Anti-Gfrα-3 Antibody

Total Page：16

File Type：pdf, Size：1020Kb

product data sheet Anti-GFRα-3 Antibody ORDERING INFORMATION SPECIFICATION SUMMARY Catalog No.: 1137 Antigen: Peptide corresponding to aa 347- Size: 100 ug IgG in PBS, pH 7.4, purified 360 of mouse GFRα-3. by immunoaffinity chroma-tography. Host Species: Rabbit Stabilizers: None BACKGROUND Preservatives: 0.02% sodium azide. Members of the glial cell line-derived neurotrophic factor (GDNF) family, including SPECIFICITY GDNF and neurturin (NTN), play key roles This antibody recognizes human, mouse, in the control of vertebrate neuronal α survivial and differentiation. A new member and rat GFR -3 (approx. 43 kD). of the GDNF family was recently identified and designated persephin. Physiological APPLICATIONS responses to these neurotrophic factors Immunoblotting: use at 1:500-1:1,000 requrie two receptor subunits, the novel dilution. glycosylphosphatidylinositol linked protein Positive control: Tissue lysates of mouse GFRα and Ret receptor tyrosine kinase kidney, liver, or heart. GFRβ. Following the identification of GFRα-1 and –2, another receptor in the DILUTION INSTRUCTIONS GFR family was identified in human and Dilute in PBS or medium which is identical mouse and designated GFRα-3. GFRα-3 to that used in the assay system. binds persephin. Thus, persephin, GFRα-3, and Ret PTK form a complex to transmit the STORAGE AND STABILITY persephin signal and to mediate persephin This antibody is stable for at least one (1) o function. year at -20 C. Avoid multiple freeze-thaw cycles. For in vitro investigational use only. Not for use in therapeutic or diagnostic procedures. QED Bioscience, Inc. Toll Free 800.929.2114 Visit our website for additional product 10919 Technology Place, Suite C Phone 858.675.2405 information and to order online. San Diego, CA 92127 Fax 858.592.1509 [email protected] qedbio.com.

Copy Link

Recommended publications

Artemin, Human Recombinant Human Artemin
Artemin, human Recombinant Human Artemin Instruction Manual Catalog Number C-60031 Synonyms ART, ARTN , EVN, NBN Description Artemin is a disulfide-linked homodimeric neurotrophic factor structurally related to GDNF, Artemin, Neurturin and Persephin. These proteins belong to the cysteine-knot superfamily of growth factors that assume stable dimeric protein structures. Artemin, GDNF, Persephin and Neurturin all signal though a multicomponent receptor system, composed of RET (receptor tyrosine kinase) and one of the four GFR-alpha (alpha1-alpha4) receptors. Artemin prefers the receptor GFRalpha3-RET, but will use other receptors as an alternative. Artemin supports the survival of all peripheral ganglia such as sympathetic, neural crest and placodally derived sensory neurons, and dompaminergic midbrains neurons. The functional human Artemin ligand is a disulfide-linked homodimer, of two 12.0 kDa polypeptide monomers. Each monomer contains seven conserved cysteine residues, one of which is used for inter-chain disulfide bridging and the others are involved in intramolecular ring formation known as the cysteine knot configuration. Recombinant human Artemin is a 24.2 kDa, disulfide-linked non-glycosylated homodimer formed by two identical 113 amino acid subunits. Recombinant Artemin has been purified using proprietary chromatographic techniques. Quantity 20 µg Molecular Mass 24.2 kDa Source E. coli Biological-Activity Artemin is fully biologically active when compared to a standard. Assay #1: Determined by its ability to stimulate the proliferation of human SH-SY5Y cells. The expected EDЊЅ for this effect is 2.0-5.0 ng/ml. Assay #2: Determined by its ability to promote neuronal survival and neurite outgrowth on dorsal root ganglion neurons.
