DOCSLIB.ORG

Catalog Update01 - EU Update 31/01/2013 08:12 Page 1

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Catalog Update01 - EU Update 31/01/2013 08:12 Page 1 Catalog Update01 - EU_Update 31/01/2013 08:12 Page 1 Catalog update High purity biochemical tools for life scientists •Receptor agonists and antagonists •Ion channel modulators •Enzyme modulators •Signaling tools € - March 2013 Discover more at www.abcam.com/biochemicals Catalog Update01 - EU_Update 31/01/2013 08:12 Page 2 Contents Receptors & Transporters Page Receptors & Transporters (continued) Page Adenosine & Purinergics Peptide Receptors 17 P1 5 Prostanoid 18 P2 5 Serotonin Adrenoceptors 5 5-HT1 18 Cannabinoid 6 5-HT2 19 Catalytic Receptors 7 5-HT3 19 Chemokine 7 5-HT4 19 Dopamine 7 5-HT5 19 Enzyme-Linked Receptors 9 5-HT6 20 G protein-coupled estrogen 10 5-HT7 20 GABA Non-selective 20 GABAA 10 Transporters 20 GABAB 10 Sigma 20 Non-selective 10 Smoothened 20 Other 11 Sphingosine 1-Phosphate Receptors 21 Transporters 11 TGR5 21 Glutamate Toll-Like Receptors 21 AMPA & Kainate 11 Transporters 21 Broad spectrum / non-selective 11 mGlu: General 12 Ion Channels Page mGlu: Group I 12 Calcium 22 mGlu: Group I & II 12 Chloride 22 mGlu: Group II 12 Cyclic nucleotide-gated 22 mGlu: Group III 13 Ionophores, indicators & chelators 22 NMDA: AP-2 binding site 13 Other 22 NMDA: Glutamate Site 13 Potassium 22 NMDA: Glycine Site 13 Sodium 23 NMDA: Ion Channel Site 13 TRP 23 NMDA: Polyamine Site 14 Transporters 14 Enzymes Page Glycine 14 ATPase & GTPase 23 Histamine 14 Caspase 24 Imidazoline 15 Cholinesterase 24 Melatonin 15 Coenzymes 24 Muscarinic 15 Cyclase 24 Nicotinic 15 Cyclooxygenase 24 Nuclear Receptors 16 Cytochrome P450 25 Opioids 16 Deacetylase 25 Orphan 7-TM Receptors 17 Dehydrogenase 25 2 Discover more at www.abcam.com/biochemicals Catalog Update01 - EU_Update 31/01/2013 08:12 Page 3 Contents Enzymes (continued) Page Signaling (continued) Page Demethylase 25 Ca2+ Signaling 34 Hydrolase 25 Cytoskeleton & motor proteins 34 Isomerase 26 DNA, RNA & protein synthesis 34 Kinase 26 Endocytosis & exocytosis 35 Oxidases 29 Epigenetics 36 Oxygenase 29 Extracellular matrix & cell adhesion 36 Phosphatase 29 Heat shock proteins 36 Phosphodiesterase 29 Immunomodulators 37 Phospholipase & Lipase 29 Lipid signaling 37 Polymerase 29 Stem Cells 38 Protease 30 Reductase 30 Signal transduction Page Secretase 30 Cytokines, NF-κB & IκB 39 Synthetase & synthase 30 G-Protein related 39 Telomerase 30 Hedgehog signaling 39 Transaminase 30 Inositol & cAMP signaling 39 Transferase 31 JAK/STAT 39 MAPK 40 Signaling Page Nitric oxide & oxidative stress 40 Amyloidogenesis 31 PI3K/Akt 41 Angiogenesis 31 Wnt signaling 41 Apoptosis & cell cycle 32 Symbol key Ç Products added since publication of 2012 catalog. É Just-Add-Water: typically water-soluble to at least 10 mM or above. Ë Country restrictions and/or license requirements may apply. Please contact customer services for further details. fi Not currently for sale in the US fi Sold under exclusive licence from Children's Medical Research Institute and Newcastle Innovation Ltd. Iminodyn-22™, Iminodyn-17™, Dynole-34-2™, Dynole-31-2™, RTIL-13™, MiTMAB™, OcTMAB™, Pitstop 1™, Pitstop 2™, Dyngo-4a™, Rhodadyn B10™, Rhodadyn C10™, are trademarks of Children's Medical Research Institute and Newcastle Innovation Ltd. fi Sold under exclusive license from Columbia University; Patent Pending fi Sold under license from Columbia University; Patent Pending fi Sold under license from Eli Lilly and company fi Sold under license from Hugin Neurochemicals fi Sold under license from Virginia Commonwealth University. fi Sold under license granted by the University of Pennsylvania. fi Sold under exclusive licence from