Paper · 17035546

Important contribution of alpha-neurexins to Ca2+-triggered exocytosis of secretory granules.

Dudanova I and 10 others. J Neurosci, 2006. Cited by 48 papers, by iCite.

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ConductScience Library. Important contribution of alpha-neurexins to Ca2+-triggered exocytosis of secretory granules. Papers, record 17035546. Release papers-2026-11-12-0.1.0, 12 Nov 2026. https://conductscience.org/library/papers/17035546

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Paper

PubMed's record of the paper, with iCite's citation figures. No abstract is shown.

Title: Important contribution of alpha-neurexins to Ca2+-triggered exocytosis of secretory granules.; PubMed
Journal: J Neurosci; PubMed
Year: 2006; PubMed
Publication types: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't; PubMed
PubMed: https://pubmed.ncbi.nlm.nih.gov/17035546/; PubMed
DOI: https://doi.org/10.1523/jneurosci.1913-06.2006; PubMed
PMC: https://pmc.ncbi.nlm.nih.gov/articles/PMC6674690/; PubMed
The journal: https://conductscience.org/library/journal-index/8102140; PubMed
Citations, by iCite: 48; iCite
Relative citation ratio, by iCite: 0.93; iCite
Revised in PubMed: 2020-02-25; PubMed

Authors11

The authors in the order PubMed's record lists them, with the ORCID iDs it states.

Order	Author	Forename
1	Dudanova I	Irina
2	Sedej S	Simon
3	Ahmad M	Mohiuddin
4	Masius H	Henriette
5	Sargsyan V	Vardanush
6	Zhang W	Weiqi
7	Riedel D	Dietmar
8	Angenstein F	Frank
9	Schild D	Detlev
10	Rupnik M	Marjan

1 to 10 of 11Source PubMed

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Topics11

NLM's MeSH indexing of the paper, its major topics first.

MeSH term	Major
Calcium	Major topic
Exocytosis	Major topic
Glycoproteins	Major topic
Neuropeptides	Major topic
Secretory Vesicles	Major topic
Animals
Calcium Channels
Cell Line
Humans
Mice
Mice, Knockout

Source PubMed

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Trials0

The trials whose ClinicalTrials.gov record lists the paper, and the trial numbers the paper's PubMed record names.

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Comments and corrections0

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References94

The papers the reference list in PubMed's record names, those in our copy of PubMed, in the list's order.

Order	PMID	Title	Journal	Year	In Papers	Source
1	10,197,529	Neurexins are functional alpha-latrotoxin receptors.	Neuron	1999	https://conductscience.org/library/papers/10197529	PubMed
2	10,212,294	Tonic dopamine inhibition of L-type Ca2+ channel activity reduces alpha1D Ca2+ channel gene expression.	J Neurosci	1999	https://conductscience.org/library/papers/10212294	PubMed
3	10,383,622	Postnatal development of GABAB receptor-mediated modulation of voltage-activated Ca2+ currents in mouse brain-stem neurons.	Eur J Neurosci	1999	https://conductscience.org/library/papers/10383622	PubMed
4	10,414,292	Interactions of presynaptic Ca2+ channels and snare proteins in neurotransmitter release.	Ann N Y Acad Sci	1999	https://conductscience.org/library/papers/10414292	PubMed
5	10,433,271	Mechanisms underlying phasic and sustained secretion in chromaffin cells from mouse adrenal slices.	Neuron	1999	https://conductscience.org/library/papers/10433271	PubMed
6	10,455,105	Association of neuronal calcium channels with modular adaptor proteins.	J Biol Chem	1999	https://conductscience.org/library/papers/10455105	PubMed
7	10,526,329	Reciprocal regulation of P/Q-type Ca2+ channels by SNAP-25, syntaxin and synaptotagmin.	Nat Neurosci	1999	https://conductscience.org/library/papers/10526329	PubMed
8	10,657,302	Synaptic assembly of the brain in the absence of neurotransmitter secretion.	Science	2000	https://conductscience.org/library/papers/10657302	PubMed
9	10,792,045	Rapid regulated dense-core vesicle exocytosis requires the CAPS protein.	Proc Natl Acad Sci U S A	2000	https://conductscience.org/library/papers/10792045	PubMed
10	10,856,612	Calcium channels and the release of large dense core vesicles from neuroendocrine cells: spatial organization and functional coupling.	Prog Neurobiol	2000	https://conductscience.org/library/papers/10856612	PubMed

1 to 10 of 94

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Cited by37

The papers in our copy of PubMed whose reference list names this one, newest first. iCite, which reads more sources, counts 48 citations.

