AB9678
Anti-GABA A Receptor α 5 Antibody
Chemicon®, from rabbit
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100 μL
₩804,286
About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
rabbit
Quality Level
antibody form
affinity purified immunoglobulin
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
rat, mouse
manufacturer/tradename
Chemicon®
technique(s)
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
dry ice
target post-translational modification
unmodified
Gene Information
human ... GABRA5(2558)
Related Categories
Specificity
GABAA Receptor alpha 5 subunit. The antibody recognizes a protein of ~55 kDa corresponding to GABAA Receptor alpha 5 subunit in lysates from rat hippocampus and thalamus.
Immunogen
Fusion protein from the Cytosolic loop of rat the GABAA Receptor alpha 5 subunit.
Application
Anti-GABA A Receptor α 5 Antibody is an antibody against GABA A Receptor α 5 for use in WB.
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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Storage Class Code
10 - Combustible liquids
WGK
WGK 2
Certificates of Analysis (COA)
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Liang Li et al.
Frontiers in neurology, 12, 591223-591223 (2021-03-13)
Post-operative cognitive dysfunction (POCD) is a common complication during the post-operative period. It affects the recovery time of the patient after surgery and the stay time in hospital, which causes a great deal of burden to patients and families emotionally
Kohei Koga et al.
Molecular pain, 14, 1744806918783478-1744806918783478 (2018-06-30)
Background Chronic pain is a persistent unpleasant sensation that produces pathological synaptic plasticity in the central nervous system. Both human imaging study and animal studies consistently demonstrate that the anterior cingulate cortex is a critical cortical area for nociceptive and
Gene expression changes in GABA(A) receptors and cognition following chronic ketamine administration in mice.
Tan, S; Rudd, JA; Yew, DT
Testing null
Muhammad Hassan et al.
International journal of molecular sciences, 23(24) (2022-12-24)
Absence seizures are hyperexcitations within the cortico-thalamocortical (CTC) network, however the underlying causative mechanisms at the cellular and molecular level are still being elucidated and appear to be multifactorial. Dysfunctional feed-forward inhibition (FFI) is implicated as one cause of absence
George Gallos et al.
American journal of physiology. Lung cellular and molecular physiology, 308(9), L931-L942 (2015-02-11)
The clinical need for novel bronchodilators for the treatment of bronchoconstrictive diseases remains a major medical issue. Modulation of airway smooth muscle (ASM) chloride via GABAA receptor activation to achieve relaxation of precontracted ASM represents a potentially beneficial therapeutic option.
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