Benzophenanthridines
Eschscholzia
Papaveraceae
The poppy plant family of the order Papaverales, subclass Magnoliidae, class Magnoliopsida. These have bisexual, regular, cup-shaped flowers with one superior pistil and many stamens; 2 or 3 conspicuous, separate sepals and a number of separate petals. The fruit is a capsule. Leaves are usually deeply cut or divided into leaflets.
Alkaloids
Crown Ethers
Macrocyclic polyethers with the repeating unit of (-CH2-CH2-O)n where n is greater than 2 and some oxygens may be replaced by nitrogen, sulfur or phosphorus. These compounds are useful for coordinating CATIONS. The nomenclature uses a prefix to indicate the size of the ring and a suffix for the number of heteroatoms.
Phosphatidylinositol 3-kinase and protein kinase C are required for the inhibition of caspase activity by epidermal growth factor. (1/443)
The mechanism by which growth factors exert an anti-apoptotic function on many cell types is not well understood. This issue is addressed in relation to epidermal growth factor (EGF) which inhibits apoptosis induced by staurosporine or wortmannin in an epithelial tumour cell line (CNE-2). The presence of EGF substantially reduced the in vitro Ac-DEVD-AMC hydrolytic activity and almost completely suppressed the intracellular cleavage of poly(ADP-ribose) polymerase in staurosporine- or wortmannin-treated cells. Staurosporine but not wortmannin caused the intracellular proteolytic processing of pro-caspase-3 and this event was transiently inhibited by EGF. Staurosporine-induced apoptosis was not inhibited by EGF in the presence of wortmannin or LY294002. Similarly, EGF failed to inhibit wortmannin-induced apoptosis in the presence of staurosporine, chelerythrine chloride or Go6850. These results suggest that phosphatidylinositol 3-kinase and protein kinase C play a role in the survival function of EGF but the reduction of cellular caspase activity cannot be satisfactorily explained by a lack of pro-caspase-3 activation. (+info)Effects of prostaglandin F2 alpha on intracellular pH, intracellular calcium, cell shortening and L-type calcium currents in rat myocytes. (2/443)
OBJECTIVE: We have studied the mechanisms underlying the positive inotropic action of prostaglandin F2 alpha (PGF2 alpha) by monitoring intracellular calcium transients, intracellular pH, L-type calcium currents and cell shortening in isolated ventricular myocytes. METHODS: Rat myocytes were loaded with fura-2AM for intracellular calcium measurements, or BCECF-AM for pH measurements. Cell shortening was recorded using an edge detection system, and L-type calcium currents measured using whole cell patch clamping. RESULTS: PGF2 alpha (3 nmol l-1-3 mumol l-1 increased single myocyte shortening and reduced resting cell length in a concentration-dependent manner. While myocyte shortening was increased by PGF2 alpha, this was not associated with any change in the amplitude of intracellular calcium transients, diastolic calcium, or L-type calcium currents. However, the same myocytes were capable of responding to catecholamines with increases in calcium transient amplitude and L-type calcium currents. PGF2 alpha (3 mumol l-1 caused a reversible rise in intracellular pH of 0.08 +/- 0.01 pH units (n = 5, p < 0.05). The Na(+)-H+ exchanger inhibitor, HOE 694 (10 mumol l-1, abolished the PGF2 alpha-induced rise in pH and the increase in cell shortening. PGF2 alpha-induced increases in cell shortening and intracellular pH were also attenuated by the protein kinase C (PKC) inhibitor, chelerythrine (2 mumol l-1. CONCLUSION: The positive inotropic action of PGF2 alpha appears to be mediated via activation of the Na(+)-H+ exchanger with the possible involvement of PKC. This suggests that PGF2 alpha-produces intracellular alkalosis, which then sensitizes cardiac myofilaments to calcium. (+info)Morphine preconditioning attenuates neutrophil activation in rat models of myocardial infarction. (3/443)
