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Relevant bibliographies by topics / Inhibitor

Academic literature on the topic 'Inhibitor'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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Journal articles on the topic "Inhibitor"

1

Sever, Natasa, Metka Filipic, Joze Brzin, and Tamara T. Lah. "Effect of Cysteine Proteinase Inhibitors on Murine B16 Melanoma Cell Invasion in vitro." Biological Chemistry 383, no. 5 (May 15, 2002): 839–42. http://dx.doi.org/10.1515/bc.2002.088.

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Abstract Various types of proteinases are implicated in the malignant progression of human and animal tumors. Proteinase inhibitors may therefore be useful as therapeutic agents in antiinvasive and antimetastatic treatment. The aims of this study were (1) to estimate the relative importance of proteinases in B16 cell invasion in vitro using synthetic, classspecific proteinase inhibitors and (2) to assess the inhibitory effect of some naturally occurring cysteine proteinase inhibitors. Serine proteinase inhibitor reduced invasiveness by up to 24%, whereas inhibition of aspartic proteinases reduced invasion by 11%. Synthetic inhibitors of cysteine proteinases markedly impaired invasion: cathepsin B inhibitors, particularly Ca 074Me, inhibited invasion from 20 40%, whereas cathepsin L inhibitor Clik 148 reduced invasion by 11%. The potato cysteine proteinase inhibitor PCPI 8.7 inhibited invasion by 21%, whereas another potato inhibitor, PCPI 6.6, and the mushroom cysteine proteinase inhibitor clitocypin had no effects. As the inhibitors that inhibited cathepsin B were in general more efficient at impairing the invasiveness, we conclude that of the two cysteine proteinases, cathepsin B plays a more important role than cathepsin L in murine melanoma cell invasion.

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Jasim, Haider Hadi, Read Abd Al-Hussain, and Ahmed Shawqi Sadeq. "Evaluation the Efficiency of Various Types of Corrosion Inhibitors Used for Basrah Water Storage Tanks." Al-Nahrain Journal for Engineering Sciences 23, no. 3 (November 21, 2020): 267–76. http://dx.doi.org/10.29194/njes.23030267.

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In this paper, the efficiency of six different types of corrosion inhibitors used in Basrah drinking water tanks was assessed using a potentiostatic test method. The mechanism of adsorption of silicate and phosphate inhibitors in AISI 316 stainless steel surfaces and the effects of different water components in inhibitors are discussed in detail. The values of corrosion rate obtained from the Potentiostatic test showed that the protection against corrosion in the presence of inhibitors is better compared to the case of absence of inhibitors. The results of the six types of corrosion inhibitors tested showed that the inhibitory efficacy is higher below the temperatures 45oC, but when raise the temperature above 45oC the inhibitory efficiency becomes to decrease. Also, the test results indicated that the corrosion inhibitor involves silicate products provided more inhibited efficiency compared to the phosphate inhibitor alone or used the combined silicate/phosphate corrosion inhibitor. The inspection of the surface of the tested samples using optical methods shows that the pitting corrosion is demonstrated on the specimen surfaces after testing with or without inhibitors.

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KUMAR, Priyadarsini, and Donal A. WALSH. "A dual-specificity isoform of the protein kinase inhibitor PKI produced by alternate gene splicing." Biochemical Journal 362, no. 3 (March 8, 2002): 533–37. http://dx.doi.org/10.1042/bj3620533.

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We have previously shown that the protein kinase inhibitor β (PKIβ) form of the cAMP-dependent protein kinase inhibitor exists in multiple isoforms, some of which are specific inhibitors of the cAMP-dependent protein kinase, whereas others also inhibit the cGMP-dependent enzyme [Kumar, Van Patten and Walsh (1997), J. Biol. Chem. 272, 20011–20020]. We have now demonstrated that the switch from a cAMP-dependent protein kinase (PKA)-specific inhibitor to one with dual specificity arises as a consequence of alternate gene splicing. We have confirmed using bacterially produced pure protein that a single inhibitor species has dual specificity for both PKA and cGMP-dependent protein kinase (PKG), inhibiting each with very high and closely similar inhibitory potencies. The gene splicing converted a protein with 70 amino acids into one of 109 amino acids, and did not change the inhibitory potency to PKA, but changed it from a protein that had no detectable PKG inhibitory activity to one that now inhibited PKG in the nanomolar range.

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Krulikas, Linas J., Ian M. McDonald, Benjamin Lee, Denis O. Okumu, Michael P. East, Thomas S. K. Gilbert, Laura E. Herring, et al. "Application of Integrated Drug Screening/Kinome Analysis to Identify Inhibitors of Gemcitabine-Resistant Pancreatic Cancer Cell Growth." SLAS DISCOVERY: Advancing the Science of Drug Discovery 23, no. 8 (May 9, 2018): 850–61. http://dx.doi.org/10.1177/2472555218773045.

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Continuous exposure of a pancreatic cancer cell line MIA PaCa-2 (MiaS) to gemcitabine resulted in the formation of a gemcitabine-resistant subline (MiaR). In an effort to discover kinase inhibitors that inhibited MiaR growth, MiaR cells were exposed to kinase inhibitors (PKIS-1 library) in a 384-well screening format. Three compounds (UNC10112721A, UNC10112652A, and UNC10112793A) were identified that inhibited the growth of MiaR cells by more than 50% (at 50 nM). Two compounds (UNC10112721A and UNC10112652A) were classified as cyclin-dependent kinase (CDK) inhibitors, whereas UNC10112793A was reported to be a PLK inhibitor. Dose–response experiments supported the efficacy of these compounds to inhibit growth and increase apoptosis in 2D cultures of these cells. However, only UNC10112721A significantly inhibited the growth of 3D spheroids composed of MiaR cells and GFP-tagged cancer-associated fibroblasts. Multiplexed inhibitor bead (MIB)–mass spectrometry (MS) kinome competition experiments identified CDK9, CLK1-4, DYRK1A, and CSNK1 as major kinase targets for UNC10112721A in MiaR cells. Another CDK9 inhibitor (CDK-IN-2) replicated the growth inhibitory effects of UNC10112721A, whereas inhibitors against the CLK, DYRK, or CSNK1 kinases had no effect. In summary, these studies describe a coordinated approach to discover novel kinase inhibitors, evaluate their efficacy in 3D models, and define their specificity against the kinome.

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Suzuki, Suzuki, Morio Arai, Kagehiro Amano, Kazuhiko Kagawa, and Katsuyuki Fukutake. "Factor VIII Inhibitor Antibodies with C2 Domain Specificity Are Less inhibitory to Factor VIII Complexed with von Willebrand Factor." Thrombosis and Haemostasis 76, no. 05 (1996): 749–54. http://dx.doi.org/10.1055/s-0038-1650655.

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SummaryIn order to clarify the potential role of von Willebrand factor (vWf) in attenuating the inactivation of factor VIII (fVIII) by those antibodies with C2 domain specificity, we investigated a panel of 14 human antibodies to fVIII. Immunoblotting analysis localized light chain (C2 domain) epitopes for four cases, heavy chain (A2 domain) epitopes in five cases, while the remaining five cases were both light and heavy chains. The inhibitor titer was considerably higher for Kogenate, a recombinant fVIII concentrate, than for Haemate P, a fVIII/vWf complex concentrate, in all inhibitor plasmas that had C2 domain specificity. In five inhibitor plasmas with A2 domain specificity and in five with both A2 and C2 domain specificities, Kogenate gave titers similar to or lower than those with Haemate P. The inhibitory effect of IgG of each inhibitor plasma was then compared with recombinant fVIII and its complex with vWf. When compared to the other 10 inhibitor IgGs, IgG concentration, which inhibited 50% of fVIII activity (IC50), was remarkably higher for the fVIII/vWf complex than for fVIII in all the inhibitor IgGs that had C2 domain reactivity. Competition of inhibitor IgG and vWf for fVIII binding was observed in an ELISA system. In 10 inhibitors that had C2 domain reactivity, the dose dependent inhibition of fVIII-vWf complex formation was observed, while, in the group of inhibitors with A2 domain specificity, there was no inhibition of the complex formation except one case. We conclude that a subset of fVIII inhibitors, those that bind to C2 domain determinants, are less inhibitory to fVIII when it is complexed with vWf that binds to overlapping region in the C2 domain.

