VAMP1 Polyclonal Antibody Catalog Number:13115-1-AP 2 Publications

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For Research Use Only VAMP1 Polyclonal antibody Catalog Number:13115-1-AP 2 Publications www.ptglab.com Catalog Number: GenBank Accession Number: Purification Method: Basic Information 13115-1-AP BC023286 Antigen affinity purification Size: GeneID (NCBI): Recommended Dilutions: 150ul , Concentration: 500 μg/ml by 6843 WB 1:500-1:2000 Nanodrop and 213 μg/ml by Bradford Full Name: IF 1:20-1:200 method using BSA as the standard; vesicle-associated membrane protein Source: 1 (synaptobrevin 1) Rabbit Calculated MW: Isotype: 117 aa, 13 kDa IgG Observed MW: Immunogen Catalog Number: 13 kDa AG3787 Applications Tested Applications: Positive Controls: IF, WB,ELISA WB : human brain tissue, Cited Applications: IF : SH-SY5Y cells, WB Species Specificity: human, mouse, rat Cited Species: mouse, rat VAMP1, also named as synaptobrevin 1, is a member of the vesicle-associated membrane protein Background Information (VAMP)/synaptobrevin family. VAMP1 is a part of the SNARE (soluble NSF-attachment protein receptor) complex. Characterized by a common sequence called the SNARE motif, SNARE proteins are involved in membrane fusion and vesicular transport (PMID: 11252968). VAMP1 is involved in synaptic vesicle exocytosis, a fundamental step in neurotransmitter release. Notable Publications Author Pubmed ID Journal Application Hailei Yu 34116208 Pharmacol Res WB Xing-Lian Duan 31962145 Neuroscience WB Storage: Storage Store at -20°C. Stable for one year after shipment. Storage Buffer: PBS with 0.02% sodium azide and 50% glycerol pH 7.3. Aliquoting is unnecessary for -20ºC storage For technical support and original validation data for this product please contact: This product is exclusively available under Proteintech T: 1 (888) 4PTGLAB (1-888-478-4522) (toll free E: [email protected] Group brand and is not available to purchase from any in USA), or 1(312) 455-8498 (outside USA) W: ptglab.com other manufacturer. Selected Validation Data human brain tissue were subjected to SDS PAGE Immunofluorescent analysis of SH-SY5Y cells using followed by western blot with 13115-1-AP (VAMP1 13115-1-AP (VAMP1 antibody) at dilution of 1:50 antibody) at dilution of 1:500 incubated at room and Alexa Fluor 488-conjugated AffiniPure Goat temperature for 1.5 hours. Anti-Rabbit IgG(H+L)..

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5850.Full.Pdf
Soluble NSF Attachment Protein Receptors (SNAREs) in RBL-2H3 Mast Cells: Functional Role of Syntaxin 4 in Exocytosis and Identification of a Vesicle-Associated This information is current as Membrane Protein 8-Containing Secretory of September 25, 2021. Compartment Fabienne Paumet, Joëlle Le Mao, Sophie Martin, Thierry Galli, Bernard David, Ulrich Blank and Michèle Roa Downloaded from J Immunol 2000; 164:5850-5857; ; doi: 10.4049/jimmunol.164.11.5850 http://www.jimmunol.org/content/164/11/5850 http://www.jimmunol.org/ References This article cites 60 articles, 36 of which you can access for free at: http://www.jimmunol.org/content/164/11/5850.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 25, 2021 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2000 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Soluble NSF Attachment Protein Receptors (SNAREs) in RBL-2H3 Mast Cells: Functional Role of Syntaxin 4 in Exocytosis and Identification of a Vesicle-Associated Membrane Protein 8-Containing Secretory Compartment1 Fabienne Paumet,* Joe¨lle Le Mao,* Sophie Martin,* Thierry Galli,† Bernard David,* Ulrich Blank,* and Miche`le Roa2* Mast cells upon stimulation through high affinity IgE receptors massively release inflammatory mediators by the fusion of spe- cialized secretory granules (related to lysosomes) with the plasma membrane.