Previous results from our laboratory have suggested that morphine can attenuate neutrophil activation in patients with acute myocardial infarction. To elucidate if morphine preconditioning (PC) has the same effects via activation of neutrophil endopeptidase 24.11 (NEP), we measured serum levels of intercellular adhesion molecule-1 (ICAM-1), gp100MEL14 and NEP in adult Wistar rats subjected to ten different protocols (n = 10 for each) at baseline, immediately after and 2 h after morphine PC. All groups were subjected to 30 min of occlusion and 2 h of reperfusion. Similarly, morphine-induced PC was elicited by 3-min drug infusions (100 micrograms/kg) interspersed with 5-min drug-free periods before the prolonged 30-min occlusion. Infarct size (IS), as a percentage of the area at risk (AAR), was determined by triphenyltetrazolium staining. Pretreatment with morphine increased NEP activities (9.86 +/- 1.98 vs. 5.12 +/- 1.10 nmol/mg protein in control group; p < 0.001). Naloxone (mu-opioid receptor antagonist) (4.82 +/- 1.02 nmol/mg protein) and phosphoramidon (NEP inhibitor) (4.66 +/- 1.00 nmol/mg protein) inhibited morphine-activated NEP, whereas glibenclamide (ATP-sensitive potassium channel antagonist) and chelerythrine (protein kinase C inhibitor) had no effects. The ICAM-1 and gp100MEL14 of the third sampling were lowest for those with morphine PC (280 +/- 30 ng/ml and 2.2 +/- 0.7 micrograms/ml; p < 0.001), but naloxone (372 +/- 38 ng/ml and 3.8 +/- 0.9 micrograms/ml) and phosphoramidon (382 +/- 40 ng/ml and 4.2 +/- 1.1 micrograms/ml) abolished the above phenomenon. IS/AAR were definitely lowest for those with morphine PC (24 +/- 7%; p < 0.05). Morphine preconditioning increases NEP activities to attenuate shedding of gp100MEL14 and to ICAM-1 and, thus, provides myocardial protection. (+info)Isoform-selective activation of protein kinase C by nitric oxide in the heart of conscious rabbits: a signaling mechanism for both nitric oxide-induced and ischemia-induced preconditioning. (4/443)
Although isoform-selective translocation of protein kinase C (PKC) epsilon appears to play an important role in the late phase of ischemic preconditioning (PC), the mechanism(s) responsible for such translocation remains unclear. Furthermore, the signaling pathway that leads to the development of late PC after exogenous administration of NO in the absence of ischemia (NO donor-induced late PC) is unknown. In the present study we tested the hypothesis that NO activates PKC and that this is the mechanism for the development of both ischemia-induced and NO donor-induced late PC. A total of 95 chronically instrumented, conscious rabbits were used. In rabbits subjected to ischemic PC (six 4-minute occlusion/4-minute reperfusion cycles), administration of the NO synthase inhibitor Nomega-nitro-L-arginine (group III), at doses previously shown to block the development of late PC, completely blocked the ischemic PC-induced translocation of PKCepsilon but not of PKCeta, indicating that increased formation of NO is an essential mechanism whereby brief ischemia activates the epsilon isoform of PKC. Conversely, a translocation of PKCepsilon and -eta quantitatively similar to that induced by ischemic PC could be reproduced pharmacologically with the administration of 2 structurally unrelated NO donors, diethylenetriamine/NO (DETA/NO) and S-nitroso-N-acetylpenicillamine (SNAP), at doses previously shown to elicit a late PC effect. The particulate fraction of PKCepsilon increased from 35+/-2% of total in the control group (group I) to 60+/-1% after ischemic PC (group II) (P<0.05), to 54+/-2% after SNAP (group IV) (P<0.05) and to 52+/-2% after DETA/NO (group V) (P<0.05). The particulate fraction of PKCeta rose from 66+/-5% in the control group to 86+/-3% after ischemic PC (P<0.05), to 88+/-2% after SNAP (P<0.05) and to 85+/-1% after DETA/NO (P<0.05). Neither ischemic PC nor NO donors had any appreciable effect on the subcellular distribution of