ANTICORPI BT-Policlonali

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ANTICORPI BT-policlonali Cat# Item Applications Reactivity Source BT-AP00001 11β-HSD1 Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat Rabbit BT-AP00002 11β-HSD1 Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat Rabbit BT-AP00003 14-3-3 β Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00004 14-3-3 β/ζ Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat Rabbit BT-AP00005 14-3-3 γ Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00006 14-3-3 ε Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00007 14-3-3 ε Polyclonal Antibody WB,IHC-p Mouse,Rat Rabbit BT-AP00008 14-3-3 ζ Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat Rabbit WB,IHC- BT-AP00009 14-3-3 ζ Polyclonal Antibody p,IP,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00010 14-3-3 ζ/δ Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00011 14-3-3 η Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00012 14-3-3 θ Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00013 14-3-3 θ/τ Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00014 14-3-3 σ Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse Rabbit BT-AP00015 14-3-3-pan (Acetyl Lys51/49) Polyclonal Antibody WB,ELISA Human,Mouse,Rat Rabbit BT-AP00016 17β-HSD11 Polyclonal Antibody WB,ELISA Human Rabbit BT-AP00017 17β-HSD4 Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat Rabbit BT-AP00018 2A5B Polyclonal Antibody WB,ELISA Human Rabbit BT-AP00019 2A5E Polyclonal Antibody WB,ELISA Human,Mouse Rabbit BT-AP00020 2A5G Polyclonal Antibody WB,ELISA Human,Mouse Rabbit BT-AP00021 2AAA Polyclonal Antibody WB,ELISA Human,Mouse Rabbit BT-AP00022 2ABG Polyclonal Antibody WB,ELISA Human,Rat,Mouse Rabbit BT-AP00023 2B1F Polyclonal Antibody WB,ELISA Human Rabbit BT-AP00024 3BHS1 Polyclonal Antibody WB,ELISA Human Rabbit BT-AP00025 3BHS2 Polyclonal Antibody WB,ELISA Human Rabbit BT-AP00026 3BP1 Polyclonal Antibody WB,ELISA Human,Mouse Rabbit BT-AP00027 3BP2 Polyclonal Antibody WB,ELISA Human Rabbit BT-AP00028 3HAO Polyclonal Antibody WB,ELISA Human,Mouse,Rat Rabbit BT-AP00029 3MG Polyclonal Antibody WB,ELISA Human Rabbit BT-AP00030 3pK Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00031 3β-HSD7 Polyclonal Antibody WB,ELISA Human,Mouse,Rat Rabbit BT-AP00032 4.1G Polyclonal Antibody WB,IHC-p,ELISA Human Rabbit BT-AP00033 4.

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Cerebral Histamine H1 Receptor Binding Potential Measured With
Cerebral Histamine H1 Receptor Binding Potential Measured with PET Under a Test Dose of Olopatadine, an Antihistamine, Is Reduced After Repeated Administration of Olopatadine Michio Senda1, Nobuo Kubo2, Kazuhiko Adachi3, Yasuhiko Ikari1,4, Keiichi Matsumoto1, Keiji Shimizu1, and Hideyuki Tominaga1 1Division of Molecular Imaging, Institute of Biomedical Research and Innovation, Kobe, Japan; 2Department of Otorhinolaryngology, Kansai Medical University, Osaka, Japan; 3Department of Mechanical Engineering, Kobe University, Kobe, Japan; and 4Micron, Inc., Kobe, Japan Some antihistamine drugs that are used for rhinitis and pollinosis have a sedative effect as they enter the brain and block the H1 Antihistamines are widely used as a medication for receptor, potentially causing serious accidents. Receptor occu- common allergic disorders such as seasonal pollinosis, pancy has been measured with PET under single-dose adminis- tration in humans to classify antihistamines as more sedating or chronic rhinitis, and urticaria. Some antihistamine drugs as less sedating (or nonsedating). In this study, the effect of re- have a sedative side effect as they enter the brain and block peated administration of olopatadine, an antihistamine, on the histamine H1 receptor, potentially causing trafﬁc accidents cerebral H1 receptor was measured with PET. Methods: A total and other serious events, but the sedative effect is difﬁcult to of 17 young men with rhinitis underwent dynamic brain PET with evaluate because of a large variation in neuropsychological 11 C-doxepin at baseline, under an initial single dose of 5 mg of measures and subjective symptoms. Measurement of cere- olopatadine (acute scan), and under another 5-mg dose after re- 11 peated administration of olopatadine at 10 mg/d for 4 wk (chronic bral histamine H1 receptor occupancy using PET with C- doxepin under a single administration of antihistamines has scan).