[Show full text]
Neurotrophic Factors and Receptors in the Immature and Adult Spinal Cord After Mechanical Injury Or Kainic Acid
The Journal of Neuroscience, May 15, 2001, 21(10):3457–3475 Neurotrophic Factors and Receptors in the Immature and Adult Spinal Cord after Mechanical Injury or Kainic Acid Johan Widenfalk, Karin Lundstro¨ mer, Marie Jubran, Stefan Brene´ , and Lars Olson Department of Neuroscience, Karolinska Institute, S-171 77 Stockholm, Sweden Delivery of neurotrophic factors to the injured spinal cord has mRNA increased in astrocytes of degenerating white matter. been shown to stimulate neuronal survival and regeneration. The relatively limited upregulation of neurotrophic factors in the This indicates that a lack of sufﬁcient trophic support is one spinal cord contrasted with the response of affected nerve factor contributing to the absence of spontaneous regeneration roots, in which marked increases of NGF and GDNF mRNA in the mammalian spinal cord. Regulation of the expression of levels were observed in Schwann cells. The difference between neurotrophic factors and receptors after spinal cord injury has the ability of the PNS and CNS to provide trophic support not been studied in detail. We investigated levels of mRNA- correlates with their different abilities to regenerate. Kainic acid encoding neurotrophins, glial cell line-derived neurotrophic fac- delivery led to only weak upregulations of BDNF and CNTF tor (GDNF) family members and related receptors, ciliary neu- mRNA. Compared with several brain regions, the overall re- rotrophic factor (CNTF), and c-fos in normal and injured spinal sponse of the spinal cord tissue to kainic acid was weak. The cord. Injuries in adult rats included weight-drop, transection, relative sparseness of upregulations of endogenous neurotro- and excitotoxic kainic acid delivery; in newborn rats, partial phic factors after injury strengthens the hypothesis that lack of transection was performed.
[Show full text]
Receptors of the Glial Cell Line-Derived Neurotrophic Factor
The Journal of Neuroscience, November 1, 1999, 19(21):9160–9169 Receptors of the Glial Cell Line-Derived Neurotrophic Factor Family of Neurotrophic Factors Signal Cell Survival through the Phosphatidylinositol 3-Kinase Pathway in Spinal Cord Motoneurons Rosa M. Soler, Xavier Dolcet, Mario Encinas, Joaquim Egea, Jose R. Bayascas, and Joan X. Comella Grup de Neurobiologia Molecular, Departament de Cie` ncies Me` diques Ba` siques, Facultat de Medicina, Universitat de Lleida, 25198 Lleida, Catalonia, Spain The members of the glial cell line-derived neurotrophic factor hybridization and reverse transcription-PCR techniques. By (GDNF) family of neurotrophic factors (GDNF, neurturin, perse- Western blot analysis and kinase assays, we demonstrate the phin, and artemin) are able to promote in vivo and in vitro ability of these factors to induce the phosphatidylinositol 3 survival of different neuronal populations, including spinal cord kinase (PI 3-kinase) and the extracellular regulated kinase motoneurons. These factors signal via multicomponent recep- (ERK)–mitogen-activated protein (MAP) kinase pathways acti- tors that consist of the Ret receptor tyrosine kinase plus a vation. To characterize the involvement of these pathways in member of the GDNF family receptor a (GRFa) family of the survival effect, we used the PI 3-kinase inhibitor LY 294002 glycosylphosphatidylinositol-linked coreceptors. Activation of and the MAP kinase and ERK kinase (MEK) inhibitor PD 98059. the receptor induces Ret phosphorylation that leads the We demonstrate that LY 294002, but not PD 98059, prevents survival-promoting effects. Ret phosphorylation causes the ac- GDNF-, neurturin-, and persephin-induced motoneuron sur- tivation of several intracellular pathways, but the biological vival, suggesting that PI 3-kinase intracellular pathway is re- effects caused by the activation of each of these pathways are sponsible in mediating the neurotrophic effect.