Children's Medical Research Institute and Newcastle Innovation Ltd. Pitstop-1™ and Pitstop-2™ is a trademark of Freie Universität Berlin, Newcastle Innovation Ltd. and Children's Medical Research Institute Discover more at www.abcam.com/biochemicals 3 Catalog Update01 - EU_Update 31/01/2013 08:12 Page 4 Great supporting data for your research Tried and tested Apoptotic stimuli biological information Every product has a detailed description including Bcl-2 Family members potency (Ki, IC50 etc.), cell permeability and solubility data. Mitochondria Apoptosome Useful references for HtrA2 SMAC cyt-c formation IAP ARTS every product antagonists Every Abcam Biochemicals product is listed with a range of useful references and citations to help you Inhibitors of XIAP Apaf-1 figure out the best conditions for your experiment - apoptosis from in vitro to in vivo; western blotting to (IAPs) immunofluorescence. Caspase 9 Initiator caspase Caspase 7 Effector Caspase 3 Find the product caspases you need • You can check chemical names, structures, formula and CAS number online. Apoptosis • Our smiles information now allows you to recreate structures using chemical drawing packages. Guides to signalling Examples include: pathways and pharmacology • Akt signaling • MAPK signaling • Apoptosis • Glutamate Visit: www.abcam.com/at-a-glance for the full range of @ a glance guides Refer to page 3 for symbol key 4 Discover more at www.abcam.com/biochemicals Catalog Update01 - EU_Update 31/01/2013 08:12 Page 5 Receptors & Transporters: Adenosine & Purinergics: P1 Cat No. Product Pack Sizes Purity Description É ab120498 Adenosine 1g: € 15 5g: € 40 25g: € 55 >99% Endogenous P1 receptor agonist É ab120240 Caffeine 1g: € 15 5g: € 30 >99% PDE inhibitor. Adenosine antagonist Ç ab120453 CGS 21680 10mg: € 205 50mg: € 895 >98% Potent, selective A2A agonist 6 ab120434 2-Chloro-N -cyclopentyladenosine (CCPA) 10mg: € 95 50mg: € 380 >98% Highly potent, selective A1 agonist É ab120037 2-Chloroadenosine (CADO) 10mg: € 30 50mg: € 70 250mg: € 305 >98% Adenosine agonist ab120442 8-(3-Chlorostyryl)caffeine 10mg: € 55 50mg: € 250 >98% Selective A2A receptor antagonist. MAO-B inhibitor. 6 ab120472 N -Cyclohexyladenosine 50mg: € 55 250mg: € 220 >98% Selective A1 receptor agonist 6 ab120398 N -Cyclopentyladenosine (CPA) 25mg: € 40 100mg: € 140 >99% Potent, selective A1 agonist ab120396 DPCPX 25mg: € 45 100mg: € 95 >99% Potent A1 antagonist ab120458 HENECA 1mg: € 70 10mg: € 185 >99% Selective A2A receptor agonist ab120438 IB-MECA 5mg: € 140 25mg: € 605 >97% Highly potent and selective A3 agonist Ç É ab120724 Inosine 100mg: € 15 1g: € 30 >99% Purine nucleoside. Adenosine metabolite. ab120452 Iodotubercidin 1mg: € 85 5mg: € 270 >95% Potent, adenosine kinase inhibitor fi ab120397 MRS 1754 10mg: € 130 50mg: € 555 >98% Selective A2B antagonist ab120440 NECA 10mg: € 40 50mg: € 110 >99% Highly potent adenosine agonist Ç ab118162 NECA fluorescent ligand (Red) 50μg: € 250 100μg: € 415 >97% Fluorescent non-selective adenosine agonist Ç ab120921 Reversine 1mg: € 30 5mg: € 135 >98% Potent selective A3 receptor antagonist ab120439 SCH-58261 10mg: € 120 50mg: € 525 >99% Potent, highly selective A2A antagonist Ç ab118163 XAC Fluorescent ligand-1 (Red) 50μg: € 250 100μg: € 415 >97% Fluorescent non-selective adenosine antagonist Ç ab118164 XAC A3 fluorescent ligand (Red) 50μg: € 250 100μg: € 415 >97% Fluorescent A3 antagonist ab120218 ZM 241385 10mg: € 120 50mg: € 515 >99% Potent, selective A2A antagonist Receptors & Transporters: Adenosine & Purinergics: P2 Cat No. Product Pack Sizes Purity Description ab120413 A 438079 10mg: € 110 50mg: € 470 >98% Potent, competitive P2X7 receptor antagonist É ab120385 ATP disodium salt 1g: € 30 5g: € 70 10g: € 130 25g: € 