ABN241
Anti-GluR1 Antibody
from rabbit, purified by affinity chromatography
Synonym(s):
Glutamate receptor 1, GluR-1, AMPA-selective glutamate receptor 1, GluR-A, GluR-K1, Glutamate receptor ionotropic, AMPA 1, GluA1
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All Photos(2)
About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
rabbit
Quality Level
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
human, mouse, rat
technique(s)
immunohistochemistry: suitable (paraffin)
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... GRIA1(2890)
mouse ... Gria1(14799)
rat ... Gria1(50592)
General description
Glutamate receptors (GluRs) are a diverse group responsible for mediating most of the excitatory synaptic transmission in the CNS of vertebrates. They can be categorized as ionotropic or metabotropic and subcategorized by their agonist preferences (NMDA, AMPA or Kainic acid). There are four types of AMPA selective GluR subunits (GluR1, GluR2, GluR3 and GluR4). Tetrameric or pentameric combinations of different subunits contributes to the functional diversity of AMPA receptors. AMPA receptors mediate fast synaptic current at most excitatory synapses, with stoichiometry characterized by subtype composition. The critical residue controlling calcium permeability is in the pore loop region. In GluR1, GluR3, and GluR4, this position is occupied by a Gln residue. The insertion or removal of GluR1/GluR4 oligomeric channels from postsynaptic membranes appears to be LTP/LTD activity dependent while GluR2/GluR3 oligomers are continuously cycling.
Specificity
This antibody recognizes the extracellular domain of GluR1.
Immunogen
KLH-conjugated linear peptide corresponding to the extracellular domain of rat GluR1.
Application
Anti-GluR1 Antibody is a highly specific rabbit polyclonal antibody, that targets GluR1 & has been tested in western blotting & IHC (Paraffin).
Immunohistochemistry Analysis: A 1:1,000 dilution from a representative lot detected GluR1 in human brain and human cerebellum tissue.
Quality
Evaluated by Western Blotting in rat brain tissue lysate.
Western Blotting Analysis: 2.0 µg/mL of this antibody detected GluR1 in 10 µg of rat brain tissue lysate.
Western Blotting Analysis: 2.0 µg/mL of this antibody detected GluR1 in 10 µg of rat brain tissue lysate.
Target description
~110 kDa observed
Linkage
Replaces: PC246-100UG
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Storage Class
12 - Non Combustible Liquids
wgk_germany
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
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Katherine J Sellers et al.
Alzheimer's & dementia : the journal of the Alzheimer's Association, 14(3), 306-317 (2017-10-23)
Synapse loss is the structural correlate of the cognitive decline indicative of dementia. In the brains of Alzheimer's disease sufferers, amyloid β (Aβ) peptides aggregate to form senile plaques but as soluble peptides are toxic to synapses. We previously demonstrated
Tao Wu et al.
Journal of biomedical science, 26(1), 79-79 (2019-10-21)
Neuronal activity-induced changes in gene expression patterns are important mediators of neuronal plasticity. Many neuronal genes can be activated or inactivated in response to neuronal depolarization. Mechanisms that activate gene transcription are well established, but activity-dependent mechanisms that silence transcription
Juhwan Kim et al.
Molecules and cells, 41(5), 454-464 (2018-05-15)
Crosstalk between G-protein signaling and glutamatergic transmission within the brain reward circuits is critical for long-term emotional effects (depression and anxiety), cravings, and negative withdrawal symptoms associated with opioid addiction. A previous study showed that Regulator of G-protein signaling 4
Ayush Singh et al.
Journal of Alzheimer's disease : JAD, 78(4), 1661-1678 (2020-11-14)
Certain individuals, here referred to as Non-Demented with Alzheimer Neuropathology (NDAN), do not show overt neurodegeneration (N-) and remain cognitively intact despite the presence of plaques (A+) and tangles (T+) that would normally be consistent with fully symptomatic Alzheimer's disease
Dipen Rajgor et al.
Cell reports, 31(12), 107785-107785 (2020-06-25)
Molecular mechanisms underlying plasticity at brain inhibitory synapses remain poorly characterized. Increased postsynaptic clustering of GABAA receptors (GABAARs) rapidly strengthens inhibition during inhibitory long-term potentiation (iLTP). However, it is unclear how synaptic GABAAR clustering is maintained to sustain iLTP. Here
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