PKCalpha, -beta1, -beta2, -gamma, -delta, - micro, or -iota/lambda; on total PKC activity; or on the subcellular distribution of total PKC activity. Thus, the effects of SNAP and DETA/NO on PKC closely resembled those of ischemic PC. The DETA/NO-induced translocation of PKCepsilon (but not that of PKCeta) was completely prevented by the administration of the PKC inhibitor chelerythrine at a dose of 5 mg/kg (group VI) (particulate fraction of PKCepsilon, 38+/-4% of total, P<0.05 versus group V; particulate fraction of PKCeta, 79+/-2% of total). The same dose of chelerythrine completely prevented the DETA/NO-induced late PC effect against both myocardial stunning (groups VII through X) and myocardial infarction (groups XI through XV), indicating that NO donors induce late PC by activating PKC and that among the 10 isozymes of PKC expressed in the rabbit heart, the epsilon isotype is specifically involved in the development of this form of pharmacological PC. In all groups examined (groups I through VI), the changes in the subcellular distribution of PKCepsilon protein were associated with parallel changes in PKCepsilon isoform-selective activity, whereas total PKC activity was not significantly altered. Taken together, the results provide direct evidence that isoform-selective activation of PKCepsilon is a critical step in the signaling pathway whereby NO initiates the development of a late PC effect both after an ischemic stimulus (endogenous NO) and after treatment with NO-releasing agents (exogenous NO). To our knowledge, this is also the first report that NO can activate PKC in the heart. The finding that NO can promote isoform-specific activation of PKC identifies a new biological function of this radical and a new mechanism in the signaling cascade of ischemic PC and may also have important implications for other pathophysiological conditions in which NO is involved and for nitrate therapy. (+info)c-myc intron element-binding proteins are required for 1, 25-dihydroxyvitamin D3 regulation of c-myc during HL-60 cell differentiation and the involvement of HOXB4. (5/443)
1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) suppresses c-myc expression during differentiation of HL-60 cells along the monocytic pathway by blocking transcriptional elongation at the first exon/intron border of the c-myc gene. In the present study, the physiological relevance of three putative regulatory protein binding sites found within a 280-base pair region in intron 1 of the c-myc gene was explored. HL-60 promyelocytic leukemia cells were transiently transfected with three different c-myc promoter constructs cloned upstream of a chloramphenicol acetyltransferase (CAT) reporter gene. With the wild-type c-myc promoter construct (pMPCAT), which contains MIE1, MIE2, and MIE3 binding sites, 1,25-(OH)2D3 was able to decrease CAT activity by 45.4 +/- 7.9% (mean +/- S.E., n = 8). The ability of 1, 25-(OH)2D3 to inhibit CAT activity was significantly decreased to 18. 5 +/- 4.3% (59.3% reversal, p < 0.02) when examined with a MIE1 deletion construct (pMPCAT-MIE1). Moreover, 1,25-(OH)2D3 was completely ineffective at suppressing CAT activity in cells transfected with pMPCAT-287, a construct without MIE1, MIE2, and MIE3 binding sites (-6.5 +/- 10.9%, p < 0.002). MIE1- and MIE2-binding proteins induced by 1,25-(OH)2D3 had similar gel shift mobilities, while MIE3-binding proteins migrated differently. Furthermore, chelerythrine chloride, a selective protein kinase C (PKC) inhibitor, and a PKCbeta antisense oligonucleotide completely blocked the binding of nuclear proteins induced by 1,25-(OH)2D3 to MIE1, MIE2, and MIE3. A 1,25-(OH)2D3-inducible MIE1-binding protein was identified to be HOXB4. HOXB4 levels were significantly increased in response to 1,25-(OH)2D3. Taken together, these results indicate that HOXB4 is one of the nuclear phosphoproteins involved in c-myc transcription elongation block during HL-60 cell differentiation by 1,25-(OH)2D3. (+info)Importance of PKC and tyrosine kinase in single or multiple cycles of preconditioning in rat hearts. (6/443)