250 >99% P2 receptor agonist. Signalling molecule. É ab120389 Brilliant Blue G 100mg: € 30 1g: € 130 >90% Potent, noncompetitive P2X7 antagonist Ç É ab120444 BzATP triethylammonium salt 1mg: € 45 5mg: € 45 25mg: € 165 >99% Potent, prototypic P2X7 agonist. P2 agonist. ab120387 (±)-Clopidogrel 10mg: € 100 50mg: € 425 >99% Potent, selective P2Y12 antagonist É ab120395 GW791343 10mg: € 120 50mg: € 525 >99% P2X7 allosteric modulator ab120421 KN-62 1mg: € 95 5mg: € 205 >98% CaM kinase II inhibitor. P2X7 antagonist. É ab120414 MRS 2179 10mg: € 165 50mg: € 735 >98% Potent, selective P2Y1 antagonist Ç É ab120445 MRS 2211 10mg: € 65 50mg: € 305 >95% Selective competitive P2Y13 antagonist É ab120454 NF023 10mg: € 85 50mg: € 345 >97% Competitive P2X1 receptor antagonist Ç É ab120415 NF 449 10mg: € 130 50mg: € 555 >95% Highly selective, potent P2X1 receptor antagonist É ab120403 β-Nicotinamide adenine dinucleotide (β-NAD) 25mg: € 30 250mg: € 95 1g: € 260 >96% Coenzyme and enzyme substrate. P2Y11 agonist. É ab120009 PPADS 10mg: € 45 50mg: € 185 250mg: € 740 P2 purinergic receptor antagonist. Ç É ab120422 Suramin hexasodium salt 100mg: € 55 500mg: € 270 >99% Non-selective P2 purinergic antagonist É ab120384 UDP-glucose 100mg: € 55 1g: € 220 >98% Highly potent P2Y14 agonist É ab120383 UDP sodium salt (Uridine 5’-diphosphate) 100mg: € 45 500mg: € 185 >98% P2Y6 agonist. P2Y14 ligand. Receptors & Transporters: Adrenoceptors Cat No. Product Pack Sizes Purity Description Ç ab118167 Alprenolol fluorescent ligand (Red) 50μg: € 250 100μg: € 415 >97% Fluorescent β2 adrenoceptor antagonist Ç ab120576 Asenapine maleate 10mg: € 45 50mg: € 185 >99% Multiple receptor antagonist. Anti-psychotic agent. Ç É ab120752 (R,S)-Atenolol 1g: € 45 >99% β1 adrenoceptor antagonist Ç ab120856 (S)-(-)-Atenolol 10mg: € 70 50mg: € 280 >98% Selective β1 adrenoceptor antagonist Ç ab120785 Atipamezole hydrochloride 10mg: € 120 50mg: € 470 >99% Selective α2 adrenergic receptor antagonist Ç ab120783 (±)-Bisoprolol hemifumarate 10mg: € 110 50mg: € 445 >99% Selective β1 antagonist Ç É ab120520 BMY 7378 dihydrochloride 10mg: € 40 50mg: € 150 >99% 5-HT1A partial agonist. α-adrenoceptor antagonist. Ç ab120806 BRL 44408 maleate 10mg: € 110 50mg: € 445 >99% Selective α2A adrenoceptor antagonist
Load more

Recommended publications
  • TABLE 1 Studies of Antagonist Activity in Constitutively Active
    TABLE 1 Studies of antagonist activity in constitutively active receptors systems shown to demonstrate inverse agonism for at least one ligand Targets are natural Gs and constitutively active mutants (CAM) of GPCRs. Of 380 antagonists, 85% of the ligands demonstrate inverse agonism. Receptor Neutral Antagonist Inverse Agonist Reference Human β2-adrenergic Dichloroisoproterenol, pindolol, labetolol, timolol, Chidiac et al., 1996; Azzi et alprenolol, propranolol, ICI 118,551, cyanopindolol al., 2001 Turkey erythrocyte β-adrenergic Propranolol, pindolol Gotze et al., 1994 Human β2-adrenergic (CAM) Propranolol Betaxolol, ICI 118,551, sotalol, timolol Samama et al., 1994; Stevens and Milligan, 1998 Human/guinea pig β1-adrenergic Atenolol, propranolol Mewes et al., 1993 Human β1-adrenergic Carvedilol CGP20712A, metoprolol, bisoprolol Engelhardt et al., 2001 Rat α2D-adrenergic Rauwolscine, yohimbine, WB 4101, idazoxan, Tian et al., 1994 phentolamine, Human α2A-adrenergic Napthazoline, Rauwolscine, idazoxan, altipamezole, levomedetomidine, Jansson et al., 1998; Pauwels MPV-2088 (–)RX811059, RX 831003 et al., 2002 Human α2C-adrenergic RX821002, yohimbine Cayla et al., 1999 Human α2D-adrenergic Prazosin McCune et al., 2000 Rat α2-adrenoceptor MK912 RX821002 Murrin et al., 2000 Porcine α2A adrenoceptor (CAM- Idazoxan Rauwolscine, yohimbine, RX821002, MK912, Wade et al., 2001 T373K) phentolamine Human α2A-adrenoceptor (CAM) Dexefaroxan, (+)RX811059, (–)RX811059, RS15385, yohimbine, Pauwels et al., 2000 atipamezole fluparoxan, WB 4101 Hamster α1B-adrenergic