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ALIAS, ZAZALI, and NORA ASYIKIN RAMLI. "PURIFICATION AND PARTIAL CHARACTERISATION OF A PROTEASE INHIBITOR FROM Mimosa diplotricha." Malaysian Applied Biology 51, no. 4 (October 31, 2022): 169–75. http://dx.doi.org/10.55230/mabjournal.v51i4.26.

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Search for inhibitors to insect proteases is one of many strategies to control pests. Previous work has demonstrated successful purification of effective inhibitors from plant origin. Thus, the current study attempted to purify protease inhibitors from locally available medicinal plants. The study demonstrated that the ethanolic extracts of Mimosa diplotricha leaves caused a significant 80% reduction in bovine trypsin activity. The inhibitory property of the proteinaceous nature of the extract was reconfirmed through qualitative analysis using the detection of trypsin inhibitors on the SDS-PAGE technique. The ammonium precipitated trypsin inhibitor was purified using Hi-Trap G25 and resolved into a single band with a molecular weight of approximately 20.8 kDa. By using the Dixon plot the competitive inhibitor has a Ki value of 2.16 × 10-4 mM. The purified protein inhibited the protease extract of Chrysomya megacephala at IC50 of 28 μg/mL. The results highlighted the presence of trypsin inhibitor in Mimosa diplotricha and its potential as a pest control agent.

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Li, Qi, Hongyu Yang, Jun Mo, Yao Chen, Yue Wu, Chen Kang, Yuan Sun, and Haopeng Sun. "Identification by shape-based virtual screening and evaluation of new tyrosinase inhibitors." PeerJ 6 (January 26, 2018): e4206. http://dx.doi.org/10.7717/peerj.4206.

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Targeting tyrosinase is considered to be an effective way to control the production of melanin. Tyrosinase inhibitor is anticipated to provide new therapy to prevent skin pigmentation, melanoma and neurodegenerative diseases. Herein, we report our results in identifying new tyrosinase inhibitors. The shape-based virtual screening was performed to discover new tyrosinase inhibitors. Thirteen potential hits derived from virtual screening were tested by biological determinations. Compound 5186-0429 exhibited the most potent inhibitory activity. It dose-dependently inhibited the activity of tyrosinase, with the IC50 values 6.2 ± 2.0 µM and 10.3 ± 5.4 µM on tyrosine and L-Dopa formation, respectively. The kinetic study of 5186-0429 demonstrated that this compound acted as a competitive inhibitor. We believe the discoveries here could serve as a good starting point for further design of potent tyrosinase inhibitor.

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Arita, Minetaro, Takaji Wakita, and Hiroyuki Shimizu. "Cellular kinase inhibitors that suppress enterovirus replication have a conserved target in viral protein 3A similar to that of enviroxime." Journal of General Virology 90, no. 8 (August 1, 2009): 1869–79. http://dx.doi.org/10.1099/vir.0.012096-0.

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Previously, we identified a cellular kinase inhibitor, GW5074, that inhibits poliovirus (PV) and enterovirus 71 replication strongly, although its target has remained unknown. To identify the target of GW5074, we searched for cellular kinase inhibitors that have anti-enterovirus activity similar or related to that of GW5074. With this aim, we performed screenings to identify cellular kinase inhibitors that could inhibit PV replication cooperatively with GW5074 or synthetically in the absence of GW5074. We identified MEK1/2 inhibitors (SL327 and U0126), an EGFR inhibitor (AG1478) and a phosphatidylinositol 3-kinase inhibitor (wortmannin) as compounds with a cooperative inhibitory effect with GW5074, and an Akt1/2 inhibitor (Akt inhibitor VIII) as a compound with a synthetic inhibitory effect with MEK1/2 inhibitors and AG1478. Individual treatment with the identified kinase inhibitors did not affect PV replication significantly, but combined treatment with MEK1/2 inhibitor, AG1478 and Akt1/2 inhibitor suppressed the replication synthetically. The effect of AG1478 in this synthetic inhibition was compensated by other receptor tyrosine kinase inhibitors (IGF-1R inhibitor II and Flt3 inhibitor II). We isolated mutants resistant to Flt3 inhibitor II and GW5074 and found that these mutants had cross-resistance to each treatment. These mutants had a common mutation in viral protein 3A that results in an amino acid change at position 70 (Ala to Thr), a mutation that was previously identified in mutants resistant to a potent anti-enterovirus compound, enviroxime. These results suggest that cellular kinase inhibitors and enviroxime have a conserved target in viral protein 3A to suppress enterovirus replication.

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Curry, V. A., I. M. Clark, H. Bigg, and T. E. Cawston. "Large inhibitor of metalloproteinases (LIMP) contains tissue inhibitor of metalloproteinases (TIMP)-2 bound to 72,000-Mr progelatinase." Biochemical Journal 285, no. 1 (July 1, 1992): 143–47. http://dx.doi.org/10.1042/bj2850143.

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Connective-tissue cells in culture produce a family of metalloproteinases which, once activated, can degrade all the components of the extracellular matrix. These potent enzymes are all inhibited by the tissue inhibitor of metalloproteinases (TIMP), and it was thought that this inhibitor was solely responsible for the inhibition of these enzymes within connective tissue. However, other inhibitors have recently been described, including large inhibitor of metalloproteinases (LIMP) present in the culture medium of human foetal lung fibroblasts. Here we show that a large proportion of the inhibitory activity of LIMP consists of 72,000-M(r)-progelatinase bound to TIMP-2, a recently discovered low-M(r) metalloproteinase inhibitor closely related to TIMP. The physiological implications of the secretion of a complex of 72,000-M(r) progelatinase and TIMP-2 are discussed, and the separation of the complex in 6 M-urea is described.

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Moon, Hyun-Jung, Su-Hoon Lee, Hak-Bong Kim, Kyoung-A. Lee, Chi-Dug Kang, and Sun-Hee Kim. "SIRT1 Inhibitor Enhances Hsp90 Inhibitor-mediated Abrogation of Hsp90 Chaperone Function and Potentiates the Cytotoxicity of Hsp90 Inhibitor in Chemo-resistant Human Cancer Cells." Journal of Life Science 26, no. 7 (July 30, 2016): 826–34. http://dx.doi.org/10.5352/jls.2016.26.7.826.

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Dissertations / Theses on the topic "Inhibitor"

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Rodkey, Elizabeth A. "INHIBITOR RESISTANCE MECHANISMS AND INHIBITOR DESIGN IN ¿¿-LACTAMASES." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1354463033.

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Shkirskiy, Viacheslav. "Corrosion inhibition of galvanized steel by LDH - inhibitor hybrids : Mechanisms of Inhibitor Release and Corrosion Reactions." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066216/document.