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A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
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Autophagy Suppresses Ras-Driven Epithelial Tumourigenesis by Limiting the Accumulation of Reactive Oxygen Species
OPEN Oncogene (2017) 36, 5576–5592 www.nature.com/onc ORIGINAL ARTICLE Autophagy suppresses Ras-driven epithelial tumourigenesis by limiting the accumulation of reactive oxygen species This article has been corrected since Advance Online Publication and a corrigendum is also printed in this issue. J Manent1,2,3,4,5,12, S Banerjee2,3,4,5, R de Matos Simoes6, T Zoranovic7,13, C Mitsiades6, JM Penninger7, KJ Simpson4,5, PO Humbert3,5,8,9,10 and HE Richardson1,2,5,8,11 Activation of Ras signalling occurs in ~ 30% of human cancers; however, activated Ras alone is not sufﬁcient for tumourigenesis. In a screen for tumour suppressors that cooperate with oncogenic Ras (RasV12)inDrosophila, we identiﬁed genes involved in the autophagy pathway. Bioinformatic analysis of human tumours revealed that several core autophagy genes, including GABARAP, correlate with oncogenic KRAS mutations and poor prognosis in human pancreatic cancer, supporting a potential tumour- suppressive effect of the pathway in Ras-driven human cancers. In Drosophila, we demonstrate that blocking autophagy at any step of the pathway enhances RasV12-driven epithelial tissue overgrowth via the accumulation of reactive oxygen species and activation of the Jun kinase stress response pathway. Blocking autophagy in RasV12 clones also results in non-cell-autonomous effects with autophagy, cell proliferation and caspase activation induced in adjacent wild-type cells. Our study has implications for understanding the interplay between perturbations in Ras signalling and autophagy in tumourigenesis,
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Selective Expression of a SNARE-Cleaving Protease in Peripheral Sensory Neurons Attenuates Pain-Related Gene Transcription and Neuropeptide Release
International Journal of Molecular Sciences Article Selective Expression of a SNARE-Cleaving Protease in Peripheral Sensory Neurons Attenuates Pain-Related Gene Transcription and Neuropeptide Release Wanzhi Wang 1, Miaomiao Kong 1, Yu Dou 1, Shanghai Xue 1, Yang Liu 1, Yinghao Zhang 1, Weiwei Chen 1, Yanqing Li 1, Xiaolong Dai 1, Jianghui Meng 1,2,* and Jiafu Wang 1,2,* 1 School of Life Sciences, Henan University, Kaifeng 475001, China; [email protected] (W.W.); [email protected] (M.K.); [email protected] (Y.D.); [email protected] (S.X.); [email protected] (Y.L.); [email protected] (Y.Z.); [email protected] (W.C.); [email protected] (Y.L.); [email protected] (X.D.) 2 School of Biotechnology, Faculty of Science and Health, Dublin City University, Glasnevin, Dublin 9, Ireland * Correspondence: [email protected] (J.M.); [email protected] (J.W.) Abstract: Chronic pain is a leading health and socioeconomic problem and an unmet need exists for long-lasting analgesics. SNAREs (soluble N-ethylmaleimide-sensitive factor attachment protein receptors) are required for neuropeptide release and noxious signal transducer surface trafﬁcking, thus, selective expression of the SNARE-cleaving light-chain protease of botulinum neurotoxin A (LCA) in peripheral sensory neurons could alleviate chronic pain. However, a safety concern to Citation: Wang, W.; Kong, M.; this approach is the lack of a sensory neuronal promoter to prevent the expression of LCA in the Dou, Y.; Xue, S.; Liu, Y.; Zhang, Y.; central nervous system. Towards this, we exploit the unique characteristics of Pirt (phosphoinositide- Chen, W.; Li, Y.; Dai, X.; Meng, J.; et al.