    [Show full text]
  • From Inverse Agonism to 'Paradoxical Pharmacology' Richard A
    International Congress Series 1249 (2003) 27-37 From inverse agonism to 'Paradoxical Pharmacology' Richard A. Bond*, Kenda L.J. Evans, Zsirzsanna Callaerts-Vegh Department of Pharmacological and Pharmaceutical Sciences, University of Houston, 521 Science and Research Bldg 2, 4800 Caltioun, Houston, TX 77204-5037, USA Received 16 April 2003; accepted 16 April 2003 Abstract The constitutive or spontaneous activity of G protein-coupled receptors (GPCRs) and compounds acting as inverse agonists is a recent but well-established phenomenon. Dozens of receptor subtypes for numerous neurotransmitters and hormones have been shown to posses this property. However, do to the apparently low percentage of receptors in the spontaneously active state, the physiologic relevance of these findings remains questionable. The possibility that the reciprocal nature of the effects of agonists and inverse agonists may extend to cellular signaling is discussed, and that this may account for the beneficial effects of certain p-adrenoceptor inverse agonists in the treatment of heart failure. © 2003 Elsevier Science B.V. All rights reserved. Keywords. Inverse agonism; GPCR; Paradoxical pharmacology 1. Brief history of inverse agonism at G protein-coupled receptors For approximately three-quarters of a century, ligands that interacted with G protein- coupled receptors (GPCRs) were classified either as agonists or antagonists. Receptors were thought to exist in a single quiescent state that could only induce cellular signaling upon agonist binding to the receptor to produce an activated state of the receptor. In this model, antagonists had no cellular signaling ability on their own, but did bind to the receptor and prevented agonists from being able to bind and activate the receptor.
    [Show full text]
  • (12) Patent Application Publication (10) Pub. No.: US 2010/0221245 A1 Kunin (43) Pub
    US 2010O221245A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2010/0221245 A1 Kunin (43) Pub. Date: Sep. 2, 2010 (54) TOPICAL SKIN CARE COMPOSITION Publication Classification (51) Int. Cl. (76) Inventor: Audrey Kunin, Mission Hills, KS A 6LX 39/395 (2006.01) (US) A6II 3L/235 (2006.01) A638/16 (2006.01) Correspondence Address: (52) U.S. Cl. ......................... 424/133.1: 514/533: 514/12 HUSCH BLACKWELL SANDERS LLP (57) ABSTRACT 4801 Main Street, Suite 1000 - KANSAS CITY, MO 64112 (US) The present invention is directed to a topical skin care com position. The composition has the unique ability to treat acne without drying out the user's skin. In particular, the compo (21) Appl. No.: 12/395,251 sition includes a base, an antibacterial agent, at least one anti-inflammatory agent, and at least one antioxidant. The (22) Filed: Feb. 27, 2009 antibacterial agent may be benzoyl peroxide. US 2010/0221 245 A1 Sep. 2, 2010 TOPCAL SKIN CARE COMPOSITION stay of acne treatment since the 1950s. Skin irritation is the most common side effect of benzoyl peroxide and other anti BACKGROUND OF THE INVENTION biotic usage. Some treatments can be severe and can leave the 0001. The present invention generally relates to composi user's skin excessively dry. Excessive use of some acne prod tions and methods for producing topical skin care. Acne Vul ucts may cause redness, dryness of the face, and can actually garis, or acne, is a common skin disease that is prevalent in lead to more acne. Therefore, it would be beneficial to provide teenagers and young adults.
