AB9848
Anti-phospho-Synapsin I (Ser62,Ser67) Antibody
Chemicon®, from rabbit
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
biological source
rabbit
Quality Level
antibody form
affinity purified immunoglobulin
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
rat
manufacturer/tradename
Chemicon®
technique(s)
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
dry ice
target post-translational modification
phosphorylation (pSer62/pSer67)
Gene Information
human ... SYN1(6853)
Specificity
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.
Immunogen
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
Physical form
ImmunoAffinity Purified
Liquid in 10 mM HEPES (pH 7.5), 150 mM NaCl, 100 ug/mL BSA and 50% glycerol.
Storage and Stability
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.
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
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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Storage Class Code
10 - Combustible liquids
WGK
WGK 2
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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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
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
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
Andrew K Evans et al.
Neurobiology of aging, 106, 241-256 (2021-07-29)
The locus coeruleus (LC) provides the primary noradrenergic input to the forebrain and hippocampus, and may be vulnerable to degeneration and contribute to age-related cognitive decline and neuroinflammation. Additionally, inhibition of noradrenergic transmission by brain-permeable beta-blockers could exacerbate cognitive impairment.
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