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Peripheral Regulation of Pain and Itch
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine 1596 Peripheral Regulation of Pain and Itch ELÍN INGIBJÖRG MAGNÚSDÓTTIR ACTA UNIVERSITATIS UPSALIENSIS ISSN 1651-6206 ISBN 978-91-513-0746-6 UPPSALA urn:nbn:se:uu:diva-392709 2019 Dissertation presented at Uppsala University to be publicly examined in A1:107a, BMC, Husargatan 3, Uppsala, Friday, 25 October 2019 at 13:00 for the degree of Doctor of Philosophy (Faculty of Medicine). The examination will be conducted in English. Faculty examiner: Professor emeritus George H. Caughey (University of California, San Francisco). Abstract Magnúsdóttir, E. I. 2019. Peripheral Regulation of Pain and Itch. Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine 1596. 71 pp. Uppsala: Acta Universitatis Upsaliensis. ISBN 978-91-513-0746-6. Pain and itch are diverse sensory modalities, transmitted by the somatosensory nervous system. Stimuli such as heat, cold, mechanical pain and itch can be transmitted by different neuronal populations, which show considerable overlap with regards to sensory activation. Moreover, the immune and nervous systems can be involved in extensive crosstalk in the periphery when reacting to these stimuli. With recent advances in genetic engineering, we now have the possibility to study the contribution of distinct neuron types, neurotransmitters and other mediators in vivo by using gene knock-out mice. The neuropeptide calcitonin gene-related peptide (CGRP) and the ion channel transient receptor potential cation channel subfamily V member 1 (TRPV1) have both been implicated in pain and itch transmission. In Paper I, the Cre- LoxP system was used to specifically remove CGRPα from the primary afferent population that expresses TRPV1.
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Martin Steinhoff Dirk Roosterman, Tobias Goerge, Stefan W
Dirk Roosterman, Tobias Goerge, Stefan W. Schneider, Nigel W. Bunnett and Martin Steinhoff Physiol Rev 86:1309-1379, 2006. doi:10.1152/physrev.00026.2005 You might find this additional information useful... This article cites 963 articles, 265 of which you can access free at: http://physrev.physiology.org/cgi/content/full/86/4/1309#BIBL Medline items on this article's topics can be found at http://highwire.stanford.edu/lists/artbytopic.dtl on the following topics: Biochemistry .. Transient Receptor Potential Channel Biochemistry .. Endopeptidases Biochemistry .. Proteolytic Enzymes Oncology .. Inflammation Medicine .. Neurogenic Inflammation Physiology .. Nerves Updated information and services including high-resolution figures, can be found at: http://physrev.physiology.org/cgi/content/full/86/4/1309 Downloaded from Additional material and information about Physiological Reviews can be found at: http://www.the-aps.org/publications/prv This information is current as of February 8, 2008 . physrev.physiology.org on February 8, 2008 Physiological Reviews provides state of the art coverage of timely issues in the physiological and biomedical sciences. It is published quarterly in January, April, July, and October by the American Physiological Society, 9650 Rockville Pike, Bethesda MD 20814-3991. Copyright © 2005 by the American Physiological Society. ISSN: 0031-9333, ESSN: 1522-1210. Visit our website at http://www.the-aps.org/. Physiol Rev 86: 1309–1379, 2006; doi:10.1152/physrev.00026.2005. Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ DIRK ROOSTERMAN, TOBIAS GOERGE, STEFAN W. SCHNEIDER, NIGEL W. BUNNETT, AND MARTIN STEINHOFF Department of Dermatology, IZKF Mu¨nster, and Boltzmann Institute for Cell and Immunobiology of the Skin, University of Mu¨nster, Mu¨nster, Germany; and Departments of Surgery and Physiology, University of California, San Francisco, California I.