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Widespread Sequence Variations in VAMP1 Across Vertebrates Suggest a Potential Selective Pressure from Botulinum Neurotoxins
Widespread Sequence Variations in VAMP1 across Vertebrates Suggest a Potential Selective Pressure from Botulinum Neurotoxins The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Peng, L., M. Adler, A. Demogines, A. Borrell, H. Liu, L. Tao, W. H. Tepp, et al. 2014. “Widespread Sequence Variations in VAMP1 across Vertebrates Suggest a Potential Selective Pressure from Botulinum Neurotoxins.” PLoS Pathogens 10 (7): e1004177. doi:10.1371/journal.ppat.1004177. http://dx.doi.org/10.1371/ journal.ppat.1004177. Published Version doi:10.1371/journal.ppat.1004177 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:12717507 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Widespread Sequence Variations in VAMP1 across Vertebrates Suggest a Potential Selective Pressure from Botulinum Neurotoxins Lisheng Peng1, Michael Adler2*, Ann Demogines3, Andrew Borrell2, Huisheng Liu4, Liang Tao1, William H. Tepp5, Su-Chun Zhang4, Eric A. Johnson5, Sara L. Sawyer3*, Min Dong1* 1 Department of Microbiology and Immunobiology, Harvard Medical School and Division of Neuroscience, New England Primate Research Center, Southborough, Massachusetts, United States of America, 2 Neurobehavioral Toxicology Branch, U.S. Army Medical Research Institute of Chemical Defense, Aberdeen
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CENTOGENE's Severe and Early Onset Disorder Gene List
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11056.Full.Pdf
11056 • The Journal of Neuroscience, October 10, 2007 • 27(41):11056–11064 Neurobiology of Disease Huntingtin-Interacting Protein 1 Influences Worm and Mouse Presynaptic Function and Protects Caenorhabditis elegans Neurons against Mutant Polyglutamine Toxicity J. Alex Parker,1,2 Martina Metzler,3 John Georgiou,4 Marilyne Mage,1,2 John C. Roder,4,5 Ann M. Rose,6 Michael R. Hayden,3 and Christian Ne´ri1,2 1Inserm, Unit 857 “Neuronal Cell Biology and Pathology,” and 2University of Paris Rene´ Descartes, Equipe d’Accueil 4059, Centre Paul Broca, 75014 Paris, France, 3Centre for Molecular Medicine and Therapeutics, Child and Family Research Institute, Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4, 4Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada M5G 1X5, 5Department of Physiology, University of Toronto, Toronto, Ontario, Canada M5S 1A8, and 6Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3 Huntingtin-interacting protein 1 (HIP1) was identified through its interaction with htt (huntingtin), the Huntington’s disease (HD) protein. HIP1 is an endocytic protein that influences transport and function of AMPA and NMDA receptors in the brain. However, little is known about its contribution to neuronal dysfunction in HD. We report that the Caenorhabditis elegans HIP1 homolog hipr-1 modulates presynaptic activity and the abundance of synaptobrevin, a protein involved in synaptic vesicle fusion. Presynaptic function was also altered in hippocampal brain slices of HIP1 Ϫ/Ϫ mice dem- onstrating delayed recovery from synaptic depression and a reduction in paired-pulse facilitation, a form of presynaptic plasticity.
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Starting a Molecular Systems View of Endocytosis
ANRV356-CB24-20 ARI 3 September 2008 19:11 ANNUAL Protein Kinases: Starting REVIEWS Further Click here for quick links to Annual Reviews content online, a Molecular Systems View including: • Other articles in this volume of Endocytosis • Top cited articles • Top downloaded articles • Our comprehensive search Prisca Liberali, Pauli Ram¨ o,¨ and Lucas Pelkmans Institute of Molecular Systems Biology, ETH Zurich, CH-8093 Zurich, Switzerland; email: [email protected] Annu. Rev. Cell Dev. Biol. 2008. 24:501–23 Key Words First published online as a Review in Advance on membrane trafﬁcking, phosphorylation, signal transduction, July 3, 2008 complexity, nonlinear systems, genetical physics The Annual Review of Cell and Developmental Biology is online at cellbio.annualreviews.org Abstract This article’s doi: The ﬁeld of endocytosis is in strong need of formal biophysical model- 10.1146/annurev.cellbio.041008.145637 ing and mathematical analysis. At the same time, endocytosis must be Copyright c 2008 by Annual Reviews. much better integrated into cellular physiology to understand the for- by Universitat Zurich- Hauptbibliothek Irchel on 04/05/13. For personal use only. All rights reserved mer’s complex behavior in such a wide range of phenotypic variations. Annu. Rev. Cell Dev. Biol. 2008.24:501-523. Downloaded from www.annualreviews.org 1081-0706/08/1110-0501$20.00 Furthermore, the concept that endocytosis provides the space-time for signal transduction can now be experimentally addressed. In this review, we discuss these principles and argue for a systematic and top-down ap- proach to study the endocytic membrane system. We provide a summary of published observations on protein kinases regulating endocytic ma- chinery components and discuss global unbiased approaches to further map out kinase regulatory networks.