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Le travail présenté essaie de comprendre les mécanismes de l’action d’un inhibiteur de corrosion présent dans un revêtement hybride sous forme de pigments intercalés dans les hydroxydes double lamellaires (HDL) pour la protection de l’acier galvanisé. Trois étapes clés ont été choisies pour ce travail : (1) l’identification d’un inhibiteur de corrosion hydrosoluble pour l’acier galvanisé avec une compréhension de sa réactivité, (2) la détermination des facteurs et des mécanismes contrôlant la libération de l’inhibiteur à partir d’HDL et (3) la compréhension des mécanismes de protection dans un système modèle avec le revêtement hybride contrôlé par la libération de l’inhibiteur et la réactivité d’inhibiteur. MoO42- a montré la meilleure efficacité d'inhibition comparable à CrO42- dans des solutions alcalines et neutres. L’effet inhibiteur de MoO42- a été associé à la formation d’un film riche en Mo(V). L'effet de cet anion sur la dissolution de l'acier à bas carbone a été également vérifié pour exclure la possibilité d'un effet d'accélération des espèces choisies. Les tests de lixiviation ont montré que la libération de MoO42- à partir d’HDL a été contrôlée par la nature des ions échangés à partir du support par un mécanisme d'échange d'ions à un pH neutre et par la dissolution du cadre de la LDH à un pH alcalin. La présence de seulement Cl- conduit à moins de 40% de libération de MoO42- après 24 h d'immersion alors que les additions des carbonates ont abouti à libération de 100% après 1 h. Les tests d'immersion ont montré léger effet d'inhibition du système de revêtement dans Cl- et une augmentation dans CO32- en accords avec le niveau plus élevé de MoO42- libéré
The current work was dedicated to the investigation of the fundamental mechanisms of the action of a layered double hydroxide (LDH) inhibitor hybrid coated systems for the corrosion protection of galvanized steel. The objective of the work was achieved by the realization of three milestones: (1) the identification of the effective water soluble inhibitor on Zn and steel substrates and the understanding the mechanisms of its action, (2) the revealing the factors and mechanisms controlling the release of the selected inhibitor from Zn2Al/-LDH hosts and (3) the understanding the mechanisms of coated system controlled by inhibitor release and its action. MoO42- showed the best inhibition efficiency comparable to CrO42- in alkaline and neutral solutions. The protective properties of MoO42- were assigned to the fast formation of Mo(V) film. The effect of MoO42- on the dissolution of low carbon steel was also verified to exclude the possible accelerating effect of chosen species. The leaching tests showed that MoO42- release from LDH was controlled by the nature of the exchanged ions from the media by ion-exchange mechanism at neutral pH and by the dissolution of the LDH framework at alkaline pH. The presence of only Cl- resulted in less than 40 % of MoO42- release after 24 hours of the immersion while the additions of the carbonates resulted in 100 % release after 1 hour. The immersion tests showed slight inhibiting effect of coated system in Cl and high in CO32- medias coherent with higher level of MoO¬42- released. The ways to control the inhibitor release and hence, the inhibition performance of coated systems were discussed in the vein of environment composition

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Hirst, Claire Elizabeth 1971. "Tissue distribution and regulation of the granzyme B inhibitor, proteinase inhibitor 9." Monash University, Dept. of Biochemistry and Molecular Biology, 2002. http://arrow.monash.edu.au/hdl/1959.1/8488.

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Roweth, Harvey George. "Mechanisms of platelet inhibition by the selective serotonin reuptake inhibitor citalopram." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/275477.

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Background: Selective serotonin reuptake inhibitor (SSRI) antidepressants prevent serotonin (5-HT) uptake by the serotonin transporter (SERT). Since blood platelets express SERT, SSRIs may modify platelet function and the risk of cardiovascular disease. However, the beneficial or adverse effects of SSRIs on arterial thrombosis are poorly characterised and detailed in vitro experimental data is limited. The SSRI citalopram is a racemate, the (S)-isomer being the more potent SERT inhibitor. Although citalopram has been shown to inhibit platelets in vitro, it is unclear whether this is mediated via SERT blockade. Aim: To determine if citalopram inhibits platelet function via SERT blockade, or through a novel mechanism of action. Findings: 5-HT uptake into platelets was blocked by both citalopram isomers at concentrations that had no apparent effect on platelet function. Despite the (S)-citalopram isomer being the more potent SERT inhibitor, (R)-citalopram was equally potent at inhibiting other platelet functions. These findings strongly suggest that inhibition of platelet function by citalopram in vitro is not mediated by blocking SERT. Subsequent experiments identified two putative mechanisms for citalopram-mediated platelet inhibition: 1) citalopram did not inhibit calcium store release induced by the platelet agonist U46619, despite blocking subsequent Rap1 activation. A credible target for this inhibitory mechanism is the calcium and diacylglycerol guanine nucleotide exchange factor-1 (CalDAG-GEFI): 2) citalopram suppressed early protein phosphorylation within the GPVI pathway, resulting in the inhibition of subsequent platelet responses. Further experiments show that other commonly used antidepressants also inhibit platelets. As with citalopram, inhibition was only observed at concentrations above those required to block SERT, suggesting that alternative inhibitory mechanism(s) are responsible. Conclusions: Data presented in this thesis support two novel putative mechanisms of citalopram-induced platelet inhibition. These findings demonstrate that citalopram and other antidepressants inhibit platelets independently of their ability to block SERT-dependent 5-HT transport. The identification of thesemechanisms provides a pharmacological approach to develop novel antiplatelet agents based on current antidepressants.

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Guzanov, Pavel. "ERAP1 inhibitor development." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:e4369016-ab8f-445d-ab1a-71129b495a37.

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ERAP1 has been associated with a set of immune-mediated diseases, including ankylosing spondylitis. Currently, there is no selective and potent ERAP1 inhibitor available that would allow in-depth research of its functions and roles in diseases. Therefore, the aim of this work is to apply fragment-based drug design approach for the development of such inhibitor. A set of 12 structurally diverse hits was identified as a result of a screen containing 1200+ fragments using orthogonal ERAP1 activity assays. These hits can be used as a basis for development of a larger lead inhibitor, which requires structural information about their binding mode to ERAP1. Three different approaches have been tried in order to obtain such information about the binding mode. Unfortunately, ERAP1 crystallisation trials did not succeed, the potential reason being heterogeneity of the protein samples due to presence of several glycoforms. A set of 31 analogues of an IRAP inhibitor, which has been shown to inhibit ERAP1 activity, was synthesised and screened providing valuable structure-activity relationship information. Taken together, the screening campaign has resulted in a novel ERAP1 inhibitor with a single digit micromolar potency against ERAP1.

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Clarke, Tyler Brooke. "Studies on the inhibitor selectivity and inhibitory signal transfer of a-Isopropylmalate synthase." Thesis, University of Canterbury. Chemistry, 2013. http://hdl.handle.net/10092/11303.

