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AB9678

Sigma-Aldrich

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

Biologische Quelle

rabbit

Qualitätsniveau

100

Antikörperform

affinity purified immunoglobulin

Antikörper-Produkttyp

primary antibodies

Klon

polyclonal

Aufgereinigt durch

affinity chromatography

Speziesreaktivität

rat, mouse

Hersteller/Markenname

Chemicon®

Methode(n)

western blot: suitable

NCBI-Hinterlegungsnummer

NM_000810.2

UniProt-Hinterlegungsnummer

P31644

Versandbedingung

dry ice

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... GABRA5(2558)

Spezifität

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.

Anwendung

Anti-GABA A Receptor α 5 Antibody is an antibody against GABA A Receptor α 5 for use in WB.

Rechtliche Hinweise

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

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Lagerklassenschlüssel

10 - Combustible liquids

WGK

WGK 2

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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
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
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
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