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S2177

Sigma-Aldrich

Anti-Synaptotagmin antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

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About This Item

Numéro MDL:
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.46

Source biologique

rabbit

Conjugué

unconjugated

Forme d'anticorps

IgG fraction of antiserum

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen 65 kDa

Espèces réactives

rat

Technique(s)

microarray: suitable
western blot: 1:5,000 using extract of rat brain membrane fraction

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... SYT1(6857)
mouse ... Syt1(20979)
rat ... Syt1(25716)

Description générale

Synaptotagmin (Syt, p65) is an abundant synaptic vesicle (SV) membrane protein. It is characterized by a short intravesicular N-terminal domain, a single transmembrane region and two copies of highly conserved internal repeats, known as the C2A and C2B domains, which are homologous to the C2 regulatory region of protein kinase C (PKC) in the cytoplasmic domain. At least eight different isoforms of synaptotagmin (SytI-VIII) are expressed in the brain, four of which (Syt IV, V, VII and VIII) are also expressed in non-neuronal tissues.

Spécificité

The sequence is highly conserved among species (SytI) and is not found in other known synaptotagmin isoforms (SytII-VIII).

Immunogène

synthetic peptide corresponding to N-terminus of synaptotagmin I (SytI) of rat origin (amino acids 1-16 with C-terminally added lysine), conjugated to KLH.

Application

Anti-Synaptotagmin antibody produced in rabbit has been used:
  • for cell surface labelling of synaptotagmin I (SytI)
  • in immunofluorescence microscopy
  • in western blotting

Actions biochimiques/physiologiques

Synaptotagmin binds Ca2+ phospholipids with high affinity and has a central role in Ca2+ regulated neurotransmitter release. Synaptotagmin functions as a Ca2+ sensor and is required for efficient exocytosis, particularly in the vesicle docking and/or fusion step with the plasma membrane. Ca2+ influx triggers synaptotagmin to interact with either syntaxin or SNAP-25 and the cytoplasmic domain of neurexin leading to fusion and exocytosis. Mutations or deletion of synaptotagmin result in severely impaired Ca2+ triggered neurotransmitter release. Synapses of SytI knockout mice lack the fast-component of Ca2+ dependent neurotransmitter release, but exhibit no changes in the slow, Ca2+ independent component of synaptic vesicle exocytosis.

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

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

nwg

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

Alzheimer-related decrease in CYFIP2 links amyloid production to tau hyperphosphorylation and memory loss
Tiwari SS, et al.
Brain, 139(10), 2751-2751 (2016)
Synaptotagmin in Ca2+dependent exocytosis: dynamic action in a flash
Tokuoka H and Goda Y
Neuron, 38(4), 521-524 (2003)
The C2B domain of synaptotagmin is a Ca2+ sensing module essential for exocytosis
Desai RC, et al.
The Journal of Cell Biology, 150(5), 1125-1136 (2000)
Zhe-Zhe Zhang et al.
Frontiers in aging neuroscience, 12, 157-157 (2020-08-11)
Age-associated impairment of spatial learning and memory (AISLM) presents substantial challenges to our health and society. Increasing evidence has indicated that embryonic exposure to inflammation accelerates the AISLM, and this can be attributable, at least partly, to changed synaptic plasticity
Zhe-Zhe Zhang et al.
Neural plasticity, 2022, 1483101-1483101 (2022-05-17)
A mounting body of evidence suggests that prenatal inflammation may enhance the rate of age-associated cognitive decline and may involve aberrant amounts of synaptic proteins in the hippocampus, including synaptotagmin-1 (Syt1) and activity-regulated cytoskeleton-associated protein (Arc). However, little is known

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