Both tyrosine kinase (TK) and protein kinase C (PKC) inhibitors have been shown individually to completely abolish the cardioprotective effects of ischemic preconditioning (IPC) in rabbits; however, blockade of both enzymes is necessary to totally abolish IPC in pigs. Recently, we have shown that TK inhibition partially attenuates the cardioprotective effect of IPC in intact rat hearts. Therefore, the present study was designed to test the hypothesis that inhibition of both TK and PKC is necessary to completely abolish IPC in the intact rat and that this effect is dependent on the intensity of the preconditioning stimulus. All animals were subjected to 30 min of coronary artery occlusion and 2 h of reperfusion. In series 1, multiple-cycle-induced IPC was produced via three 5-min occlusions interspersed with 5 min of reperfusion (3 x 5 IPC). Genistein (5 mg/kg), a TK inhibitor infused 30 min before IPC, and chelerythrine chloride (5 mg/kg), a PKC inhibitor infused 5 min before the prolonged ischemic insult, were administered alone or in combination in the absence or presence of 3 x 5 IPC. 3 x 5 IPC produced a marked reduction in infarct size as a percentage of area at risk compared with control (8.0 +/- 0.8 vs. 56.1 +/- 0.8%). The effects of 3 x 5 IPC were partially blocked by pretreatment with genistein (34.0 +/- 2.0%) or chelerythrine (26.4 +/- 2.8%) alone; however, combined administration of genistein and chelerythrine completely abolished the effects of 3 x 5 IPC (50.7 +/- 3.6%). In series 2, single-cycle IPC was elicited by one 5-min occlusion followed by 10 min of reperfusion (1 x 5 IPC). Compared with control, 1 x 5 IPC also significantly reduced infarct size (15.4 +/- 3.0%). Genistein or chelerythrine administered alone completely abolished 1 x 5 IPC-induced cardioprotection. These results suggest that the efficacy of TK and PKC inhibition to block IPC depends on the intensity of the preconditioning stimulus and that these kinases may work through parallel pathways. (+info)Chloride channel inhibition blocks the protection of ischemic preconditioning and hypo-osmotic stress in rabbit ventricular myocardium. (7/443)
The objective of this study was to examine the role of chloride (Cl-) channels in the myocardial protection of ischemic preconditioning (IP). Isolated rabbit ventricular myocytes were preconditioned with 10-minute simulated ischemia (SI) and 20-minute simulated reperfusion (SR) or not preconditioned (control). The myocytes then received 180-minute SI or 45-minute SI/120-minute SR. Indanyloxyacetic acid 94 (IAA-94, 10 micromol/L) or 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB, 1 micromol/L) was administered before IP or before SI or SI/SR to inhibit Cl- channels. Electrophysiological studies indicate that these drugs, at the concentrations used, selectively abolished Cl- currents activated under hypo-osmotic conditions (215 versus 290 mOsm). IP significantly (P<0.001) reduced the percentage of dead myocytes after 60-minute (30.8+/-1.3%, mean+/-SEM), 90-minute (35.3+/-1.3%), and 120-minute (39.2+/-1.7%) SI compared with controls (44.7+/-1.6%, 54.5+/-1.3%, and 58.9+/-1.8%, respectively) and after 45-minute SI/120-minute SR (36.3+/-0.6%) compared with control (56.6+/-2.2%). Hypo-osmotic stress also produced protection similar to IP. IAA-94 or NPPB abolished the protection of both IP and hypo-osmotic stress. In buffer-perfused rabbit hearts preconditioned with three 5-minute ischemia/10-minute reperfusion cycles given before the 40-minute long ischemia and 60-minute reperfusion, IP significantly (P<0.0001) reduced infarct size (IP+vehicle, 4.7+/-0.9%, versus control+vehicle, 26.6+/-3.3%; mean+/-SEM). Again, IAA-94 or NPPB abolished the protection of IP. Our results implicate Cl- channels in the IP protection of the myocardium against ischemic/reperfusion injury and demonstrate that hypo-osmotic stress is capable of preconditioning cardiomyocytes. (+info)Nuclear factor-kappaB plays an essential role in the late phase of ischemic preconditioning in conscious rabbits. (8/443)