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Peng et al. Clin Transl Allergy (2019) 9:49 https://doi.org/10.1186/s13601-019-0288-1 Clinical and Translational Allergy LETTER TO THE EDITOR Open Access Histamine H4 receptor regulates IL-6 and INF-γ secretion in native monocytes from healthy subjects and patients with allergic rhinitis Hua Peng1†, Jian Wang1†, Xiao Yan Ye2,3, Jie Cheng1, Cheng Zhi Huang1, Li Yue Li2,3, Tian Ying Li2,3 and Chun Wei Li2,3* Abstract Histamine H1 receptor (H1R) and histamine H4 receptor (H4R) are essential in allergic infammation. The roles of H4R have been characterized in T cell subsets, whereas the functional properties of H4R in monocytes remain unclear. In the current study, the responses of H4R in peripheral monocytes from patients with allergic rhinitis (AR) were investigated. The results confrmed that H4R has the functional efects of mediating cytokine production (i.e., down- regulating IFN-γ and up-regulating IL-6) in cells from a monocyte cell line following challenge with histamine. We demonstrated that when monocytes from AR patients were stimulated with allergen extracts of house dust mite (HDM), IFN-γ secretion was dependent on H4R activity, but IL-6 secretion was based on H1R activity. Furthermore, a combination of H1R and H4R antagonists was more efective at blocking the infammatory response in monocytes than treatment with either type of antagonist alone. Keywords: Histamine H4 receptor, Histamine H1 receptor, Allergic rhinitis, Native human monocyte, Th1 and Th2 cytokines To the editor of H4R in monocyte-derived macrophages and dendritic Allergic rhinitis (AR) has long been considered to be cells in atopic dermatitis [6, 7]; in addition, two stud- mainly mediated by activation of histamine H1 receptor ies have indicated the functional roles of H4R in native (H1R) [1], although the use of histamine H1R antago- monocytes from healthy subjects by inhibiting CCL2 nists to treat this disease has produced unsatisfactory production or IL-12p70 secretion [8, 9].
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Sharada Laidlay
Bioassay-guided isolation and biochemical characterisation of vasorelaxant compounds extracted from a Dalbergia species Sharada Laidlay A thesis submitted in partial fulfilment of the requirements of the University of Brighton for the degree of Doctor of Philosophy 2016 Thesis Abstract Natural products have been the source of many of our successful drugs providing us with an unrivalled chemical diversity combined with drug-like properties. The search for bioactive compounds can be helped considerably by the phytotherapeutic knowledge held by indigenous communities. In this study solvent extracts from the bark of a Dalbergia species and used by a community in Borneo, will be investigated to isolate, identify and biochemically characterise compounds showing vasorelaxation. At the core of this study is the hypertensive model, which uses phenylephrine precontracted rat aortic rings as a bioassay to identify solvent extracts, fractions and sub-fractions that cause relaxation. These fractions are generated using chromatographic techniques and solvent systems developed specifically for this purpose. Structural elucidation of the isolated compounds was undertaken by studying extensive data from UV, MS, 1D and 2D 1H and 13C NMR spectra. This study also undertook the pharmacological characterisation of the isolated compounds using the same bioassay together with enzyme and receptor inhibitors to identify the signalling pathways involved. In this study the plant was identified as a Dalbergia species using DNA profiling techniques and in particular sequences from the matK and rpoC1 barcoding genes to construct a phylogenetic tree. Solvent extracts of the bark showed the presence of compounds that caused both vascular relaxation and contraction. From the hexane extract which showed only relaxation two related bioactive compounds were isolated and identified as 5,7-dihydroxy, 6, β’,4’,5’-tetramethoxy isoflavone or Caviunin (S/F4) and its isomer 5,7-dihydroxy, 8, β’,4’,5’- tetramethoxy isoflavone or Isocaviunin (S/F3) not previously investigated for there vascular activity.