[Show full text]
Potential Ciliary Neurotrophic Factor Application in Dental Stem Cell Therapy Patrick Suezaki University of the Pacific
University of the Pacific Scholarly Commons Dugoni School of Dentistry Faculty Articles Arthur A. Dugoni School of Dentistry 2-2017 Potential Ciliary Neurotrophic Factor Application in Dental Stem Cell Therapy Patrick Suezaki University of the Pacific Nan (Tori) Xiao University of the Pacific, [email protected] Follow this and additional works at: https://scholarlycommons.pacific.edu/dugoni-facarticles Part of the Dentistry Commons Recommended Citation Suezaki, P., & Xiao, N. (2017). Potential Ciliary Neurotrophic Factor Application in Dental Stem Cell Therapy. Journal of Dentistry and Oral Biology, 2(3), 1–2. https://scholarlycommons.pacific.edu/dugoni-facarticles/415 This Article is brought to you for free and open access by the Arthur A. Dugoni School of Dentistry at Scholarly Commons. It has been accepted for inclusion in Dugoni School of Dentistry Faculty Articles by an authorized administrator of Scholarly Commons. For more information, please contact [email protected]. Mini Review Journal of Dentistry and Oral Biology Published: 08 Feb, 2017 Potential Ciliary Neurotrophic Factor Application in Dental Stem Cell Therapy Patrick Suezaki1 and Nan Xiao2* 1Doctor of Dental Surgery Program, Arthur A. Dugoni School of Dentistry University of the Pacific, USA 2Department of Biomedical Sciences, Arthur A. Dugoni School of Dentistry University of the Pacific, USA Abstract Neurotrophic factors have long been considered growth factors that promote survival and growth of various neuronal tissues. Recent studies showed that neurotrophic factors are also present in dental pulp and periodontal ligament. This paper reviews the literature about the ciliary neurotrophic factor (CNTF), a member of the neurotrophic factor family, and indicates the potential clinical application of CNTF in dental stem cell therapy.
[Show full text]
Revisiting the Role of Neurotrophic Factors in Inflammation
cells Review Revisiting the Role of Neurotrophic Factors in Inﬂammation Lucas Morel, Olivia Domingues, Jacques Zimmer and Tatiana Michel * Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, L-4354 Esch-sur Alzette, Luxembourg; [email protected] (L.M.); [email protected] (O.D.); [email protected] (J.Z.) * Correspondence: [email protected]; Tel.: +352-26970-264 Received: 6 March 2020; Accepted: 31 March 2020; Published: 2 April 2020 Abstract: The neurotrophic factors are well known for their implication in the growth and the survival of the central, sensory, enteric and parasympathetic nervous systems. Due to these properties, neurturin (NRTN) and Glial cell-derived neurotrophic factor (GDNF), which belong to the GDNF family ligands (GFLs), have been assessed in clinical trials as a treatment for neurodegenerative diseases like Parkinson’s disease. In addition, studies in favor of a functional role for GFLs outside the nervous system are accumulating. Thus, GFLs are present in several peripheral tissues, including digestive, respiratory, hematopoietic and urogenital systems, heart, blood, muscles and skin. More precisely, recent data have highlighted that different types of immune and epithelial cells (macrophages, T cells, such as, for example, mucosal-associated invariant T (MAIT) cells, innate lymphoid cells (ILC) 3, dendritic cells, mast cells, monocytes, bronchial epithelial cells, keratinocytes) have the capacity to release GFLs and express their receptors, leading to the participation in the repair of epithelial barrier damage after inflammation. Some of these mechanisms pass on to ILCs to produce cytokines (such as IL-22) that can impact gut microbiota.
