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      Call for Papers: Sex and Gender in Neurodegenerative Diseases

      Submit here before September 30, 2024

      About Neurodegenerative Diseases: 3.0 Impact Factor I 4.3 CiteScore I 0.695 Scimago Journal & Country Rank (SJR)

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      Secretion and Molecular Forms of NESP55, a Novel Genomically Imprinted Neuroendocrine-Specific Protein from AtT-20 Cells

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          Abstract

          NESP55 (neuroendocrine secretory protein of M<sub>r</sub> 55,000) is a paternally imprinted proteoglycan, expressed specifically in endocrine cells and the nervous system. We investigated the subcellular localization and secretion of NESP55 in AtT-20 cells. NESP55 accumulated in the medium linearly over 24 h exceeding its intracellular content 3.7-fold by that time. Incubation of cells at 16°C, to block protein export, inhibited basal secretion by 79%. Stimulation of AtT-20 cells with 8-Br-cAMP increased secretion of NESP55 by only 45%. The NESP55 secretory vesicles sedimented at a density of 1.2–1.4 M, which is slightly lighter than that of the large dense core vesicles. Immunofluorescence studies revealed immunoreactivity in the Golgi apparatus and a punctuate staining of processes or neurites. Our data demonstrate that NESP55 is mainly sorted to and released from a population of constitutive secretory vesicles, which are transported out of the perikarya into processes or axons. In addition, some NESP55 is also routed to the regulated pathway. The signal peptide of NESP55, as determined with peptide antisera, is 46 amino acids long and represents the best conserved region of this molecule suggesting that the signal peptide may have a function of its own. The subcellular localization and export of NESP55 from cells are reminiscent of neuronal proteoglycans forming the extracellular matrix, which are implicated in the development and maintenance of neuronal circuits and mechanisms of axonal guidance.

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          Most cited references29

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          A protein related to extracellular matrix proteins deleted in the mouse mutant reeler.

          The autosomal recessive mouse mutation reeler leads to impaired motor coordination, tremors and ataxia. Neurons in affected mice fail to reach their correct locations in the developing brain, disrupting the organization of the cerebellar and cerebral cortices and other laminated regions. Here we use a previously characterized reeler allele (rl(tg)) to close a gene, reelin, deleted in two reeler alleles. Normal but not mutant mice express reelin in embryonic and postnatal neurons during periods of neuronal migration. The encoded protein resembles extracellular matrix proteins involved in cell adhesion. The reeler phenotype thus seems to reflect a failure of early events associated with brain lamination which are normally controlled by reelin.
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            Defective neuromuscular synaptogenesis in agrin-deficient mutant mice.

            During neuromuscular synapse formation, motor axons induce clustering of acetylcholine receptors (AChRs) in the muscle fiber membrane. The protein agrin, originally isolated from the basal lamina of the synaptic cleft, is synthesized and secreted by motoneurons and triggers formation of AChR clusters on cultured myotubes. We show here postsynaptic AChR aggregates are markedly reduced in number, size, and density in muscles of agrin-deficient mutant mice. These results support the hypothesis that agrin is a critical organizer of postsynaptic differentiation does occur in the mutant, suggesting the existence of a second-nerve-derived synaptic organizing signal. In addition, we show that intramuscular nerve branching and presynaptic differentiation are abnormal in the mutant, phenotypes which may reflect either a distinct effect of agrin or impaired retrograde signaling from a defective postsynaptic apparatus.
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              The chromogranins A and B: The first 25 years and future perspectives

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                Author and article information

                Journal
                NSG
                Neurosignals
                10.1159/issn.1424-862X
                Neurosignals
                S. Karger AG
                1424-862X
                1424-8638
                2004
                December 2004
                23 December 2004
                : 13
                : 6
                : 298-307
                Affiliations
                Departments of aPharmacology and bAnatomy and Histology, Innsbruck Medical University, Innsbruck, Austria; cDepartment of Neurochemistry, Institute of Zoology, J.W. Goethe University of Frankfurt, Frankfurt, Germany
                Article
                81965 Neurosignals 2004;13:298–307
                10.1159/000081965
                15627817
                5b639132-c7eb-4a9f-b6e5-11712af62c50
                © 2004 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 26 July 2004
                : 18 August 2004
                Page count
                Figures: 8, Tables: 1, References: 34, Pages: 10
                Categories
                Original Paper

                Geriatric medicine,Neurology,Cardiovascular Medicine,Neurosciences,Clinical Psychology & Psychiatry,Public health
                Constitutive secretion,Neuroendocrine secretory protein,Chromogranin,Genomic imprinting

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