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Supplemental Material
Supplemental material Systems Pharmacology Approach to Prevent Retinal Degeneration in Stargardt Disease Yu Chen, Grazyna Palczewska, Debarshi Mustafi, Marcin Golczak, Zhiqian Dong, Osamu Sawada, Tadao Maeda, Akiko Maeda, and Krzysztof Palczewski Table of Contents: 1. Supplemental Table 1. 2. Supplemental Table 2. 3. Supplemental Table 3. 4. References. 1 Supplemental Table 1. Expression of GPCRs in the eye and retina of C57BL/6J mice and the retina of a human donor eye (normalized FPKM values)A. Genes B6 mouse B6 mouse Human retina eye retina Rho 6162.04 11630.18 6896.09 Rgr 355.74 97.66 123.98 Opn1sw 125.13 198.54 31.69 Drd4 93.84 241.78 139.49 Opn1mw 62.97 95.77 172.56 Gprc5b 29.82 12.95 22.85 Gpr162 29.37 73.32 46.29 Gpr37 28.47 41.28 66.65 Ednrb 22.27 1.94 5.77 Rorb 21.69 23.52 24.31 Gpr153 20.42 37.18 15.31 Gabbr1 19.78 40.24 35.38 Rrh 19.29 9.23 40.34 2 Gpr152 18.55 40.46 3.05 Adora1 16.20 18.26 13.55 Lphn1 15.98 29.73 31.85 Tm2d1 15.56 10.31 17.63 Cxcr7 14.30 3.58 2.37 Ppard 13.68 19.37 21.61 Agtrap 13.64 17.21 8.18 Cd97 12.93 1.77 1.55 Gpr19 12.21 8.45 1.11 Fzd1 11.99 3.29 7.35 Fzd6 11.34 1.85 2.76 Gpr87 11.34 0.04 0.00 Lgr4 11.09 9.50 18.07 Drd2 10.82 23.10 26.33 Smo 10.75 6.35 5.91 S1pr1 10.66 11.21 11.78 Bai1 10.08 27.10 10.82 3 Glp2r 9.94 34.85 0.31 Ptger1 9.59 14.88 0.94 Gpr124 9.56 8.94 19.82 F2r 9.31 5.32 0.15 Adra2c 8.96 7.17 2.38 Gpr146 8.91 7.49 6.17 Vipr2 8.79 14.33 10.69 Fzd5 8.69 10.01 7.73 Gpr110 8.59 0.08 0.02 Adrb1 8.43 20.18 3.84 S1pr3 8.42 6.95 3.56 Gabbr2 7.80 17.03 10.57 Lphn2 7.66 9.02 8.79 Lpar1 7.47 0.91
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G Protein-Coupled Receptors in the Hypothalamic Paraventricular and Supraoptic Nuclei – Serpentine Gateways to Neuroendocrine Homeostasis
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Frontiers in Neuroendocrinology 33 (2012) 45–66 Contents lists available at ScienceDirect Frontiers in Neuroendocrinology journal homepage: www.elsevier.com/locate/yfrne Review G protein-coupled receptors in the hypothalamic paraventricular and supraoptic nuclei – serpentine gateways to neuroendocrine homeostasis Georgina G.J. Hazell, Charles C. Hindmarch, George R. Pope, James A. Roper, Stafford L. Lightman, ⇑ David Murphy, Anne-Marie O’Carroll, Stephen J. Lolait Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Dorothy Hodgkin Building, School of Clinical Sciences, University of Bristol, Whitson Street, Bristol BS1 3NY, UK article info abstract Article history: G protein-coupled receptors (GPCRs) are the largest family of transmembrane receptors in the mamma- Available online 23 July 2011 lian genome. They are activated by a multitude of different ligands that elicit rapid intracellular responses to regulate cell function. Unsurprisingly, a large proportion of therapeutic agents target these receptors. Keywords: The paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus are important G protein-coupled receptor mediators in homeostatic control. Many modulators of PVN/SON activity, including neurotransmitters Paraventricular nucleus and hormones act via GPCRs – in fact over 100 non-chemosensory GPCRs have been detected in either Supraoptic nucleus the PVN or SON. This review provides a comprehensive summary of the expression of GPCRs within Vasopressin the PVN/SON, including data from recent transcriptomic studies that potentially expand the repertoire Oxytocin Corticotropin-releasing factor of GPCRs that may have functional roles in these hypothalamic nuclei.