[Show full text]
Neuregulin Expression at Neuromuscular Synapses Is Modulated by Synaptic Activity and Neurotrophic Factors
The Journal of Neuroscience, March 15, 2002, 22(6):2206–2214 Neuregulin Expression at Neuromuscular Synapses Is Modulated by Synaptic Activity and Neurotrophic Factors Jeffrey A. Loeb,1 Abdelkrim Hmadcha,1 Gerald D. Fischbach,3 Susan J. Land,2 and Vaagn L. Zakarian1 1Department of Neurology and Center for Molecular Medicine and Genetics and 2Institute of Environmental Health Sciences, Wayne State University School of Medicine, Detroit, Michigan 48201, and 3Columbia University, College of Physicians and Surgeons, New York, New York 10032 The proper formation of neuromuscular synapses requires on- brain-derived neurotrophic factor and neurotrophin 3 expres- going synaptic activity that is translated into complex structural sion in muscle without appreciably changing the expression of changes to produce functional synapses. One mechanism by these same factors in spinal cord. Adding back these or other which activity could be converted into these structural changes neurotrophic factors restores synaptic neuregulin expression is through the regulated expression of speciﬁc synaptic regu- and maintains normal end plate band architecture in the pres- latory factors. Here we demonstrate that blocking synaptic ence of activity blockade. The expression of neuregulin protein activity with curare reduces synaptic neuregulin expression in a at synapses is independent of spinal cord and muscle neuregu- dose-dependent manner yet has little effect on synaptic agrin or lin mRNA levels, suggesting that neuregulin accumulation at a muscle-derived heparan sulfate proteoglycan. These changes synapses is independent of transcription. These ﬁndings sug- are associated with a fourfold increase in number and a twofold gest a local, positive feedback loop between synaptic regula- reduction in average size of synaptic acetylcholine receptor tory factors that translates activity into structural changes at clusters that appears to be caused by excessive axonal sprout- neuromuscular synapses.
[Show full text]
Glial Cell Line-Derived Neurotrophic Factor and Neurturin Inhibit Neurite Outgrowth and Activate Rhoa Through GFR␣2B, an Alternatively Spliced Isoform of GFR␣2
The Journal of Neuroscience, May 23, 2007 • 27(21):5603–5614 • 5603 Cellular/Molecular Glial Cell Line-Derived Neurotrophic Factor and Neurturin Inhibit Neurite Outgrowth and Activate RhoA through GFR␣2b, an Alternatively Spliced Isoform of GFR␣2 Li Foong Yoong1 and Heng-Phon Too1,2 1Department of Biochemistry, National University of Singapore, Singapore 119260, and 2Molecular Engineering of Biological and Chemical System/Chemical Pharmaceutical Engineering, Singapore–Massachusetts Institute of Technology Alliance, Singapore 117576 The glial cell line-derived neurotrophic factor (GDNF) and neurturin (NTN) belong to a structurally related family of neurotrophic factors. NTN exerts its effect through a multicomponent receptor system consisting of the GDNF family receptor ␣2 (GFR␣2), RET, and/or NCAM (neural cell adhesion molecule). GFR␣2 is alternatively spliced into at least three isoforms (GFR␣2a, GFR␣2b, and GFR␣2c). It is currently unknown whether these isoforms share similar functional and biochemical properties. Using highly specific and sensitive quantitative real-time PCR, these isoforms were found to be expressed at comparable levels in various regions of the human brain. When stimulated with GDNF and NTN, both GFR␣2a and GFR␣2c, but not GFR␣2b, promoted neurite outgrowth in transfected Neuro2A cells. These isoforms showed ligand selectivity in MAPK (mitogen-activated protein kinase) [ERK1/2 (extracellular signal- regulated kinase 1/2)] and Akt signaling. In addition, the GFR␣2 isoforms regulated different early-response genes when stimulated with GDNF or NTN. In coexpression studies, GFR␣2b was found to inhibit ligand-induced neurite outgrowth by GFR␣2a and GFR␣2c. Stimulation of GFR␣2b also inhibited the neurite outgrowth induced by GFR␣1a, another member of the GFR␣.