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α-Isopropylmalate synthase (α-IPMS) is responsible for catalysing the first committed step in leucine biosynthesis. This pathway is found in plants and microorganisms, including pathogenic bacteria such as Mycobacterium tuberculosis and Neisseria meningitidis. α-IPMS catalyses a Claisen condensation reaction between α-ketoisovalerate (KIV) and acetyl coenzyme A (AcCoA) to form the product α-isopropylmalate (IPM). This enzyme undergoes feedback inhibition by the end product of the pathway, leucine. This regulation allows the control of the rate leucine biosynthesis. This project focuses on the α-IPMS enzymes from M. tuberculosis and N. meningitidis (MtuIPMS and NmeIPMS). These α-IPMS enzymes are homodimeric in structure. Each monomer consists of a catalytic domain which comprises of a (β/α)8 barrel fold, two subdomains and a regulatory domain, to which the allosteric binding of the natural inhibitor leucine occurs. The mechanism by which the allosteric binding of leucine leads to a decrease in enzymatic activity is not yet fully understood. Citramalate synthase (CMS) is responsible for catalysing the first committed step of threonine-independent isoleucine biosynthesis. This enzyme is extremely similar to α-IPMS in both the reaction which it catalyses and the catalytic and regulatory domain structure. CMS catalyses a Claisen condensation reaction between pyruvate and AcCoA to produce citramalate (CM). CMS is also feedback inhibited by the end product of its pathway, isoleucine. The similarity between α-IPMS and CMS enzymes resulted in and examination of the inhibitor selectivity of MtuIPMS. Amino acids in the leucine binding site were altered to their counterparts in the isoleucine binding site of the CMS enzyme to see if the selectivity of the leucine binding site could be interchanged. Results from this study show that it is possible to change inhibitor selectivity with a single amino acid substitution. However, changing the selectivity from leucine to isoleucine was unsuccessful. Instead, one of the MtuIPMS variants displayed significantly increased sensitivity to an alternative amino acid, norvaline. The MtuIPMS variants were expressed and purified using immobilised metal affinity chromatography and size-exclusion chromatography. These variants were then kinetically characterised and displayed similar binding affinities and turnover rates for the natural substrates to the wild-type enzyme. As expected changes to the leucine binding pocket had drastic effects on the sensitivity of the enzyme to its natural inhibitor. This work is described in Chapter 2 of this thesis. The mechanism by which the regulatory signal is transferred from the allosteric leucine binding site to the catalytic site in α-IPMS is not fully understood. NmeIPMS variants were created based on preliminary molecular dynamic simulations which indicated that significant changes in residue contacts were associated with leucine binding. Chapter 3 describes studies that explore the effect of single amino acid substitutions of NmeIPMS. The NmeIPMS variants were expressed and purified similarly to MtuIPMS, using immobilised metal affinity chromatography and size-exclusion chromatography. Variants were subsequently characterised via mass spectrometry, differential scanning fluorimetry and kinetic assays. It was found that each variant generated retained sensitivity to leucine but displayed significant differences in the catalytic efficiencies with AcCoA. One of the generated variants also displayed a significant increase in thermal stability. Results are drawn together in Chapter 4 along with future directions of this research. This chapter details knowledge gained into protein structure and allosteric mechanisms in this thesis.

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Menon, V. "Molecular and functional aspects of hydrolyases / inhibitors with emphasis on aspartic protease inhibitor." Thesis(Ph.D.), CSIR-National Chemical Laboratory, Pune, 2012. http://dspace.ncl.res.in:8080/xmlui/handle/20.500.12252/2401.

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Miyazaki, Hiroshi. "Studies on Inhibitors of Plasminogen Activator Inhibitor-1(PAI-1) and Inhibitors of PAI-1 Production as Antithrombotic Agents." 京都大学 (Kyoto University), 2010. http://hdl.handle.net/2433/126818.

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Ahtyamova, Daria. "Cholinesterase inhibitor: pharmacological application." Thesis, Київський національний університет технологій та дизайну, 2019. https://er.knutd.edu.ua/handle/123456789/13033.

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McCready, Tara Lyn. "Inhibition of protein phosphatase-1 by endogenous inhibitor proteins and natural product toxins." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0032/NQ46885.pdf.

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Books on the topic "Inhibitor"

1

Li, Rongshi, and Jeffrey A. Stafford, eds. Kinase Inhibitor Drugs. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2009. http://dx.doi.org/10.1002/9780470524961.

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2

A, Stafford Jeffrey, ed. Kinase inhibitor drugs. Hoboken, N.J: J. Wiley, 2009.

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Chang, Henry E. HIV protease inhibitor report. 2nd ed. Brooklyn, NY (72 Orange St., #3C, Brooklyn 11201): National AIDS Treatment Advocacy Project, 1996.

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Bashein, Abdulla Masood. Vitreous-derived inhibitor of angiogenesis. Manchester: University of Manchester, 1995.

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C, Shirley Anne, ed. Trends in serotonin uptake inhibitor research. Hauppauge, NY: Nova Science Pub., 2004.

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Krämer, Oliver H., ed. HDAC/HAT Function Assessment and Inhibitor Development. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2788-4.

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Krämer, Oliver H., ed. HDAC/HAT Function Assessment and Inhibitor Development. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6527-4.

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Lendeckel, Uwe, and Nigel M. Hooper, eds. Viral Proteases and Antiviral Protease Inhibitor Therapy. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2348-3.

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Miskei, Gyorgy Zsolt. Studies on lung lavage alphai proteinase inhibitor. Birmingham: University of Birmingham, 1998.

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H, Kennedy Sidney, ed. Clinical advances in monoamine oxidase inhibitor therapies. Washington, DC: American Psychiatric Press, 1994.

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Book chapters on the topic "Inhibitor"

1

Weik, Martin H. "inhibitor." In Computer Science and Communications Dictionary, 782. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/1-4020-0613-6_8998.

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Gooch, Jan W. "Inhibitor." In Encyclopedic Dictionary of Polymers, 388. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_6312.

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Bährle-Rapp, Marina. "Inhibitor." In Springer Lexikon Kosmetik und Körperpflege, 280. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_5204.

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Davis, Alvin E. "C1 Inhibitor." In Advances in Experimental Medicine and Biology, 185–94. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5391-5_18.

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Makkar, Harinder P. S., P. Siddhuraju, and Klaus Becker. "Trypsin Inhibitor." In Plant Secondary Metabolites, 1–6. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-425-4_1.

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Makkar, Harinder P. S., P. Siddhuraju, and Klaus Becker. "Chymotrypsin Inhibitor." In Plant Secondary Metabolites, 7–9. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-425-4_2.

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Lahiri, Cecile Delille, Jeffrey Lennox, and Ighovwerha Ofotokun. "Protease Inhibitor." In Encyclopedia of AIDS, 1–8. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-9610-6_443-1.

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Kapadia, Shashi, and Marshall J. Glesby. "Maturation Inhibitor." In Encyclopedia of AIDS, 1–5. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-9610-6_452-1.

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Floresco, Stan, Robert Kessler, Ronald L. Cowan, Robert Kessler, Ronald L. Cowan, Mark Slifstein, Andrea Cipriani, et al. "Receptor Inhibitor." In Encyclopedia of Psychopharmacology, 1126. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_4503.

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Hoyer, Daniel, Eric P. Zorrilla, Pietro Cottone, Sarah Parylak, Micaela Morelli, Nicola Simola, Nicola Simola, et al. "COMT Inhibitor." In Encyclopedia of Psychopharmacology, 324. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_948.

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Conference papers on the topic "Inhibitor"

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Booth, N. A., A. Reith, and B. Bennett. "A PLASMINOGEN ACTIVATOR INHIBITOR (PAI-2) CIRCULATES IN TWO HIGH MOLECULAR WEIGHT FORMS IN PREGNANCY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644459.

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Normal vascular endothelium and platelet α-granules contain an inhibitor of plasminogen activator (PAI-1) of about 48000 molecular weight, which is released by stimuli such as thrombin. An immunologically distinct inhibitor (PAI-2) of about 47000 molecular weight has been purified from placenta and from a histiocytic cell line U-937. The level of PA-inhibition in plasma is raised in late pregnancy and this may be due to increases in PAI-1 or in PAI-2 or in both.Using SDS-PAGE and zymography on fibrin/plasminogen /u-PA detector gels, we have found that normal plasma contains a band of inhibition of apparent molecular weight 40000, which can be neutralised by antiserum raised against PAI-1. Pregnancy plasma contained this band as well as additional inhibitor bands of apparent molecular weights 75000 and 130000. The novel high molecular weight PA-inhibitors were detectable by zymography at about 12 weeks gestation. They were specific for plasminogen activator and did not inhibit plasmin. They were inhibited by antiserum raised against PAI-2 from U-937 cells (a gift from Dr EKO Kruithof) and thus are immunologically related to PAI-2. They may represent circulating complexes of PAI-2 with another protein or aggregates of PAI-2, which retain inhibitory activity after SDS-PAGE. PAI-2 appears to represent a pregnancy associated protein that circulates in a number of different molecular weight forms.