    [Show full text]
  • Ciproxifan, a Histamine H3 Receptor Antagonist, Reversibly Inhibits Monoamine Oxidase a and B Received: 05 September 2016 S
    www.nature.com/scientificreports OPEN Ciproxifan, a histamine H3 receptor antagonist, reversibly inhibits monoamine oxidase A and B Received: 05 September 2016 S. Hagenow1, A. Stasiak2, R. R. Ramsay3 & H. Stark1 Accepted: 07 December 2016 Ciproxifan is a well-investigated histamine H receptor (H3R) inverse agonist/antagonist, showing Published: 13 January 2017 3 an exclusively high species-specific affinity at rodent compared to human H3R. It is well studied as reference compound for H3R in rodent models for neurological diseases connected with neurotransmitter dysregulation, e.g. attention deficit hyperactivity disorder or Alzheimer’s disease. In a screening for potential monoamine oxidase A and B inhibition ciproxifan showed efficacy on both enzyme isoforms. Further characterization of ciproxifan revealed IC50 values in a micromolar concentration range for human and rat monoamine oxidases with slight preference for monoamine oxidase B in both species. The inhibition by ciproxifan was reversible for both human isoforms. Regarding inhibitory potency of ciproxifan on rat brain MAO, these findings should be considered, when using high doses in rat models for neurological diseases. As the H3R and monoamine oxidases are all capable of affecting neurotransmitter modulation in brain, we consider dual targeting ligands as interesting approach for treatment of neurological disorders. Since ciproxifan shows only moderate activity at human targets, further investigations in animals are not of primary interest. On the other hand, it may serve as starting point for the development of dual targeting ligands. Ciproxifan (cyclopropyl 4-(3-(1H-imidazol-4-yl)propyloxy)phenyl methanone) is a well characterized species-specific histamine 3H receptor (H3R) inverse agonist/antagonist (Fig.
    [Show full text]
  • Overview and Perspective on RTK Heterointeractions Michael D
    Review Cite This: Chem. Rev. 2019, 119, 5881−5921 pubs.acs.org/CR The RTK Interactome: Overview and Perspective on RTK Heterointeractions Michael D. Paul and Kalina Hristova* Department of Materials Science and Engineering, Institute for NanoBioTechnology, and Program in Molecular Biophysics, Johns Hopkins University, Baltimore, Maryland 21218, United States ABSTRACT: Receptor tyrosine kinases (RTKs) play important roles in cell growth, motility, differentiation, and survival. These single-pass membrane proteins are grouped into subfamilies based on the similarity of their extracellular domains. They are generally thought to be activated by ligand binding, which promotes homodimerization and then autophosphorylation in trans. However, RTK interactions are more complicated, as RTKs can interact in the absence of ligand and heterodimerize within and across subfamilies. 19 Here, we review the known cross-subfamily RTK heterointeractions and their possible biological implications, as well as the methodologies which have been used to study them. Moreover, we demonstrate how thermodynamic models can be used to study RTKs and to explain many of the complicated biological effects which have been described in the literature. Finally, we discuss the concept of the RTK interactome: a putative, extensive network of interactions between the RTKs. This RTK interactome can produce unique signaling outputs; can amplify, inhibit, and modify signaling; and can allow for signaling backups. The existence of the RTK interactome could provide an explanation for the irreproducibility of experimental data from different studies and for the failure of some RTK inhibitors to produce the desired therapeutic effects. We argue that a deeper knowledge of RTK interactome thermodynamics can lead to a better understanding of fundamental RTK signaling processes in health and disease.