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The Molecular Basis of Transcriptional Activation by the CDP/Cux Transcription Factor
The Molecular Basis of Transcriptional Activation by the CDP/Cux Transcription Factor Mary Truscott A thesis submitted to the Faculty of Graduate and Post-doctoral Studies in partial fulfillment of the requirements for the degree of Doctor of Philosophy Department of B iochemistry McGill University Montreal, Quebec, Canada August 2006 © Mary Truscott, 2006 Library and Bibliothèque et 1+1 Archives Canada Archives Canada Published Heritage Direction du Branch Patrimoine de l'édition 395 Wellington Street 395, rue Wellington Ottawa ON K1A ON4 Ottawa ON K1A ON4 Canada Canada Your file Votre référence ISBN: 978-0-494-32391-5 Our file Notre référence ISBN: 978-0-494-32391-5 NOTICE: AVIS: The author has granted a non L'auteur a accordé une licence non exclusive exclusive license allowing Library permettant à la Bibliothèque et Archives and Archives Canada to reproduce, Canada de reproduire, publier, archiver, publish, archive, preserve, conserve, sauvegarder, conserver, transmettre au public communicate to the public by par télécommunication ou par l'Internet, prêter, telecommunication or on the Internet, distribuer et vendre des thèses partout dans loan, distribute and sell th es es le monde, à des fins commerciales ou autres, worldwide, for commercial or non sur support microforme, papier, électronique commercial purposes, in microform, et/ou autres formats. paper, electronic and/or any other formats. The author retains copyright L'auteur conserve la propriété du droit d'auteur ownership and moral rights in et des droits moraux qui protège cette thèse. this thesis. Neither the thesis Ni la thèse ni des extraits substantiels de nor substantial extracts from it celle-ci ne doivent être imprimés ou autrement may be printed or otherwise reproduits sans son autorisation.
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Gene Expression Analysis in the Parvalbuminimmunoreactive PV1 Nucleus of the Mouse Lateral Hypothalamus
Published in (XURSHDQ-RXUQDORI1HXURVFLHQFH ± which should be cited to refer to this work. Gene expression analysis in the parvalbumin- immunoreactive PV1 nucleus of the mouse lateral hypothalamus F. Girard,1 Z. Meszar,1 C. Marti,1 F. P. Davis2 and M. Celio1 1Division of Anatomy and Program in Neuroscience, Universite´ de Fribourg, Route A. Gockel 1, CH1700 Fribourg, Switzerland 2Janelia Farm Research Campus, Howard Hughes Medical Institute, Ashburn, VA, USA Keywords: brain, calcium-binding protein, glutamate, lateral tuberal nucleus Abstract A solitary, elongated cluster of parvalbumin-immunoreactive neurons has been previously observed in the rodent ventrolateral hypothalamus. However, the function of this so-called PV1 nucleus is unknown. In this article, we report the results of an unbiased, broad and in-depth molecular characterization of this small, compact group of neurons. The Allen Brain Atlas database of in situ hybridization was screened in order to identify genes expressed in the PV1-nucleus-containing area of the hypothalamus, and those that might be co-expressed with parvalbumin. Although GABA is the principal neurotransmitter in parvalbumin-expressing cells in various other brain areas, we found that PV1 neurons express the vesicular glutamate transporter (VGlut) VGlut2-encoding gene Slc17a6 and are negative for the glutamic acid decarboxylase 1 (GAD1) gene. These cells also express the mRNA for the neuropeptides Adcyap1 and possibly Nxph4, express several types of potassium and sodium channels, are under the control of the neurotransmitter acetylcholine, bear receptors for the glial-derived neurotrophic factor, and produce an extracellular matrix rich in osteopontin. The PV1 nucleus is thus composed of glutamatergic nerve cells, expressing some typical markers of long-axon, projecting neurons (e.g.