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Beretz, A., F. Lanza, A. Stierlé, and J.-P. Cazenave. "CYCLIC NUCLEOTIDE PHOSPHODIESTERASE INHIBITORS PREVENT AGGREGATION AND SECRETION OF HUMAN PLATELETS BY RAISING CYCLIC AMP AND REDUCING CYTOPLASMIC FREE CALCIUM MOBILIZATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643586.

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Drugs that raise platelet cyclic AMP (cAMP) are potent inhibitors of platelet activation. We have studied the effects of 5 inhibitors of cyclic nucleotide phosphodiesterase (PDE) of different chemical structures (quercetin, Ro 15-2041, HL-725, cilostamide and MY-5445), which are all potent inhibitors of platelet function. The concentrations that inhibit by 50 % crude cAMP-PDE activity (IC50) from human platelets are: 0.06 μM(HL-725), 0.15 μM(Ro 15-2041 ), 0.23 μM(cilostamide), 6.9 μM(MY-5445) and 44.4 μM(quercetin). We measured on the same preparation of washed human platelets loaded with quin2, the aggregation and the increase in intracellular Ca2+ ([Ca2+]i) induced by 5 μM ADP alone or in the presence of PDE inhibitors.PGE1 (2 nM) potentiates significantly (1.6 to 3.3 fold) the inhibitory effects of PDE inhibitors on [Ca2+]i rises and platelet aggregation. Adrenaline, an inhibitor of adenylate cylase, prevents the effect of PDE inhibitors on ADP-induced [Ca2+]i rise and platelet aggregation. These results suggest that these compounds inhibit [Ca2+]i mobilization and subsequent ADP-induced aggregation through a rise in cAMP, because both effects are potentiated by PGE1 and inhibited by adrenaline. The inhibitor concentrations which potentiate the action of PGE1, on [ Ca2+]i levels also potentiate the rise in platelet cAMP induced by PGE-<. These results suggest that PDE inhibitors inhibit platelet aggregation Ly raising cAMP levels and subsequently inhibiting [Ca2+]i mobilization.

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Liu, Keshun, and Mike Woolman. "Developing an optimized method for measuring chymotrypsin inhibitor activity in protein products." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/yucc6741.

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Protease inhibitors of protein nature, such as trypsin inhibitors and chymotrypsin inhibitors, are rich in seeds of legume crops. Soybeans contain Kunitz inhibitor and Bowman-Birk inhibitor. The former mainly inhibits trypsin, while the latter inhibits both trypsin and chymotrypsin. Other legumes contain similar types. Historically, trypsin inhibitor activity in legume products has been of primary interest for measurement due to its antinutritional implication. However, Bowman-Birk inhibitor has been shown therapeutic. It is also more resistant to heat than Kunitz inhibitor. As increasing volumes of plant proteins are being used for food or feed in recent years, there is a growing interest in monitoring chymotrypsin inhibitor activity (CIA) in these products as well. Yet, reported methods for CIA assay vary greatly, with no standard method being available. Three years ago, at our USDA lab, we developed an improved method for measuring trypsin inhibitor activity, which was later adopted as AOCS Official Method, Ba 12a-2020. This presentation reports our new effort in developing a method for measuring CIA, using N-benzoyl-L-tyrosine p-nitroanilide (BTpNA) as a substrate. Unlike the substrate for measuring trypsin inhibitor activity, BTpNA is not water soluble, an organic solvent that is miscible with water must be present. Therefore, the assay system for measuring CIA was much more complicated than that for measuring trypsin inhibitor activity. This made the method development more difficult than originally thought. After investigating effects of many assay parameters, such as organic solvent, the sequence of adding reagents, % chymotrypsin inhibition, etc., an optimized method for CIA measurement was finally developed. It featured dimethylformamide as the organic solvent, the enzyme-last sequence, 5 mL total assay volume, and calculation of the inhibitor activity based on % chymotrypsin inhibition. The proposed method was reliable and robust and could be standardized for measuring CIA in various protein products.

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Saeki, T., K. HARADA, T. Youshimura, Y. Nakamura, T. Fujimori, K. E. Katayama, Y. Yamagish, I. Yamastu, and I. Ikeda. "MODE OF ACTION OF A NOVEL ANTI-PLATELET AGENT (E-5510)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643427.

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A novel anti-platelet agent, 4-cyano-5,5-bis(4-methoxy-phenyl)-4-pentenoic acid(E-5510), has been shown to inhibit platelet aggregation and secretion induced by thrombin as well as by other inducers such as ADP, collagen and PAF. Although E-5510 can act as a cyclooxygenase inhibitor,inhibition of cyclooxygenase may not be the primary mode of action since this compound effectively inhibits thrombin-induced platelet activation. In this paper, effects^of E-5510 on arachidonic acid (AA) metabolism, intracellular Ca++ and cAMP in human platelets are examined.(1) Effect on AA metabolism. Platelets prelabeled with [14 C]-AA were stimulated with thrombin. E-5510 inhibited not only thromboxane A2 and HHT generation but also 12-HETE generation in a dose-dependent fashion. The total AA released was also reduced by E-5510. An almost 50% reduction was obtained by 10 uM of this compound. On the other hand, a cyclooxygenase inhibitor such as U-53059 increased 12-HETE generation in a dose-dependent fashion. In addition to the inhibition of AA metabolism, E-5510 exerted inhibitory effects on phosphatidic acidgeneration, which suggests the possible inhibition of phospholipase C activity by this compound.(2) Effect on intracellular Ca++ and protein phosphorylation. Intracellular Ca++ mobilization was examined using Fura-2 loaded human platelet suspension. The increase in intracellular Ca induced by thrombin was inhibited by E-5510 and the increase in phosphorylation of 40 K protein was also suppressed by this compound after the stimulation of human platelets by thrombin.(3) Effect on cAMP. Platelets were incubated with 10-100 uM of E-5510 and the cAMP content in human platelets was measured. E-5510 increased the cAMP content in a dose-dependent fashion. In platelet homogenate, E-5510 inhibited phosphodiesterase activity with an IC50 of 10 uM.These results suggest that E-5510 may inhibit platelet aggregation and secretion through the multiple modes of action, such as inhibition of phospholipase C, phosphodiesterase and cyclooxygenase, in the process of platelet activation.

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Tans, G., T. Janssen-Claessen, J. Rosing, and J. H. Griffin. "APPLICATION OF SPECIFIC SERINE PROTEASE INHIBITORS IN ASSAYS FOR ACTIVATED CONTACT FACTORS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643301.