    [Show full text]
  • A Molecular Dynamics Simulation Study for Variant Drug Responses Due to FMS-Like Tyrosine Kinase 3 Cite This: RSC Adv.,2017,7, 29871 G697R Mutation†
    RSC Advances View Article Online PAPER View Journal | View Issue A molecular dynamics simulation study for variant drug responses due to FMS-like tyrosine kinase 3 Cite this: RSC Adv.,2017,7, 29871 G697R mutation† Chien-Cheng Lee,a Yu-Chung Chuang,b Yu-Lin Liub and Chia-Ning Yang *b FMS-like tyrosine kinase 3 (FLT3) is an attractive target for acute myeloid leukemia. Recent studies have suggested that the application of small-molecule kinase inhibitors is a promising treatment strategy for patients with primary activating mutations of FLT3; however, the development of secondary mutations, including those of A627T, N676D, F691I, and G697R, that confer acquired resistance to kinase inhibitors has become a severe problem. In this study, we conducted a series of molecular dynamics simulations on PKC412- and sorafenib-bound FLT3 kinases and different apo forms of the FLT3 kinase to explain the minor and severe G697R mutation-induced resistance to sorafenib and PKC412, respectively. Structural analysis on our simulation results revealed that the type II kinase inhibitor sorafenib (IC50 ¼ 9 nM) Creative Commons Attribution 3.0 Unported Licence. assesses its binding site through either the adenine pocket entrance or the back pocket entrance, whereas the type I kinase inhibitor PKC412 (IC50 ¼ 35 nM) intercalates to its binding site from the front pocket entrance. The G697 residue is located at the end of the FLT3 kinase hinge segment and is close to the front and adenine pockets. In G697R mutation where the substituted R697 residue affects both the front and adenine pocket entrances in different manners, sorafenib may approach its binding site Received 11th April 2017 through the back pocket entrance, whereas PKC412 is blocked by the FLT3 kinase.
    [Show full text]
  • Marine Drugs
    marine drugs Article Neuroprotective Effect of Carotenoid-Rich Enteromorpha prolifera Extract via TrkB/Akt Pathway against Oxidative Stress in Hippocampal Neuronal Cells Seung Yeon Baek and Mee Ree Kim * Department of Food and Nutrition, Chungnam National University, Daejeon 34134, Korea; [email protected] * Correspondence: [email protected]; Tel.: +82-42-821-6837; Fax: +82-42-821-8887 Received: 27 June 2020; Accepted: 17 July 2020; Published: 19 July 2020 Abstract: In this study, we found that E. prolifera extract (EAEP) exhibits neuroprotective effects in oxidative stress-induced neuronal cells. EAEP improved cell viability as well as attenuated the formation of intracellular reactive oxygen species (ROS) and apoptotic bodies in glutamate-treated hippocampal neuronal cells (HT-22). Furthermore, EAEP improved the expression of brain-derived neurotrophic factor (BDNF) and antioxidant enzymes such as heme oxygenase-1 (HO-1), NAD(P)H quinine oxidoreductase-1 (NQO-1), and glutamate–cysteine ligase catalytic subunit (GCLC) via the tropomyosin-related kinase receptor B/ protein kinase B (TrkB/Akt) signaling pathway. In contrast, the pre-incubation of K252a, a TrkB inhibitor, or MK-2206, an Akt-selective inhibitor, ameliorated the neuroprotective effects of EAEP in oxidative stress-induced neuronal cells. These results suggest that EAEP protects neuronal cells against oxidative stress-induced apoptosis by upregulating the expression of BDNF and antioxidant enzymes via the activation of the TrkB/Akt pathway. In conclusion, such an effect of EAEP, which is rich in carotenoid-derived compounds, may justify its application as a food supplement in the prevention and treatment of neurodegenerative disorders. Keywords: Enteromorpha prolifera; oxidative stress; apoptosis; BDNF; TrkB/Akt pathway 1.
    [Show full text]
  • Lipid Metabolic Reprogramming: Role in Melanoma Progression and Therapeutic Perspectives
    cancers Review Lipid metabolic Reprogramming: Role in Melanoma Progression and Therapeutic Perspectives 1, 1, 1 2 1 Laurence Pellerin y, Lorry Carrié y , Carine Dufau , Laurence Nieto , Bruno Ségui , 1,3 1, , 1, , Thierry Levade , Joëlle Riond * z and Nathalie Andrieu-Abadie * z 1 Centre de Recherches en Cancérologie de Toulouse, Equipe Labellisée Fondation ARC, Université Fédérale de Toulouse Midi-Pyrénées, Université Toulouse III Paul-Sabatier, Inserm 1037, 2 avenue Hubert Curien, tgrCS 53717, 31037 Toulouse CEDEX 1, France; [email protected] (L.P.); [email protected] (L.C.); [email protected] (C.D.); [email protected] (B.S.); [email protected] (T.L.) 2 Institut de Pharmacologie et de Biologie Structurale, CNRS, Université Toulouse III Paul-Sabatier, UMR 5089, 205 Route de Narbonne, 31400 Toulouse, France; [email protected] 3 Laboratoire de Biochimie Métabolique, CHU Toulouse, 31059 Toulouse, France * Correspondence: [email protected] (J.R.); [email protected] (N.A.-A.); Tel.: +33-582-7416-20 (J.R.) These authors contributed equally to this work. y These authors jointly supervised this work. z Received: 15 September 2020; Accepted: 23 October 2020; Published: 27 October 2020 Simple Summary: Melanoma is a devastating skin cancer characterized by an impressive metabolic plasticity. Melanoma cells are able to adapt to the tumor microenvironment by using a variety of fuels that contribute to tumor growth and progression. In this review, the authors summarize the contribution of the lipid metabolic network in melanoma plasticity and aggressiveness, with a particular attention to specific lipid classes such as glycerophospholipids, sphingolipids, sterols and eicosanoids.