Although it is recognized that late preconditioning (PC) results from upregulation of cardioprotective genes, the specific transcription factor(s) that govern this genetic adaptation remains unknown. The aim of this study was to test the hypothesis that the development of late PC is mediated by nuclear factor-kappaB (NF-kappaB) and to elucidate the mechanisms that control the activation of NF-kappaB after an ischemic stimulus in vivo. A total of 152 chronically instrumented, conscious rabbits were used. A sequence of six 4-minute coronary occlusion/4-minute reperfusion cycles, which elicits late PC, induced rapid activation of NF-kappaB, as evidenced by a marked increase in p65 content (+164%; Western immunoblotting) and NF-kappaB DNA binding activity (+306%; electrophoretic mobility shift assay) in nuclear extracts isolated 30 minutes after the last reperfusion. These changes were attenuated 2 hours after ischemic PC and resolved by 4 hours. Competition and supershift assays confirmed the specificity of the NF-kappaB DNA complex signals. The mobility of the NF-kappaB DNA complex was shifted by anti-p65 and anti-p50 antibodies but not by anti-c-Rel antibodies, indicating that the subunits of NF-kappaB involved in gene activation after ischemic PC consist of p65-p50 heterodimers. Pretreatment with the NF-kappaB inhibitor diethyldithiocarbamate (DDTC; 150 mg/kg IP 15 minutes before ischemic PC) completely blocked the nuclear translocation and increased DNA binding activity of NF-kappaB. The same dose of DDTC completely blocked the cardioprotective effects of late PC against both myocardial stunning and myocardial infarction, indicating that NF-kappaB activation is essential for the development of this phenomenon in vivo. The ischemic PC-induced activation of NF-kappaB was also blocked by pretreatment with Nomega-nitro-L-arginine (L-NA), a nitric oxide synthase (NOS) inhibitor, N-2-mercaptopropionyl glycine (MPG), a reactive oxygen species (ROS) scavenger, chelerythrine, a protein kinase C (PKC) inhibitor, and lavendustin A, a tyrosine kinase inhibitor (all given at doses previously shown to block late PC), indicating that ischemic PC activates NF-kappaB via formation of NO and ROS and activation of PKC- and tyrosine kinase-dependent signaling pathways. A subcellular redistribution and increased DNA binding activity of NF-kappaB quantitatively similar to those induced by ischemic PC could be reproduced pharmacologically by giving the NO donor diethylenetriamine/NO (DETA/NO) (at a dose previously shown to elicit late PC), demonstrating that NO in itself can activate NF-kappaB in the heart. Taken together, these results provide direct evidence that activation of NF-kappaB is a critical step in the signal transduction pathway that underlies the development of the late phase of ischemic PC in conscious rabbits. The finding that four different pharmacological manipulations (L-NA, MPG, chelerythrine, and lavendustin A) produced similar inhibition of NF-kappaB suggests that this transcription factor is a common downstream pathway through which multiple signals elicited by ischemic stress (NO, ROS, PKC, tyrosine kinases) act to induce gene expression. To our knowledge, this is the first demonstration that NO can promote NF-kappaB activation in the heart, a finding that identifies a new biological function of NO and may have important implications for various pathophysiological conditions in which NO is involved and for nitrate therapy. (+info)
CHELERYTHRINE CHLORIDE | 3895-92-9
The Anticancer Effect of Sanguinarine: A Review | Bentham Science
Frontiers | Molecular determinants of sensitivity or resistance of cancer cells towards sanguinarine | Pharmacology
Molecular determinants of sensitivity or resistance of cancer cells toward sanguinarine<...
