Evidence map›Paper›PMID 10880438›Full record

ArticleThe EMBO journal2000

alpha-latrotoxin triggers transmitter release via direct insertion into the presynaptic plasma membrane.

M Khvotchev, T C Südhof

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Insecticidal toxins from black widow spider venom.Toxicon : official journal of the International Society on Toxinology · 2007
    Review
  8. N-terminal insertion and C-terminal ankyrin-like repeats of alpha-latrotoxin are critical for Ca2+-dependent exocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  9. Article
  10. Article
  11. Article
  12. The alpha-latrotoxin mutant LTXN4C enhances spontaneous and evoked transmitter release in CA3 pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    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

2 authors at 1 institution in 1 country.

M KhvotchevCenter for Basic Neuroscience, Department of Molecular Genetics and Howard Hughes Medical Institute, The University of Texas Southwestern Medical Center at Dallas, TX 75235, USA.
T C Südhof
Howard Hughes Medical Institute · US

Funding

FUNCTION OF NEUREXINSR37MH052804 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI SUDHOF, THOMAS C. · 2000 to 2019
$9.3M
Function of NeurexinsR01MH052804 · NIMH · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI SUDHOF, THOMAS C. · 1994 to 2024
$3.7M
NIMH NIH HHS R0I-MH52804NIMH NIH HHS R37 MH052804
6 · The paper itself

Abstract

alpha-latrotoxin, a component of black widow spider venom, binds to presynaptic nerve terminals and stimulates massive neurotransmitter release. Previous studies have demonstrated that alpha-latrotoxin first binds to two high-affinity receptors on nerve terminals, neurexins and CLs (CIRLs and latrophilins), and then executes a critical, second step of unknown nature that stimulates neurotransmitter release. We now demonstrate that incubation of alpha-latrotoxin with synaptosomes at 0 degrees C results in its peripheral membrane association. Incubation at 37 degrees C, however, converts the toxin into an operationally integral membrane protein, and induces generation of a protease-resistant fragment that consists of the entire N-terminal domain of alpha-latrotoxin and becomes protease sensitive after lysis of synaptosomes. Our data suggest that alpha-latrotoxin inserts into the presynaptic plasma membrane after receptor binding, resulting in an intracellular location of the N-terminal sequences. Membrane insertion of the N-terminal domain of alpha-latrotoxin occurs spontaneously, independently of membrane recycling or transmembrane ion gradients. We postulate that alpha-latrotoxin acts intracellularly in triggering release, and propose that non-selective cation channels induced by alpha-latrotoxin may be a by-product of membrane insertion.

Indexed as

AnimalsBiological TransportCell MembraneHot TemperatureHydrolysisMicePeptide FragmentsPresynaptic TerminalsRatsRecombinant ProteinsSpider VenomsSynaptosomesTrypsinalpha-latrotoxinPeptide FragmentsRecombinant ProteinsSpider VenomsTrypsin

Identifiers

PMID10880438
PMCPMC313948
OpenAlexW2063566914

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.