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MRGPRX4 Is a Novel Bile Acid Receptor in Cholestatic Itch Huasheng Yu1,2,3, Tianjun Zhao1,2,3, Simin Liu1, Qinxue Wu4, Omar
bioRxiv preprint doi: https://doi.org/10.1101/633446; this version posted May 9, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 MRGPRX4 is a novel bile acid receptor in cholestatic itch 2 Huasheng Yu1,2,3, Tianjun Zhao1,2,3, Simin Liu1, Qinxue Wu4, Omar Johnson4, Zhaofa 3 Wu1,2, Zihao Zhuang1, Yaocheng Shi5, Renxi He1,2, Yong Yang6, Jianjun Sun7, 4 Xiaoqun Wang8, Haifeng Xu9, Zheng Zeng10, Xiaoguang Lei3,5, Wenqin Luo4*, Yulong 5 Li1,2,3* 6 7 1State Key Laboratory of Membrane Biology, Peking University School of Life 8 Sciences, Beijing 100871, China 9 2PKU-IDG/McGovern Institute for Brain Research, Beijing 100871, China 10 3Peking-Tsinghua Center for Life Sciences, Beijing 100871, China 11 4Department of Neuroscience, Perelman School of Medicine, University of 12 Pennsylvania, Philadelphia, PA 19104, USA 13 5Department of Chemical Biology, College of Chemistry and Molecular Engineering, 14 Peking University, Beijing 100871, China 15 6Department of Dermatology, Peking University First Hospital, Beijing Key Laboratory 16 of Molecular Diagnosis on Dermatoses, Beijing 100034, China 17 7Department of Neurosurgery, Peking University Third Hospital, Peking University, 18 Beijing, 100191, China 19 8State Key Laboratory of Brain and Cognitive Science, CAS Center for Excellence in 20 Brain Science and Intelligence Technology (Shanghai), Institute of Biophysics, 21 Chinese Academy of Sciences, Beijing, 100101, China 22 9Department of Liver Surgery, Peking Union Medical College Hospital, Chinese bioRxiv preprint doi: https://doi.org/10.1101/633446; this version posted May 9, 2019.
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Page 1 of 89 Diabetes Insulin and glucose alter death-associated protein kinase 3 (DAPK3) DNA methylation in human skeletal muscle Jonathan M. Mudry1, David G. Lassiter1, Carolina Nylén1, Sonia García-Calzón2, Erik Näslund3, Anna Krook2, Juleen R. Zierath1,2,4. Running title: DAPK3 DNA methylation in human skeletal muscle 1Department of Molecular Medicine and Surgery, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden. 2Department of Physiology and Pharmacology, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden. 3Division of Surgery, Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden. 4Section of Integrative Physiology, The Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Science, University of Copenhagen, Copenhagen, Denmark. Juleen R. Zierath Department of Molecular Medicine and Surgery, Section of Integrative Physiology, Karolinska Institutet, von Eulers väg 4a, SE 171 77 Stockholm, Sweden Phone: +46 (0)8 524 87581 Fax: +46 (0) 8 33 54 36 E-mail: [email protected] Diabetes Publish Ahead of Print, published online December 23, 2016 Diabetes Page 2 of 89 Abstract DNA methylation is altered by environmental factors. We hypothesized DNA methylation is altered in skeletal muscle in response to either insulin or glucose exposure. We performed a genome-wide DNA methylation analysis in muscle from healthy men before and after insulin exposure. DNA methylation of selected genes was determined in muscle from healthy and type 2 diabetic men before and after a glucose tolerance test. Insulin altered DNA methylation in the 3’UTR of the calcium pump ATP2A3 gene. Insulin increased DNA methylation in the gene body of DAPK3, a gene involved in cell proliferation, apoptosis and autophagy.
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