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Antiplatelet effect of sanguinarine is correlated to calcium mobilization, thromboxane and cAMP production<...
A study on Sanguinarine as an antileukemic agent- Involvement of react by Anees Rahman Cheratta
Sanguinarine induces apoptosis of human pancreatic carcinoma AsPC-1 and BxPC-3 cells via modulations in Bcl-2 family proteins |...
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Positive Inotropy Mediated by Diacylglycerol in Rat Ventricular Myocytes | Circulation Research
BBA - Molecular Cell Research (v.1823, #4) | www.chemweb.com
Frontiers | Exogenous 10 kDa-Heat Shock Protein Preserves Mitochondrial Function After Hypoxia/Reoxygenation | Pharmacology
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Fagaronine chloride [52259-64-0] glixxlabs.com High quality biochemicals supplier
Evaluation of anticancer activities of benzo phenanthridine alkaloid sanguinarine in oral squamous cell carcinoma cell line. |...
CAS 20267-87-2 (+/-)-Chelidonine - BOC Sciences
Protein kinase C activation induces tyrosine phosphorylation of the NR2A and NR2B subunits of the NMDA receptor. - Department...
POLD1 | Cancer Genetics Web
Differential contributions of protein kinase C isoforms in the regulation of group IIA secreted phospholipase A2 expression in...
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NK314 | CAS#208237-49-4 | Chk1 inhibitor | topoisomerase II inhibitor | MedKoo Biosciences
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Structural Perturbation of Chromatin by Plant Alkaloid Sanguinarine and Its Functional Consequences
Toddalin chloride | Abcam
Calphostin C | PKC inhibitor | Hello Bio
Investigation of signaling pathways that mediate the inotropic effect of urotensin-II in human heart | USC Research Bank -...
Different roles of protein kinase C α and δ isoforms in the regulation of neutral sphingomyelinase activity in HL-60 cells |...
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Dexmedetomidine-induced Contraction Involves Phosphorylation of Caldesmon by JNK in Endothelium-denuded Rat Aortas [Abstract]
Quantitative 1 H NMR metabolomics reveals extensive metabolic reprogramming of primary and secondary metabolism in elicitor...
Bloodroot Plant Care: Learn How To Grow Bloodroot (Sanguinaria Canadensis) - igrowplants.net
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Keltamo (Chelidonium majus) - villimies.fi
Sanguinaria canadensis - Wikibooks, open books for an open world
Corydalis | definition of Corydalis by Medical dictionary
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Role of PKC in the novel synergistic action of urotensin II and angiotensin II and in urotensin II-induced vasoconstriction |...
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
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Zanthoxylum austrosinense
The root contains benzophenanthridines and quinolines. Alkaloids: dictamnine. dimethylaheleryth-rine, austrosinensine, 8- ...
Zanthoxylum zanthoxyloides
Dupont, C; Couillerot, E; Gillet, R; Caron, C; Zeches-Hanrot, M; Riou, JF; Trentesaux, C (2005). "The benzophenanthridine ... It also contains fagaronine, a benzophenanthridine alkaloid. A study by Williams, Soelberg and Jäger (2016) showed than ...
Fagaronine
... is a benzophenanthridine alkaloid found in Zanthoxylum zanthoxyloides and other species in the genus Zanthoxylum. ... Dupont, C; Couillerot, E; Gillet, R; Caron, C; Zeches-Hanrot, M; Riou, JF; Trentesaux, C (2005). "The benzophenanthridine ...
Chelidonine
This benzophenanthridine alkaloid can induce apoptosis in some transformed or malignant cell lines. D-Chelidonine, the main ... C. majus contains various isoquinoline alkaloids with protopine, protoberberine and benzophenanthridine structures. ...