    [Show full text]
  • Short-Term Rapamycin Persistently Improves Cardiac Function After Cessation of Treatment in Aged Male and Female Mice
    Short-term rapamycin persistently improves cardiac function after cessation of treatment in aged male and female mice. Ellen Quarles A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy University of Washington 2017 Reading Committee: Peter Rabinovitch, Chair Michael MacCoss David Marcinek Program Authorized to Offer Degree: Pathology © Copyright 2017 Ellen Quarles University of Washington Abstract Short-term rapamycin persistently improves cardiac function after cessation of treatment in aged male and female mice. Ellen Quarles Chair of the Supervisory Committee: Peter Rabinovitch, Professor and Vice Chair of Research Department of Pathology Cardiac aging is an intrinsic process that results in impaired cardiac function and dysregulation of cellular and molecular quality control mechanisms. These effects are evident in the decline of diastolic function, increase in left ventricular hypertrophy, metabolic substrate shifts, and alterations to the cardiac proteome. This thesis covers the quality control mechanisms that are associated with cardiac aging, results from an anti-aging intervention in aged mice, and a review of mitochondrial dysfunction in the heart. Chapter one is a review of the quality control mechanisms in aging myocardium. Chapter two consists of the results of several mouse experiments that compare the cardiac function, proteomes, and metabolomes of aged and young controls, along with rapamycin treated aged mice. The novelty of this study comes from the inclusion of a group of animals treated only transiently with the drug, then followed for eight weeks post-drug-removal. This persistence cohort may hold clues to deriving long-lasting benefits of rapamycin with only transient treatment.
    [Show full text]
  • The Role of Neurotrophin Receptors in Female Germ-Cell Survival in Mouse and Human Norah Spears1,*, Michael D
    Research article 5481 The role of neurotrophin receptors in female germ-cell survival in mouse and human Norah Spears1,*, Michael D. Molinek1, Lynne L. L. Robinson2, Norma Fulton2, Helen Cameron1, Kohji Shimoda1, Evelyn E. Telfer3, Richard A. Anderson2 and David J. Price1 1Biomedical Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK 2Medical Research Council Human Reproductive Sciences Unit, Centre for Reproductive Biology, The University of Edinburgh Chancellor’s Building, 49 Little France Crescent, Edinburgh EH16 4SA, UK 3Institute of Cellular and Molecular Biology, University of Edinburgh, Darwin Building, Kings Buildings, Edinburgh, UK *Author for correspondence (e-mail: [email protected]) Accepted 4 July 2003 Development 130, 5481-5491 © 2003 The Company of Biologists Ltd doi:10.1242/dev.00707 Summary During mammalian ovary formation, the production of follicle formation in the mouse. In situ hybridisation ovarian follicles is accompanied by an enormous loss of showed that TrkB was expressed primarily in the germ cells germ cells. It is not known how this loss is regulated. We before and after follicle formation. Mouse neonatal and have investigated the role of the Trk tyrosine kinase fetal ovaries and human fetal ovaries were cultured in the receptors, primarily TrkB, in this process. The ovaries of presence of K252a, a potent inhibitor of all Trk receptors. TrkB–/– and TrkC–/– mice with a mixed (129Sv × C57BL/6) In mice, K252a inhibited the survival of germ cells in newly genetic background were examined shortly after birth. formed (primordial) follicles. This effect was rescued by the Around 50% of TrkB–/– mice had grossly abnormal ovaries addition of basic fibroblast growth factor (bFGF) to the that contained greatly reduced numbers of follicles.