[Show full text]
Neuroscience Booklet Updated.Indd
Neuroscience Research Related Cytokine Products Neuroscience Research Related Cytokine Products Copyright © 2017 by PeproTech, Inc. PeproTech, Inc. 5 Crescent Avenue Rocky Hill, NJ 08553-0275 Tel: (800) 436-9910 (609) 497-0253 Fax: (609) 497-0321 email: [email protected] [email protected] [email protected] www.peprotech.com All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the publisher. Printed in the United States of America. 1 Neuroscience Research Related Cytokine Products Introduction Neuroscience is the biological study of the nervous system, encompassing those scientific disciplines concerned with the development, molecular and cellular structure, chemistry, functionality, evolution, and pathology of the neural networks constructing the nervous system. The vertebrate nervous system is a sophisticated networking of neural cells that function through the transmission of excitatory or inhibitory signaling to process information and orchestrate all bodily functions, including the capacity for motor and sensory function, cognition, and emotion. Arising from the ectoderm, the most exterior of the three germ cell layers, this system is comprised of both the central and peripheral nervous systems. The central nervous system, consisting of the brain and spinal cord, functions to receive, interpret, and respond to the nerve impulses
[Show full text]
The Mouse Soluble Gfra4 Receptor Activates RET Independently of Its Ligandpersephin
Oncogene (2007) 26, 3892–3898 & 2007 Nature Publishing Group All rights reserved 0950-9232/07 $30.00 www.nature.com/onc SHORT COMMUNICATION The mouse soluble GFRa4 receptor activates RET independently of its ligandpersephin J Yang, P Runeberg-Roos, V-M Leppa¨ nen and M Saarma Institute of Biotechnology, Viikki Biocenter, University of Helsinki, Helsinki, Finland Glial cell line-derived neurotrophic factor (GDNF) family There are four different ligands, all of which belong to ligands (GFLs) all signal through the transmembrane the glial cell line-derived neurotrophic factor (GDNF) receptor tyrosine kinase RET. The signalling complex family (GDNF, neurturin, artemin, persephin), and consists of GFLs, GPI-anchoredligandbinding GDNF correspondingly four different GPI-anchored co-recep- family receptor alphas (GFRas) andRET. Signalling via tors, which are named GDNF family receptor alpha RET is requiredfor the development of the nervous system (GFRa) 1–4 (Airaksinen and Saarma, 2002). The andthe kidney,as well as for spermatogenesis. However, persephin binding co-receptor GFRa4 is of special constitutive activation of RET is implicatedas a cause in interest, as its restricted expression pattern suggests that several diseases. Mutations of the RET proto-oncogene it may play a role in the MEN 2 syndrome (Lindahl cause the inherited cancer syndrome multiple endocrine et al., 2000, 2001). Several splice variants of GFRa4 neoplasia type 2 (MEN 2). Recently, it has been suggested have been found both in the human and in the mouse that mutations in the persephin binding GFRa4 receptor (Lindahl et al., 2000, 2001). The variants have been may have a potentially modifying role in MEN 2.
[Show full text]
Neurotrophic Factors and Parkinson's Disease
Review Article CLINICAL INVESTIGATION Neurotrophic factors and Parkinson’s disease Abstract Rajat Bhardwaj1 and Rahul Deshmukh2* Neurotrophins play a major role in adult neuronal survival, maintenance and regeneration. 1Neuropharmacology Division, Alterations in their levels have been implicated in various neurodegenerative disorders, including Department of Pharmacology, ISF Parkinson’s disease (PD). It has been reported that, the pathophysiology of PD progress is College of Pharmacy, Moga- 142001, essentially depends on various striatal signaling cascade, which consists handful of neurotrophic Punjab, India. factors namely, cerebral dopamine neurotrophic factor (CDNF), glial derived neurotrophic factor 2Department of Pharmaceutical Sciences (GDNF), mesencephalic astrocyte-derived neurotrophic factor (MANF), brain derived neurotrophic & Technology, factor (BDNF), nerve growth factor (NGF). Although, the exact pathophysiology of PD is remained Maharaja Ranjit Singh Punjab Technical elusive however, the loss of dopaminergic neurons and dopamine deficiency has considered as a University, Bathinda -151001, Punjab, major consequence for the movement disability as seen in PD. It has been proposed that loss of India dopaminergic neurons in PD may be conducted by inadequate neurotrophic activity which leads *Author for correspondence: to neuronal apoptosis. In addition, stimulation of neurotrophic factors in the striatal brain region E-mail: [email protected]; [email protected]; has been reported to be beneficial in experimental models of PD. In the current review we have [email protected] detailed out the neurotrophic factors and their role in pathogenesis of Parkinson’s disease. Keywords: Parkinson’s disease . Neurotrophic factors . NGF . BDNF . GDNF . MANF . CDNF Movement disorders Submitted Date: 08 February 2018; Accepted Date: 24 February 2018; Published Date: 03 March 2018 Abbreviations plants in a pot.