Chelerythrine
... is a benzophenanthridine alkaloid present in the plant Chelidonium majus (greater celandine). It is a potent, ... "The actions of benzophenanthridine alkaloids, piperonyl butoxide and (S)-methoprene at the G-protein coupled cannabinoid CB₁ ...
Dihydrobenzophenanthridine oxidase
Park SU, Yu M, Facchini PJ (2002). "Antisense RNA-mediated suppression of benzophenanthridine alkaloid biosynthesis in ... Dihydrobenzophenanthridine oxidase produces oxidized forms of benzophenanthridine alkaloids: In Sanguinaria canadensis ( ... cell suspensions and immobilized cultures for production of benzophenanthridine alkaloids". Appl. Microbiol. Biotechnol. 36 (5 ...
Protopine 6-monooxygenase
... the central enzyme in benzophenanthridine alkaloid biosynthesis". Phytochemistry. 29 (4): 1113-1122. doi:10.1016/0031-9422(90) ...
Nitidine
... is a benzophenanthridine alkaloid found in species of the genus Zanthoxylum , notably in Zanthoxylum nitidum. This ...
Reticuline oxidase
... an enzyme essential to the formation of benzophenanthridine alkaloids in the response of plants to pathogenic attack". Proc. ... a covalently flavinylated oxidase of benzophenanthridine alkaloid biosynthesis in plants". J. Biol. Chem. 270 (41): 24475-81. ...
Cannabidiolic acid synthase
... a covalently flavinylated oxidase of benzophenanthridine alkaloid biosynthesis in plants". The Journal of Biological Chemistry ...
Sanguinaria
Sanguinarine is a benzophenanthridine alkaloid (see phenanthridine), which, unlike most other alkaloids, has a red color in ...
Aristolochia grandiflora
Maiti, M.; G. S. Kumar (27 September 2007). "Molecular aspects on the interaction of protoberberine, benzophenanthridine, and ...
Piperonyl butoxide
"The actions of benzophenanthridine alkaloids, piperonyl butoxide and (S)-methoprene at the G-protein coupled cannabinoid CB₁ ...
T. R. Govindachari
... benzophenanthridines, pyridophenanthridines, dibenzoquinolizines, terpenes, flavones, and furocoumarins. Tylophorine from ...
Zanthoxylum clava-herculis
The benzophenanthridine alkaloid chelerythrine is the major active natural product found in Z. clava-herculis, exhibiting anti- ...
Mark Cushman
... versatile transformation has been used to generate polysubstituted lactam carboxylic acids and to prepare benzophenanthridine ...
Black salve
The extract of bloodroot is called sanguinarine, a quaternary benzophenanthridine alkaloid which attacks and destroys living ...
Zanthoxylum
Species identified in Nigeria contains several types of alkaloids including benzophenanthridines (nitidine, dihydronitidine, ...
Ivan Addae Mensah
A phenolic benzophenanthridine alkaloid from Fagara xanthoxyloides (1973) Torto, F.G.; Mensah, I.A. (April 1970). "Alkaloids of ... Comparative examination of two Zanthoxylum benzophenanthridine alkaloids for effects in rabbits (1989) Essential oils of Lippia ...
BBE-like enzymes
... benzophenanthridine, phthalide isoquinoline or rhoeadine metabolic pathways. Research on this matter is rare since it is very ...
Papaveraceae
They are derived from berberine, tetrahydroberberine, protopine and benzophenanthridine in Papaveroideae, and from ...
Controlling Powdery Mildew of Greenhouse Roses Using Quartenary Benzophenanthridine Alkaloids in: HortScience Volume 31 Issue 4...
Quartenary benzophenanthridine alkaloids (QBAs) are known to be effective in the control of crop damaging fungal diseases. QBAs ... Quartenary benzophenanthridine alkaloids (QBAs) are known to be effective in the control of crop damaging fungal diseases. QBAs ... Controlling Powdery Mildew of Greenhouse Roses Using Quartenary Benzophenanthridine Alkaloids in HortScience ...
