Evidence map›Paper›PMID 8464926›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1993

Association of GAD-65, but not of GAD-67, with the Golgi complex of transfected Chinese hamster ovary cells mediated by the N-terminal region.

M Solimena, D Aggujaro, C Muntzel, R Dirkx, M Butler, P De Camilli, A Hayday

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
9.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Article
  3. Advances in the cellular immunological pathogenesis of type 1 diabetes.Journal of cellular and molecular medicine · 2014
    Review
  4. Review
  5. Article
  6. Review
  7. A Role for GAT-1 in Presynaptic GABA Homeostasis?Frontiers in cellular neuroscience · 2011
    Article
  8. Article
  9. Article
  10. Article
  11. Expression and function of SNAP-25 as a universal SNARE component in GABAergic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006
    Article
  12. Article
  13. Article
  14. Article
  15. Autoimmunity to beta IV spectrin in paraneoplastic lower motor neuron syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2001
    Article
  16. Article
  17. Article
  18. Widespread expression of an autoantigen-GAD65 transgene does not tolerize non-obese diabetic mice and can exacerbate disease.Proceedings of the National Academy of Sciences of the United States of America · 1998
    Article
  19. Motifs and structural fold of the cofactor binding site of human glutamate decarboxylase.Protein science : a publication of the Protein Society · 1998
    Article
  20. GAD-reactive CD4+ Th1 cells induce diabetes in NOD/SCID mice.The Journal of clinical investigation · 1998
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

M SolimenaHoward Hughes Medical Institute, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06510.
D Aggujaro
C Muntzel
R Dirkx
M Butler
P De Camilli
A Hayday
Howard Hughes Medical Institute · US

Funding

CELLULAR AND MOLECULAR BASIS OF AUTOIMMUNE DIABETESP01DK043078 · NIDDK · YALE UNIVERSITY · PI JANEWAY, CHARLES A · 1990 to 1995
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AUTOIMMUNITY TO GABA-ERGIC NEURONS IN STIFF-MAN SYNDROMER01AI030248 · NIAID · YALE UNIVERSITY · PI DE CAMILLI, PIETRO V · 1990 to 1992
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NIAID NIH HHS AI 30248-01NIDDK NIH HHS DK 43078-01PHS HHS 43708
6 · The paper itself

Abstract

Glutamic acid decarboxylase (GAD) is the enzyme responsible for synthesis of the neurotransmitter gamma-aminobutyric acid in neurons and pancreatic beta cells. It is represented by two isoforms, GAD-65 and GAD-67, which are the products of two different genes and differ substantially only at their N-terminal regions. GAD-65 is a dominant autoantigen in stiff-man syndrome and insulin-dependent diabetes mellitus. In neurons and beta cells, GAD is concentrated around synaptic vesicles and synaptic-like microvesicles, respectively, as well as in the area of the Golgi complex. The mechanisms responsible for specific targeting of GAD to these organelles are not yet understood. The elucidation of the mechanism of subcellular targeting of GAD may be relevant to understanding its role as an autoantigen. In this study, the cloned genes for GAD-65 and GAD-67 were expressed separately in Chinese hamster ovary (CHO) cells and COS cells. While GAD-67 had a diffuse cytoplasmic localization, GAD-65 had a punctate distribution, with most of the immunoreactivity being concentrated in the area of the Golgi complex. A chimeric protein in which the 88 N-terminal amino acids of GAD-67 were replaced by the 83 N-terminal amino acids of GAD-65 was targeted to the Golgi complex, indicating that the N-terminal region of GAD-65 contains a targeting signal sufficient for directing the remaining portion of the molecule, highly similar in GAD-65 and GAD-67, to the Golgi complex-associated structures.

Indexed as

Amino Acid SequenceAnimalsBase SequenceBlotting, WesternCell LineCHO CellsCloning, MolecularCricetinaeFluorescent Antibody TechniqueGlutamate DecarboxylaseGolgi ApparatusIsoenzymesMolecular Sequence DataOligodeoxyribonucleotidesPeptidesPolymerase Chain ReactionGlutamate DecarboxylaseIsoenzymesOligodeoxyribonucleotidesPeptidesRecombinant Fusion Proteins

Identifiers

PMID8464926
PMCPMC46239
OpenAlexW2051936025

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.