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We developed amidolytic assays to determine human Factor Xlla, Factor XIa and plasma kallikrein in mixtures containing variable amounts of each enzyme. The commercially available chromogenic substrates pro-phe-arg-pNA (S2302 or chromozym PK), glu-pro-arg-pNA (S2366), ile-glu-(piperidyl)-gly-arg-pNA (S2337), and ile-glu-gly-arg-pNA (S2222) were tested for their suitability as substrates in these assays. 8-Factor Xlla, Factor XIa and plasma kallikrein each exhibit considerable activity towards a number of these substrates. This precludes direct quantitation of the individual enzymes when large amounts of other activated contact factors are present. Several serine protease inhibitors were tested on their ability to selectively inhibit those contact factors that may interfere with the factor tested for. Soybean trypsin inhibitor efficiently inhibits kallikrein, inhibits Factor XIa at moderate concentrations, but did not affect the amidolytic activity of Factor Xlla. Therefore, this inhibitor can be used to abolish a kallikrein and Factor XIa contribution in a Factor Xlla assay. We also report the rate constants of inhibition of contact activation factors by three different chloromethylketones. D-phe-pro-arg-CH 2 Cl was moderately active against contact factors (k - 2271 M-ls-1 at pH 8.3) but showed no differences in specif ity. D-phe-phe-arg-CH2 Cl was a very efficient inhibitor of kallikrein (k = 118,000 M-ls-1 at pH 8.3) whereas it slowly inhibited Factor Xlla (k = 1389 M-ls-1) and Factor XIa (k = 110 M-ls-1). Also dansyl-glu-gly-arg-CH2Cl was more reactive towards kallikrein (k 15,662 M-ls-1) than towards Factor Xlla (k = 462 M-ls-1) and Factor XIa (k = 63 M-ls-1). Since phe-phe-arg-CH2Cl is highly specific for kallikrein it can be used in a Factor XIa assay to selectively inhibit kallikrein. Based on the catalytic efficiencies of chromogenic substrate conversion and the inhibition characteristics of serine protease inhibitors and chloromethyl ketones we were able to develop quantitative assays for Factor Xlla, Factor XIa and kallikrein in mixtures of contact activation factors.

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Steinert, Bruce W., James M. Onoda, Bonnie F. Sloane, John D. Taylor, and Kenneth V. Honn. "CYCLOOXYGENASE AND LIPOXYGENASE PRODUCTS SYNERGISTICALLY MODULATE TUMOR CELL INDUCED PLATELET AGGREGATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644668.

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There has been considerable controversy surrounding the ability of inhibitors of arachidonic acid metabolism to concomitantly inhibit tumor cell induced platelet aggregation (TCIPA). Reconciliation of this controversy has been difficult due to the wide variability of experimental conditions (e.g., inhibitor concentration, strength of the inducing agonist).In the present study, we examined the effects of several cyclooxygenaseand lipoxygenase inhibitors on the induction of platelet aggregation by Walker 256 carcinosarcoma (W256) cells. We have previously demonstrated that aggregation of platelet rich plasma (PRP), induced by W256 cells, was initiated via a thrombin dependent mechanism. Platelet aggregation was induced by the addition of W256 cells (75,000-J500,000 cells/cuvette) to rat PRP preincubated with inhibitor(s) or diluent. The strength of the inducing stimulus affected both the degree of aggregation and the production of thromboxane A2 (TXA2) in a dose dependent manner. A weak stimulus (low concentration of W256 cells) produced only a low level of aggregation and low TXA2 production, whereas aggregation induced by a strong stimulus (high concentration of W256 cells) resulted in significant aggregation and increased TXA2 production. Preincubation (5 min., 37°C) of rat PRP with cyclooxygenase inhibitors (e.g., aspirin, indomethacin, ibuprofen) resulted in complete inhibition of platelet aggregation at low agonist concentration (75,000 W256 cells), whereas when a high agonist concentration (500,000 W256 cells) was used to induce aggregation, the inhibitors failed to inhibit TCIPA. The addition of fewer than 50,000W256 cells failed to induce any measurable platelet aggregation in the presence or absence of inhibitors. TCIPA was not affected by lipoxygenaseinhibitors (e.g.,quercetin) alone regardless of agonist concentration. Both cyclooxygenase and lipoxygenase inhibitors, however, were required to significantly inhibit TCIPA induced by high agonist concentration. Compounds which inhibited both the cycloogygenase and lipoxygenase pathways (e.g.,hydroquinone, BW755c) inhibited TCIPA at all agonist concentrations. Nafazatrom failed to inhibit TCIPA consistant with a lack of effect on platelet cyclooxygenase and lipoxygenase. Therefore, we conclude cyclooxygenase (e.g., TXA2) and lipoxygenase (e.g., 12-HETE) products of platelet arachidonic acid metabolism and the strength of the inducingagonist are important criteria in TCIPA. This study may help to clarify the current controversy regarding the inhibition of TCIPA by inhibitors of arachidonic acid metabolism.

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Jansen, J. W. C. M. "EFFECTS OF INHIBITORS ON COLLAGEN INDUCED PLATELET AGGREGATION IN SIX DIFFERENT SPECIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643445.

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One approach to the development of antithrombotics is inhibition of platelet aggregation. The pharmacological approach often used is to test compounds on collagen induced platelet aggregation measured in platelet rich plasma. Therefore we have compared inhibitors with different mechanism of action on aggregation of platelets from six different species commonly used in pharmacological studies. Aggregation was induced with submaximal amounts of collagen (Hormone Chemie).Inhibitors of the cyclooxygenase system, aspirin and indomethacin, were very potent in inhibiting aggregation of platelets from humans guinea pig and dog (IC50 20-60 and 1-3 ¼M resp.). Aggregation of pig and rat platelets was poorly inhibited by both of these compounds (IC5: 700-900 ¼M), whereas platelets from mice showed intermediate sensitivety (IC50 ca.100 ¼M).The combined lipoxygenase/cyclooxygenase inhibitor BW755C, was extremely active on platelets of guinea pig (IC50 1 ¼M) and was poorly active in mice platelets (IC50 300 ¼M). In the other species the inhibitory activity ranged from 20-80 ¼M.The phosphodiesterase inhibitors, papaverine and BL3459 inhibited aggregation in all species (IC50 50-100 and 1-5 ¼M resp.). Dipyridamole inhibited aggregation also in all species but with lower activity (IC50 > 100 ¼M).Conclusion: remarkable species differences are present with respect to inhibition of collagen induced platelet aggregation by the various compounds e.g. rat and porcine platelet aggregation was hardly inhibited by cyclooxygenase inhibitors. The effects of the compounds on human platelets are comparable to the effects on canine plateletes.

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Albaiz, A., T. Almubarak, F. Alissa, A. Owais, and N. Aljeaban. "Calcium Sulfate Scale Inhibitor: Does the Carbon Backbone Length Matter?" In International Petroleum Technology Conference. IPTC, 2024. http://dx.doi.org/10.2523/iptc-23506-ea.

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Abstract Calcium sulfate (CaSO4) scale precipitation is a challenge faced in the oil and gas industry where it can cause a variety of issues that lead to productivity decline. Amino-phosphonate-base scale inhibitors are used to prevent this type of inorganic scale and have shown great success in the industry. A common misconception is to believe that high molecular weight amino-phosphonates perform better than their low molecular weight counterparts. This study systematically compares performance of scale inhibitors which have the same number of functional groups but different molecular size and backbone chain length. The study shows the influence of changing the molecular size and backbone chain length on the inhibition efficiency. Two amino-phosphonate-based scale inhibitors are tested in this work: Ethylenediamine tetramethylenephosphonic acid (EDTMP) and Hexamethylenediaminetetramethylene phosphonic acid (HDTMP). These inhibitors have the same number of functional groups, but they differ in the length of the carbon backbone chain. The inhibition efficiency of each inhibitor is measured through its ability to prevent formation of CaSO4 in a brine containing up to 6,000 ppm calcium ions (Ca2+) and an equivalent amount of sulphate ions (SO42-). Moreover, the remaining concentration of Ca2+ in the solution is measured using Inductive Coupled Plasma (ICP). The results of the study shows that the inhibitor molecules with shorter chain length, EDTMP, have higher inhibition efficiency than the ones with longer chain length, HDTMP. That is because a small dose of EDTMP can efficiently inhibit CaSO4 precipitation while a big dose of HDTMP to do the same job efficiently. Environmental scanning electron microscope (ESEM) is employed to study the effect of the inhibitors on the morphology of the formed scale. The morphology of the formed scale after using the low doses of the inhibitors are investigated by Environmental Scanning Electron Microscope (ESEM), and the resulted images show that the CaSO4 precipitates exhibit deformed shapes compared to the CaSO4 precipitates where no inhibitor is used.