MeSH Browser
Benzophenanthridines Preferred Term Term UI T658134. Date11/10/2005. LexicalTag NON. ThesaurusID NLM (2007). ... Benzophenanthridines Preferred Concept UI. M0491452. Registry Number. 0. Scope Note. Compounds of four rings containing a ... Benzophenanthridines. Tree Number(s). D03.132.089. D03.633.300.633.207. D03.633.400.131. Unique ID. D053119. RDF Unique ...
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Antiinflammatory activity of quaternary benzophenanthridine alkaloids from Chelodium majus. J Med Plant Res 1981; 43:161-165. ... Antiinflammatory activity of quaternary benzophenanthridine alkaloids from Chelodium majus. J Med Plant Res 1981; 43:161-165. ... Antiinflammatory activity of quaternary benzophenanthridine alkaloids from Chelodium majus. . J Med Plant Res. 1981. ; 43. :. ... Antiinflammatory activity of quaternary benzophenanthridine alkaloids from Chelodium majus. . J Med Plant Res. 1981. ; 43. :. ...
Chelerythrine Chloride | Cell Signaling Technology
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Biological and Pharmaceutical Bulletin
CCCC 1975, Volume 40, Issue 3, Abstracts pp. 705-711, Articles by the same authors | Collection of Czechoslovak Chemical...
DeCS
Natural isoquinoline alkaloids as potential multi-target agents against Alzheimerandprime;s disease| Abstract
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Dicentrine production in cell suspensions and hairy root cultures of Stephania suberosa
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Amaryllidaceae Alkaloids | Harvard Catalyst Profiles | Harvard Catalyst
Nitidine chloride induces caspase 3/GSDME-dependent pyroptosis by inhibting PI3K/Akt pathway in lung cancer | Chinese Medicine ...
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Chelerythrine chloride (1330) | Bio-Techne
Anticancer activity of Nigerian medicinal plants: a review | Future Journal of Pharmaceutical Sciences | Full Text
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Guineensine, an Acyl-CoA: cholesterol acyltransferase inhibitor, from the fruits of Piper longum.下载|翻译|阅读
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DeCS 2007 - New terms
DeCS 2007 - New terms
DeCS 2007 - New terms
Alkaloid5
- Chelerythrine is a benzophenanthridine alkaloid that elicits a wide range of biological responses. (cellsignal.com)
- Transcriptional down regulation of hTERT and induction of senescence in HepG2 cells by the benzophenanthridine alkaloid chelidonine. (uni-heidelberg.de)
- Enhanced benzophenanthridine alkaloid production and protein expression with combined elicitor in Eschscholtzia californica suspension cultures. (tci-thaijo.org)
- Differential induction of protein expression and benzophenanthridine alkaloid accumulation in Eschscholtzia californica suspension cultures by methyl jasmonate and yeast extract. (tci-thaijo.org)
- Antiproliferative and antiangiogenic effects of the of the Benzophenanthridine alkaloid Sanguinarine in melanoma. (science-medic.com)
Alkaloids2
- Quartenary benzophenanthridine alkaloids (QBAs) are known to be effective in the control of crop damaging fungal diseases. (ashs.org)
- Lee Angoline and chelerythrine, benzophenanthridine alkaloids that do not inhibit protein kinase C. J.Biol.Chem. (bio-techne.com)
Chelerythrine1
- On the other hand, from the stem bark of Z. schreberi were isolated 2 protoberberines (berberine and columbamine) and a benzophenanthridine (chelerythrine). (alliedacademies.org)
Protoberberine2
- MolecularAspects on the Interaction of Protoberberine, Benzophenanthridine, and. (csircentral.net)
- Natural Berberine and Sanguinarine both are isoquinoline derivatives and belong to protoberberine and benzophenanthridines, respectively. (underherb.com)