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M2694

Sigma-Aldrich

Anti-Munc-18-1 antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Synonyme(s) :

Anti-Munc-18α, Anti-STXBP1, Anti-Syntaxin-binding protein 1, Anti-rb-Sec-1

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About This Item

Numéro MDL:
MFCD07370408
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

200

Conjugué

unconjugated

Forme d'anticorps

IgG fraction of antiserum

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen 67 kDa

Espèces réactives

mouse, rat

Technique(s)

indirect immunofluorescence: 1:250-1:500 using mouse fibroblast NIH3T3 cell line
microarray: suitable
western blot: 1:2,000-1:4,000 using rat brain extract (S1 fraction) and PC12 whole cell extract.

Numéro d'accès UniProt

O08599

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... STXBP1(6812)
mouse ... Stxbp1(20910)
rat ... Stxbp1(25558)

Description générale

Munc-18-1 (67 kDa) is an abundant neuronal protein that tightly binds to the synaptic fusion protein syntaxin. It is primarily expressed in neuronal tissues. Both Munc-18-1 and 2 isoforms bind tightly to syntaxins 1A, 2, and 3.

Immunogène

synthetic peptide corresponding to amino acids 577-594 located at the C-terminus of rat Munc-18-1 conjugated to KLH. This sequence is identical in mouse, chicken, bovine, and human Munc-18-1. It does not share homology with the Munc-18-2 and Munc-18-3 isoforms.

Application

Anti-Munc-18-1 antibody produced in rabbit has been used in immunoblotting and immunofluorescence.

Actions biochimiques/physiologiques

Munc-18-1 functions in synaptic vesicle exocytosis. It modulates neurotransmission by associating with syntaxin 1. Munc-18-1 binds to both syntaxin 1A and 1B isoforms, inhibiting the binding of t-soluble N-ethylmaleimide-sensitive factor-attached protein receptor (SNARE) synaptobrevin/vesicle-associated membrane protein (VAMP) and SNAP25 to syntaxin 1 and preventing SNARE assembly. Munc-18 is required for neurotransmitter secretion from synaptic vesicles throughout development and has been implicated in axonal branching in hippocampal neurons.

Forme physique

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Clause de non-responsabilité

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

Overexpression of neuronal Sec1 enhances axonal branching in hippocampal neurons
Steiner P, et al.
Neuroscience, 113(4), 893-905 (2002)
Sec1/Munc18 proteins: mediators of membrane fusion moving to center stage.
R Jahn
Neuron, 27(2), 201-204 (2000-09-14)
Gülçin Vardar et al.
eLife, 10 (2021-08-25)
Syntaxin-1 (STX1) and Munc18-1 are two requisite components of synaptic vesicular release machinery, so much so synaptic transmission cannot proceed in their absence. They form a tight complex through two major binding modes: through STX1's N-peptide and through STX1's closed
Mints as adaptors Direct binding to neurexins and recruitment of munc18
Biederer T and Sudhof TC
Test, 275(51), 39803-39806 (2000)
Ouada Nebie et al.
Journal of biomedical science, 26(1), 89-89 (2019-11-02)
Effective neurorestorative therapies of neurodegenerative diseases must be developed. There is increasing interest in using human platelet lysates, rich in neurotrophic factors, as novel disease-modifying strategy of neurodegeneration. To ensure virus safety, pathogen reduction treatments should be incorporated in the
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