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M6194

Sigma-Aldrich

Monoclonal Anti-Munc13/1 antibody produced in mouse

~2 mg/mL, clone Munc13-71, purified immunoglobulin, buffered aqueous solution

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About This Item

Numéro MDL:
MFCD08705591
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

mouse

Conjugué

unconjugated

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

Munc13-71, monoclonal

Forme

buffered aqueous solution

Espèces réactives

rat, mouse

Concentration

~2 mg/mL

Technique(s)

microarray: suitable
western blot: 1-2 μg/mL using cytosolic rat brain S1 fraction

Isotype

IgG2b

Numéro d'accès UniProt

Q4KUS2

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

mouse ... Unc13a(382018)
rat ... Unc13a(64829)

Description générale

Monoclonal Anti-Munc13-1 (mouse IgG2b isotype) is derived from the hybridoma Munc13-71 produced by the fusion of mouse myeloma cells (NS1 cells) and splenocytes from BALB/c mice immunized with a synthetic peptide of rat Munc13-1, conjugated to KLH. Protein unc-13 homolog A (Munc13-1) contains a diacylglycerol (DAG)/b phorbol ester-binding C1 domain. Munc13-1 are expression in axon is observed at various synapse populations.
Munc13/1 is a diacylglycerol receptor which is expressed in the presynaptic area.

Immunogène

synthetic peptide corresponding to amino acid 10-27 of rat munc13/1, conjugated to KLH.

Application

Monoclonal Anti-Munc13/1 antibody produced in mouse has been used in enzyme linked immunosorbent assay (ELISA) and immunoblotting.

Actions biochimiques/physiologiques

Munc13/1 has a crucial role in synaptic vesicle priming. It interacts with Syntaxin 1A and helps it to bind to soluble NSF attachment protein receptor (SNARE) proteins. Thus it contributes to the stability of the SNARE complex. Deletion of Munc13/1 leads to complete arrest synaptic transmission.

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

ELKS/Voltage-dependent Ca2+ channel-beta subunit module regulates polarized Ca2+ influx in pancreatic beta cells
Ohara-Imaizumi M, et al.
Testing, 26(5), 1213-1226 (2019)
Differential control of vesicle priming and short-term plasticity by Munc13 isoforms
Rosenmund C, et al.
Neuron, 33(3), 411-424 (2002)
Edwin P Kwan et al.
Diabetes, 55(5), 1421-1429 (2006-04-29)
Munc13-1 is a diacylglycerol (DAG) receptor that is essential for synaptic vesicle priming. We recently showed that Munc13-1 is expressed in rodent and human islet beta-cells and that its levels are reduced in islets of type 2 diabetic humans and
Stefan Kalla et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 26(50), 13054-13066 (2006-12-15)
GFP (green fluorescent protein) fusion proteins have revolutionized research on protein dynamics at synapses. However, corresponding analyses usually involve protein expression methods that override endogenous regulatory mechanisms, and therefore cause overexpression and temporal or spatial misexpression of exogenous fusion proteins
Lijun Kang et al.
Cell metabolism, 3(6), 463-468 (2006-05-16)
Munc13-1 is a presynaptic protein that is essential for synaptic vesicle priming. Deletion of Munc13-1/unc13 causes total arrest of synaptic transmission due to a complete loss of fusion-competent synaptic vesicles. The requirement of Munc13-1 for large dense-core vesicles (LDCVs), however
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