    [Show full text]
  • Chemical Biology of Natural Indolocarbazole Products: 30 Years Since the Discovery of Staurosporine
    The Journal of Antibiotics (2009) 62, 17–26 & 2009 Japan Antibiotics Research Association All rights reserved 0021-8820/09 $32.00 www.nature.com/ja REVIEW ARTICLE Chemical biology of natural indolocarbazole products: 30 years since the discovery of staurosporine Hirofumi Nakano and Satoshi O¯ mura Staurosporine was discovered at the Kitasato Institute in 1977 while screening for microbial alkaloids using chemical detection methods. It was during the same era that protein kinase C was discovered and oncogene v-src was shown to have protein kinase activity. Staurosporine was first isolated from a culture of Actinomyces that originated in a soil sample collected in Mizusawa City, Japan. Thereafter, indolocarbazole compounds have been isolated from a variety of organisms. The biosynthesis of staurosporine and related indolocarbazoles was finally elucidated during the past decade through genetic and biochemical studies. Subsequently, several novel indolocarbazoles have been produced using combinatorial biosynthesis. In 1986, 9 years since its discovery, staurosporine and related indolocarbazoles were shown to be nanomolar inhibitors of protein kinases. They can thus be viewed as forerunners of today’s crop of novel anticancer drugs. The finding led many pharmaceutical companies to search for selective protein kinase inhibitors by screening natural products and through chemical synthesis. In the 1990s, imatinib, a Bcr-Abl tyrosine kinase inhibitor, was synthesized and, following human clinical trials for chronic myelogenous leukemia, it was approved for use in the USA in 2001. In 1992, mammalian topoisomerases were shown to be targets for indolocarbazoles. This opened up new possibilities in that indolocarbazole compounds could selectively interact with ATP- binding sites of not only protein kinases but also other proteins that had slight differences in ATP-binding sites.
    [Show full text]
  • Title Page CEP-26401 (Irdabisant), a Potent and Selective Histamine H3 Receptor Antagonist/ Inverse Agonist with Cognition-Enhan
    JPET Fast Forward. Published on October 14, 2011 as DOI: 10.1124/jpet.111.186585 JPET FastThis articleForward. has not Published been copyedited on and October formatted. 14,The final2011 version as DOI:10.1124/jpet.111.186585 may differ from this version. Title Page CEP-26401 (Irdabisant), a potent and selective histamine H3 receptor antagonist/ inverse agonist with cognition-enhancing and wake promoting activities Downloaded from Rita Raddatz, Robert L. Hudkins, Joanne R. Mathiasen*, John A. Gruner*, Dorothy G. Flood*, Lisa D. Aimone, Siyuan Le*, Hervé Schaffhauser*, Maciej Gasior*, Donna jpet.aspetjournals.org Bozyczko-Coyne, Michael J. Marino*, Mark A. Ator, Edward R. Bacon, John P. Mallamo and Michael Williams* at ASPET Journals on September 24, 2021 Discovery Research Cephalon, Inc. 145 Brandywine Parkway West Chester, PA 19380 USA Copyright 2011 by the American Society for Pharmacology and Experimental Therapeutics. JPET Fast Forward. Published on October 14, 2011 as DOI: 10.1124/jpet.111.186585 This article has not been copyedited and formatted. The final version may differ from this version. JPET #186585 2 Running Title H3 Receptor Antagonist CEP-26401 Corresponding author: Rita Raddatz Cephalon, Inc. 145 Brandywine Parkway West Chester, PA 19380 USA PHONE : (610) 738-6728 FAX: (610) 738-6305 Downloaded from [email protected] Text Pages: 48 Tables: 6 jpet.aspetjournals.org Figures: 7 References: 40 at ASPET Journals on September 24, 2021 Abstract (# of words): 240 Introduction (# of words): 490 Discussion (# of words): 1500 Abbreviations: H3R, histamine H3 receptor; CEP-26401, 6-{4-[3-((R)-2-methyl- pyrrolidin-1-yl)-propoxy]-phenyl}-2H-pyridazin-3-one HCl; ABT-239, 4-(2-{2-[(2R)-2- methyl-1-pyrrolidinyl]ethyl}-1-benzofuran-5-yl)benzonitrile (L) tartrate; RAMH, R-α- methylhistamine; GTPγS, guanosine 5`-(γ-thio)triphosphate; PPI, prepulse inhibition; [3H]NAMH, [3H]N-α-methylhistamine; RID, ratio of investigation duration; DTT, dithiothreitol; EEG, electroencephalographic; EMG, electromyographic; SWS, slow wave sleep; REMS, rapid eye movement sleep.
    [Show full text]