AB9848
Anti-phospho-Synapsin I (Ser62,Ser67) Antibody
Chemicon®, from rabbit
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100 μL
651,00 €
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100 μL
651,00 €
About This Item
Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41
Source biologique
rabbit
Niveau de qualité
Forme d'anticorps
affinity purified immunoglobulin
Type de produit anticorps
primary antibodies
Clone
polyclonal
Produit purifié par
affinity chromatography
Espèces réactives
rat
Fabricant/nom de marque
Chemicon®
Technique(s)
western blot: suitable
Numéro d'accès NCBI
Numéro d'accès UniProt
Conditions d'expédition
dry ice
Modification post-traductionnelle de la cible
phosphorylation (pSer62/pSer67)
Informations sur le gène
human ... SYN1(6853)
Spécificité
Synapsin I, phospho Serine 62,67. The antibody recognizes a protein doublet of ~78 kDa corresponding to Synapsin I, phospho Serine 62,67 in lysates from rat cortex. Immunolableing is blocked by preadsorption with the phospho-peptide used as the immunogen but not by the corresponding dephospho-peptide.
The immunogen has 100% homology with mouse and bovine.
Immunogène
Synthetic peptide of amino acids surrounding the phosphoSerine 62,67 site of rat Synapsin I.
Application
Anti-phospho-Synapsin I Antibody (Ser62, Ser67) detects level of phospho-Synapsin I (Ser62) & has been published & validated for use in WB.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Synapse & Synaptic Biology
Synapse & Synaptic Biology
Forme physique
ImmunoAffinity Purified
Liquid in 10 mM HEPES (pH 7.5), 150 mM NaCl, 100 ug/mL BSA and 50% glycerol.
Stockage et stabilité
Maintain at -20degC in undiluted for up to 6 months after date of receipt. Avoid repeated freeze/thaw cycles. Do not store in a self defrosting freezer.
Informations légales
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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 2
Certificats d'analyse (COA)
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Chongbo Zhong et al.
Frontiers in neural circuits, 16, 978837-978837 (2022-10-11)
Modulation of the release of glutamate by activation of presynaptic nicotinic acetylcholine receptors (nAChRs) is one of the most prevalent mechanism of nicotinic facilitation of glutamatergic transmission in cortico-limbic circuits. By imaging gene chimeric co-cultures from mouse, we examined the
Soledad Bárez-López et al.
Molecular & cellular proteomics : MCP, 22(5), 100544-100544 (2023-04-09)
The cell bodies of hypothalamic magnocellular neurones are densely packed in the hypothalamic supraoptic nucleus, whereas their axons project to the anatomically discrete posterior pituitary gland. We have taken advantage of this unique anatomical structure to establish proteome and phosphoproteome
Soledad Bárez-López et al.
Neuroendocrinology, 113(10), 1008-1023 (2023-06-05)
Despite the widespread use of general anaesthetics, the mechanisms mediating their effects are still not understood. Although suppressed in most parts of the brain, neuronal activity, as measured by FOS activation, is increased in the hypothalamic supraoptic nucleus (SON) by
Julie Fourneau et al.
Journal of neurochemistry, 147(2), 240-255 (2018-05-29)
In human, a chronic sensorimotor perturbation (SMP) through prolonged body immobilization alters motor task performance through a combination of peripheral and central factors. Studies performed on a rat model of SMP have shown biomolecular changes and a reorganization of sensorimotor
Ellen R Bowen et al.
Discover mental health, 3(1), 27-27 (2023-12-01)
Schizophrenia is a debilitating condition necessitating more efficacious therapies. Previous studies suggested that schizophrenia development is associated with aberrant synaptic pruning by glial cells. We pursued an interdisciplinary approach to understand whether therapeutic reduction in glial cell-specifically astrocytic-phagocytosis might benefit
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