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Donaldson, V. H., and M. D. B. H. Mitchell. "INTERACTIONS OF DYSFUNCTIONAL Cl-INHIBITORS FROM PATIENTS WITH TYPE II HEREDITARY ANGIONEUROTIC EDEMA (HANE) WITH ACTIVATED HAGEMAN FACTOR (FACTOR XIIa)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643302.

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Type II HANE is characterized by a deficiency of Cl-inhibitor (Cl-INH) activity in serum which is associated with a dysfunctional inhibitor protein having a normal or increased quantity o|_the antigenic properties of normal serum Cl-inhibitor. Dysfunctional Cl-INH proteins were purified from members_of eight different kindred with Type II HANE and compared to normal Cl-inhibitor with respect to their inhibitory activity directed against the amidolytic and clot-promoting properties of purified activated Hageman factor. All but one dysfunctional Cl-inhibitor blocked the amidolytic activity of ellagic acid-activated Hageman factor; all eight blocked the clot-promoting activity of Hageman factor activated in solutions of sulfatides and BSA. The inhibition _of amidolytic activity was equal to or greater than that of normal Cl-INH (Donaldson, et al., 3. Clin. Invest. 75:124,1985). The impairment of the specific Hageman factor coagulant activity of activated Hageman factor by six^f the eight dysfunctional inhibitors was less than that of the normal Cl-inhibitor, although readily measured. Dysfunctional Cl-inhibitor proteins were also heterogeneous with respect to their formation of stable complexes and their susceptibility to cleavage by Hageman factor activated with BSA-sulfatides when analyzed in SDS-gel electrophoresis. Although these observatons cannot be directly applied to in vivo pathophysiologic changes in plasma, dysfunctional Cl-inhibitors do have the potential of regulating activated Hageman factor.

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Dai, Chong, Zhaoyi Dai, Samiridhdi Paudyal, Saebom Ko, Yue Zhao, Xin Wang, Xuanzhu Yao, Amy Kan, and Mason Tomson. "New Kinetic Turbidity Test Method and Prediction Model for Calcite Inhibition." In SPE International Conference on Oilfield Chemistry. SPE, 2021. http://dx.doi.org/10.2118/204398-ms.

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Abstract Calcite, as one of the most common scales in oilfield can be inhibited by common scale inhibitors. The measurement of calcite nucleation and inhibition is a challenge, because of the difficulty to control pH as a result of CO2 partitioning in and out of the aqueous phase. A new kinetic turbidity test method was developed so that the partial pressure of CO2, pH, and SI can be precisely controlled. Calcite nucleation and inhibition batch tests were conducted under various conditions (SI = 0.24-2.41, T = 4-175 °C, and pH = 5.5-7.5) in the presence of common phosphonate and polymeric inhibitors. Based on experimental results, calcite nucleation and inhibition semi-empirical models are proposed, and the logarithm of the predicted induction time is in good agreement with the measured induction time. The models are also validated with laboratory and field observations. Furthermore, a new BCC CSTR Inhibition (BCIn) test method that applied the Continuous Stirred Tank Reactor (CSTR) theory has been developed, for the first time. This BCIn method was used for calcite inhibitor screening tests and minimum inhibitor concentration (MIC) estimation. By only running one experiment (< 1 hour) for each inhibitor, BCIn method selected the effective inhibitors among 18 common inhibitors under the conditions of SI = 1.23 at 90 °C and pH = 6. It was also found that the critical concentration (Ccrit) from BCIn method has a correlation with the MIC from batch tests. This study provided a simple and reliable solution for conducting calcite scale inhibition tests in an efficient and low-cost way. Furthermore, the newly developed prediction models can be used as guidance for laboratory tests and field applications, potentially saving enormous amounts of time and money.

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Reports on the topic "Inhibitor"

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Lance, Richard, and Xin Guan. Variation in inhibitor effects on qPCR assays and implications for eDNA surveys. Engineer Research and Development Center (U.S.), August 2021. http://dx.doi.org/10.21079/11681/41740.

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Aquatic environmental DNA (eDNA) surveys are sometimes impacted by polymerase chain reaction (PCR) inhibitors. We tested varying concentrations of different inhibitors (humic, phytic, and tannic acids; crude leaf extracts) for impacts on quantitative PCR (qPCR) assays designed for eDNA surveys of bighead and silver carp (Hypophthalmichthys nobilis and Hypophthalmichthys molitrix). We also tested for inhibition by high concentrations of exogenous DNA, hypothesizing that DNA from increasingly closely related species would be increasingly inhibitory. All tested inhibitors impacted qPCR, though only at very high concentrations — likely a function, in part, of having used an inhibitor-resistant qPCR solution. Closer phylogenetic relatedness resulted in inhibition at lower exogenous DNA concentrations, but not at relatively close phylogenetic scales. Inhibition was also influenced by the qPCR reporter dye used. Importantly, different qPCR assays responded differently to the same inhibitor concentrations. Implications of these results are that the inclusion of more than one assay for the same target taxa in an eDNA survey may be an important countermeasure against false negatives and that internal positive controls may not, in the absence of efforts to maximize inhibition compatibility, provide useful information about the inhibition of an eDNA assay.

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Beavers, Gui, and Sridhar. PR-186-073508-R01 Environmental and Stress Factors that Produce SCC in Existing Ethanol Facilities. Chantilly, Virginia: Pipeline Research Council International, Inc. (PRCI), February 2011. http://dx.doi.org/10.55274/r0010441.

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The potential exists for stress corrosion cracking (SCC) of carbon steel pipelines transporting fuel grade ethanol (FGE) and FGE- gasoline blends. The objective of SCC 4-3 Phase 2 was determine if inhibitors are effective in preventing SCC growth under more realistic field conditions than those found in the slow strain rate (SSR) tests performed previously. The results of the research demonstrated that: 1. Un-notched SSR test results generally correlated well with the results of the crack growth tests using precracked CT specimens, although the latter test technique was somewhat more aggressive. 2. The notched SSR test technique was so aggressive that it was not useful for screening SCC inhibitors. 3. E-50, prepared with a simulated FGE was consistently more potent as a cracking agent than SFGE. 4. Some commercial inhibitors were effective in inhibiting ethanol SCC under many of the test conditions. 5. The commercial inhibitors, in general, were less effective in E-50 than in SFGE. 6. Ammonium hydroxide, at a relatively low concentration, was by far the most effective inhibitor evaluated. 7. For one commercial inhibitor, a higher concentration was needed to inhibit SCC in one lot of corn based FGE than in SFGE. 8. Water inhibited, but did not completely arrest, SCC in the crack growth tests in SFGE. 9. Sustained crack growth was observed in SFGE in which no chloride was added. 10. Evidence of loss of inhibition, at low concentrations, was observed in an inhibition scheme for batching of FGE with gasoline in which a high initial dose, followed by a low maintenance dose was used.