[Show full text]
RT² Profiler PCR Array (Rotor-Gene® Format) Human Growth Factors
RT² Profiler PCR Array (Rotor-Gene® Format) Human Growth Factors Cat. no. 330231 PAHS-041ZR For pathway expression analysis Format For use with the following real-time cyclers RT² Profiler PCR Array, Rotor-Gene Q, other Rotor-Gene cyclers Format R Description The Human Growth Factors RT² Profiler PCR Array profiles the expression of 84 genes related to growth factors. Growth factors play a vital role in various normal biological processes such as embryogenesis, wound healing and inflammation. This array contains angiogenic growth factors and regulators of apoptosis. Genes involved in cell differentiation are included as well. Also represented are genes related to embryonic development as well as genes involved in tissue-specific development. Using real-time PCR, you can easily and reliably analyze expression of a focused panel of genes related to the growth factors with this array. For further details, consult the RT² Profiler PCR Array Handbook. Shipping and storage RT² Profiler PCR Arrays in the Rotor-Gene format are shipped at ambient temperature, on dry ice, or blue ice packs depending on destination and accompanying products. For long term storage, keep plates at –20°C. Note: Ensure that you have the correct RT² Profiler PCR Array format for your real-time cycler (see table above). Note: Open the package and store the products appropriately immediately on receipt. Sample & Assay Technologies Array layout The 96 real-time assays in the Rotor-Gene format are located in wells 1–96 of the Rotor-Disc™ (plate A1–A12=Rotor-Disc 1–12, plate B1–B12=Rotor-Disc 13–24, etc.).
[Show full text]
Glial Cell Line-Derived Neurotrophic Factor Promotes the Survival of Early Postnatal Spinal Motor Neurons in the Lateral and Medial Motor Columns in Slice Culture
The Journal of Neuroscience, May 15, 2002, 22(10):3953–3962 Glial Cell Line-Derived Neurotrophic Factor Promotes the Survival of Early Postnatal Spinal Motor Neurons in the Lateral and Medial Motor Columns in Slice Culture Wojtek P. Rakowicz,1,2,5 Christopher S. Staples,2 Jeffrey Milbrandt,3 Janice E. Brunstrom,1,2 and Eugene M. Johnson Jr1,4 Departments of 1Neurology, 2Cell Biology and Physiology, 3Pathology and Internal Medicine, and 4Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, Missouri 63110, and 5Department of Neurology, Addenbrooke’s Hospital, Cambridge CB2 2QQ, United Kingdom The mechanisms by which trophic factors bring about spinal alone was sufficient to maintain all “rescuable” MNs for at least motor neuron (MN) survival and regulate their number during 1 week. Analysis of MN survival in GFR␣-1 Ϫ/Ϫ mice demon- development are not well understood. We have developed an strated that the trophic effect of GDNF was completely medi- organotypic slice culture model for the in vitro study of the ated by its preferred coreceptor, GDNF family receptor ␣-1 trophic requirements and cell death pathways in MNs of post- (GFR␣-1). None of the other GDNF family ligands supported natal day 1–2 mice. Both lateral motor column (LMC) and significant MN survival, suggesting that there is little ligand– medial motor column (MMC) neurons died within 72 hr when coreceptor cross talk within the slice preparation. Although MN grown in serum-free medium without trophic factors. Brain- subtypes can be clearly defined by both anatomical distribution derived neurotrophic factor, ciliary neurotrophic factor, and and ontogenetic specification, the pattern of trophic factor 8-(4-chlorophenylthio)-cAMP promoted the survival of a pro- responsiveness of neurons from the MMC was indistinguish- portion of the neurons, but glial cell line-derived neurotrophic able from that seen in the LMC.
[Show full text]