AB9678
Anti-GABA A Receptor α 5 Antibody
Chemicon®, from rabbit
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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)
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
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.
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
Guobin Xia et al.
Molecular psychiatry, 26(7), 2837-2853 (2021-03-27)
The high comorbidity between obesity and mental disorders, such as depression and anxiety, often exacerbates metabolic and neurological symptoms significantly. However, neural mechanisms that underlie reciprocal control of feeding and mental states are largely elusive. Here we report that melanocortin
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
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