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Membrane Trafficking in Health and Disease Rebecca Yarwood*, John Hellicar*, Philip G
© 2020. Published by The Company of Biologists Ltd | Disease Models & Mechanisms (2020) 13, dmm043448. doi:10.1242/dmm.043448 AT A GLANCE Membrane trafficking in health and disease Rebecca Yarwood*, John Hellicar*, Philip G. Woodman‡ and Martin Lowe‡ ABSTRACT KEY WORDS: Disease, Endocytic pathway, Genetic disorder, Membrane traffic, Secretory pathway, Vesicle Membrane trafficking pathways are essential for the viability and growth of cells, and play a major role in the interaction of cells with Introduction their environment. In this At a Glance article and accompanying Membrane trafficking pathways are essential for cells to maintain poster, we outline the major cellular trafficking pathways and discuss critical functions, to grow, and to accommodate to their chemical how defects in the function of the molecular machinery that mediates and physical environment. Membrane flux through these pathways this transport lead to various diseases in humans. We also briefly is high, and in specialised cells in some tissues can be enormous. discuss possible therapeutic approaches that may be used in the For example, pancreatic acinar cells synthesise and secrete amylase, future treatment of trafficking-based disorders. one of the many enzymes they produce, at a rate of approximately 0.5% of cellular protein mass per hour (Allfrey et al., 1953), while in Schwann cells, the rate of membrane protein export must correlate School of Biological Sciences, Faculty of Biology, Medicine and Health, with the several thousand-fold expansion of the cell surface that University of Manchester, Manchester, M13 9PT, UK. occurs during myelination (Pereira et al., 2012). The population of *These authors contributed equally to this work cell surface proteins is constantly monitored and modified via the ‡Authors for correspondence ([email protected]; endocytic pathway.
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Downregulation of Carnitine Acyl-Carnitine Translocase by Mirnas
Page 1 of 288 Diabetes 1 Downregulation of Carnitine acyl-carnitine translocase by miRNAs 132 and 212 amplifies glucose-stimulated insulin secretion Mufaddal S. Soni1, Mary E. Rabaglia1, Sushant Bhatnagar1, Jin Shang2, Olga Ilkayeva3, Randall Mynatt4, Yun-Ping Zhou2, Eric E. Schadt6, Nancy A.Thornberry2, Deborah M. Muoio5, Mark P. Keller1 and Alan D. Attie1 From the 1Department of Biochemistry, University of Wisconsin, Madison, Wisconsin; 2Department of Metabolic Disorders-Diabetes, Merck Research Laboratories, Rahway, New Jersey; 3Sarah W. Stedman Nutrition and Metabolism Center, Duke Institute of Molecular Physiology, 5Departments of Medicine and Pharmacology and Cancer Biology, Durham, North Carolina. 4Pennington Biomedical Research Center, Louisiana State University system, Baton Rouge, Louisiana; 6Institute for Genomics and Multiscale Biology, Mount Sinai School of Medicine, New York, New York. Corresponding author Alan D. Attie, 543A Biochemistry Addition, 433 Babcock Drive, Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin, (608) 262-1372 (Ph), (608) 263-9608 (fax), [email protected]. Running Title: Fatty acyl-carnitines enhance insulin secretion Abstract word count: 163 Main text Word count: 3960 Number of tables: 0 Number of figures: 5 Diabetes Publish Ahead of Print, published online June 26, 2014 Diabetes Page 2 of 288 2 ABSTRACT We previously demonstrated that micro-RNAs 132 and 212 are differentially upregulated in response to obesity in two mouse strains that differ in their susceptibility to obesity-induced diabetes. Here we show the overexpression of micro-RNAs 132 and 212 enhances insulin secretion (IS) in response to glucose and other secretagogues including non-fuel stimuli. We determined that carnitine acyl-carnitine translocase (CACT, Slc25a20) is a direct target of these miRNAs.
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