf senescence, which occurs before changes in senescence parameters are observed, and while other PM ATPase enzymes still retain about 50% of their activities. A general pattern of increased phosphorylation of PM proteins with advanced senescence, which could be modified by plant hormones applied in vivo (BA) or in vitro (ABA), sa found. Taken together, all this indirect evidence indicate that [Ca2+]cyt is elevated due to the senescence-induced decrease in the ability to extrude Ca2+, which results particularly from reduced PM Ca2++-transport capability rather than increased operation of Ca2+ channels or elevated Ins(1,4,5)P3 levels. The direct proof for such a senescence-related elevation in [Ca2+]cyt was provided for the first time by the Ca2+ imaging measures with fura-2, showing a rise in [Ca2+]cyt of mesophyll cells upon senescence induction, which preceeded changes in typical senescence characteristics. This research provides strong evidence for regarding the rise in [Ca2+]cyt as a primary event in induction of the senescence syndrome in detached leaves. The findings have also broad implications for postharvest handling of leafy crops and ornamentals, and open new avenues for employing Ca2+-related inhibitors to delay leaf senescence.