PMID	Title	Journal	Year	In Papers	Source
42,211,283	Roles of NRXN1 in neuropsychiatric disorders: from genetic lesion to molecular mechanism.	Front Neurosci	2026	https://conductscience.org/library/papers/42211283	PubMed
41,831,576	Cerebellar hypoplasia caused by calcium/calmodulin-dependent serine protein kinase deficiency.	Mol Cells	2026	https://conductscience.org/library/papers/41831576	PubMed
41,333,154	Alpha-neurexins in health and disease.	Front Mol Neurosci	2025	https://conductscience.org/library/papers/41333154	PubMed
39,521,920	Neurexin facilitates glycosylation of Dystroglycan to sustain muscle architecture and function in Drosophila.	Commun Biol	2024	https://conductscience.org/library/papers/39521920	PubMed
38,891,114	Conditional Knockout of Neurexins Alters the Contribution of Calcium Channel Subtypes to Presynaptic Ca2+ Influx.	Cells	2024	https://conductscience.org/library/papers/38891114	PubMed
38,167,109	Neurexin-1-dependent circuit activity is required for the maintenance of photoreceptor subtype identity in Drosophila.	Mol Brain	2024	https://conductscience.org/library/papers/38167109	PubMed
34,323,517	Social behavior in prepubertal neurexin 1α deficient rats: A model of neurodevelopmental disorders.	Behav Neurosci	2021	https://conductscience.org/library/papers/34323517	PubMed
33,224,013	Application of Chromosome Microarray Analysis in the Investigation of Developmental Disabilities and Congenital Anomalies: Single Center Experience and Review of NRXN3 and NEDD4L Deletions.	Mol Syndromol	2020	https://conductscience.org/library/papers/33224013	PubMed
31,893,021	Increased Ca2+ signaling in NRXN1α+/- neurons derived from ASD induced pluripotent stem cells.	Mol Autism	2019	https://conductscience.org/library/papers/31893021	PubMed
31,758,607	Dysfunction of the corticostriatal pathway in autism spectrum disorders.	J Neurosci Res	2020	https://conductscience.org/library/papers/31758607	PubMed

1 to 10 of 37

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PubMed: 2026-11-06; PubMed
iCite: 2026-11-05; iCite
PMC's ID file: 2026-11-05; PMC's ID file
NIH RePORTER's grant and paper links: 2026-11-01; NIH RePORTER's grant and paper links
Trials: 2026-11-12
Gene search: 2026-11-11
Pipelines: 2026-09-18

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ClinicalTrials.govNo license stated
HGNCCC0
iCiteCC BY 4.0
NCBI GenePublic domain (US government)
NIH RePORTER's grant and paper linksPublic domain
Open TargetsCC0 1.0
PMC's ID filePublic domain (US government)
PubMedNLM's terms
PubTator 3Public domain
UniProtCC BY 4.0

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ChEMBL, through Open TargetsCC BY-SA 3.0, for the parts from ChEMBL. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
ClinicalTrials.govnone stated
HGNCCC0: https://www.genenames.org/about/license/
iCiteCC BY 4.0
NCBI GeneNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
NIH RePORTER's grant and paper linksPublic domain (NIH RePORTER)
Open TargetsCC0 1.0. Open Targets asks that users cite its latest paper: Buniello et al. 2025, Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery, Nucleic Acids Research 53(D1):D1467, PMID 39657122. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
PMC's ID fileNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
PubMedNLM's terms
PubTator 3Public domain
UniProtCC BY 4.0. UniProt's licence file: "All databases and documents in the UniProt FTP directory may be copied and redistributed freely, without advance permission, provided that this copyright statement is reproduced with each copy." UniProt asks that users cite its latest paper: The UniProt Consortium, UniProt: the Universal Protein Knowledgebase in 2025, Nucleic Acids Research 53:D609-D617, https://doi.org/10.1093/nar/gkae1010. Read on 9 Nov 2026 at https://www.uniprot.org/help/license

ClinicalTrials.gov's data carry an international copyright outside the United States: https://clinicaltrials.gov/about-site/terms-conditions.

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