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Sisler, Edward C., Raphael Goren, and Akiva Apelbaum. Controlling Ethylene Responses in Horticultural Crops at the Receptor Level. United States Department of Agriculture, October 2001. http://dx.doi.org/10.32747/2001.7580668.bard.

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Ethylene is a plant hormone that controls many plant responses, such as growth, senescence, ripening, abscission and seed germination. Recently, 1-methy- cyclopropene (1-MCP), was shown to bind to ethylene receptor for a certain period of time and prevent ethylene action. The objectives of this research were to synthesize analogues of 1-MCP and test their potency to block the ethylene receptor and inhibit ethylene action. During the course of this project, procedures for synthesis and shipment of the cyclopropene compounds were developed as well assay procedures for each compound were worked out. Thirteen new compounds were synthesized. All of them are structural analogues of 1-MCP, with substitution in the 1-position and a side chain containing 2 to 10 carbons. After preliminary studies, nine promising compounds were selected for in-depth study. The potency of the compounds to inhibit ethylene action was tested on a wide scope of systems like: climacteric fruits (banana, avocado and tomato), the triple response (etiolated peas), and leaf abscission (citrus). As the putative inhibitors are suspected to compete for the site of binding and a competitive type of inhibition could be considered, a high concentration of ethylene (300 m1.L-1) was used to induce ripening and other physiological processes. The tests were conducted under extreme conditions which hasten ripening like treatment and storage at 22 to 25oC. There were fluctuations in the responses as related to the concentrations of the inhibitors. Some required much higher concentration to exert the same effect, while some, when applied at the same concentration, blocked the receptor for a longer period of time than the others. Some fruits and other plant organs responded differently to the same inhibitor, indicating differences in characteristics and availability of the ethylene receptors in the various tissues. The potency of the putative inhibitors was found to be greatly affected by their molecular structural and size. In addition, it was found that treatment with the inhibitor should be given before the onset of ethylene action In the case of fruit, treatment should be carried out before the pre-climacteric stage. Simultaneous treatment with ethylene and the inhibitors reduced the inhibitors' effect. The relationship between ethylene and the inhibitors is of a non-competitive nature. All the fruits treated with the putative inhibitors resumed normal ripening after recovery from the inhibition. This fact is of great importance when considering the inhibitors for practical use. The advantage of using inhibitors of ethylene action over inhibitors of ethylene production lies in the ability of the inhibitors of ethylene action to protect the tissue against both endogenous and exogenous ethylene, thus providing better overall protection. Our findings indicate that 1-MCP and its structural analogues are potent inhibitors of ethylene action capable of providing good protection against endogenous and exogenous ethylene. The fact that the compounds are in a gas phase and are non-phytotoxic, odorless and effective at minute concentrations, renders them promising candidates for commercial use. However, the development of water-soluble inhibitors will expand the potential use of the inhibitors in agriculture.

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Wilmarth, W. R. Results of Aluminosilicate Inhibitor Testing. Office of Scientific and Technical Information (OSTI), June 2001. http://dx.doi.org/10.2172/782672.

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Rochelle, J. KH-30 Parafin Inhibitor Treatment. Office of Scientific and Technical Information (OSTI), September 2001. http://dx.doi.org/10.2172/793837.

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Banda, Michael J. Novel Breast Tumor Metalloproteinase Inhibitor. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada411303.

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Banda, Michael J. Novel Breast Tumor Metalloproteinase Inhibitor. Fort Belvoir, VA: Defense Technical Information Center, October 2000. http://dx.doi.org/10.21236/ada392495.

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Been, Lu, and King. 3DWXATZ Inhibitive Effect of Organics on Near-neutral pH SCC. Chantilly, Virginia: Pipeline Research Council International, Inc. (PRCI), January 2008. http://dx.doi.org/10.55274/r0011184.

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The objectives of the current project are to confirm the earlier observation of an inhibitive effect of organic soils on the stress corrosion cracking of pipeline steels and to determine the mechanism of this inhibition.� Identification of an inhibitor for near-neutral pH SCC that may be naturally present in some locations could perhaps be deliberately added in other locations.

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Bowes, Kevin M., John Buffin, Richard Kamin, and Douglas Mearns. Fuel System Icing Inhibitor Concentration Reduction Study. Fort Belvoir, VA: Defense Technical Information Center, November 2013. http://dx.doi.org/10.21236/ada618863.

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Naim, Michael, Andrew Spielman, Shlomo Nir, and Ann Noble. Bitter Taste Transduction: Cellular Pathways, Inhibition and Implications for Human Acceptance of Agricultural Food Products. United States Department of Agriculture, February 2000. http://dx.doi.org/10.32747/2000.7695839.bard.

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Abstract:

Historically, the aversive response of humans and other mammals to bitter-taste substances has been useful for survival, since many toxic constituents taste bitter. Today, the range of foods available is more diverse. Many bitter foods are not only safe for consumption but contain bitter constituents that provide nutritional benefits. Despite this, these foods are often eliminated from our current diets because of their unacceptable bitterness. Extensive technology has been developed to remove or mask bitterness in foods, but a lack of understanding of the mechanisms of bitterness perception at the taste receptor level has prevented the development of inhibitors or efficient methods for reducing bitterness. In our original application we proposed to: (a) investigate the time course and effect of selected bitter tastants relevant to agricultural products on the formation of intracellular signal molecules (cAMP, IP3, Ca2+) in intact taste cells, in model cells and in membranes derived therefrom; (b) study the effect of specific bitter taste inhibitors on messenger formation and identify G-proteins that may be involved in tastant-induced bitter sensation; (c) investigate interactions and self-aggregation of bitter tastants within membranes; (d) study human sensory responses over time to these bitter-taste stimuli and inhibitors in order to validate the biochemical data. Quench-flow module (QFM) and fast pipetting system (FPS) allowed us to monitor fast release of the aforementioned signal molecules (cGMP, as a putative initial signal was substituted for Ca2+ ions) - using taste membranes and intact taste cells in a time range below 500 ms (real time of taste sensation) - in response to bitter-taste stimulation. Limonin (citrus) and catechin (wine) were found to reduce cellular cAMP and increase IP3 contents. Naringin (citrus) stimulated an IP3 increase whereas the cheese-derived bitter peptide cyclo(leu-Trp) reduced IP3 but significantly increased cAMP levels. Thus, specific transduction pathways were identified, the results support the notion of multiple transduction pathways for bitter taste and cross-talk between a few of those transduction pathways. Furthermore, amphipathic tastants permeate rapidly (within seconds) into liposomes and taste cells suggesting their availability for direct activation of signal transduction components by means of receptor-independent mechanisms within the time course of taste sensation. The activation of pigment movement and transduction pathways in frog melanophores by these tastants supports such mechanisms. Some bitter tastants, due to their amphipathic properties, permeated (or interacted with) into a bitter tastant inhibitor (specific phospholipid mixture) which apparently forms micelles. Thus, a mechanism via which this bitter taste inhibitor acts is proposed. Human sensory evaluation experiments humans performed according to their 6-n-propyl thiouracil (PROP) status (non-tasters, tasters, super-tasters), indicated differential perception of bitterness threshold and intensity of these bitter compounds by different individuals independent of PROP status. This suggests that natural products containing bitter compounds (e.g., naringin and limonin in citrus), are perceived very differently, and are in line with multiple transduction pathways suggested in the biochemical experiments. This project provides the first comprehensive effort to explore the molecular basis of bitter taste at the taste-cell level induced by economically important and agriculturally relevant food products. The findings, proposing a mechanism for bitter-taste inhibition by a bitter taste inhibitor (made up of food components) pave the way for the development of new, and perhaps more potent bitter-taste inhibitors which may eventually become economically relevant.

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