AB9678

Anti-GABA A Receptor α 5 Antibody

Name: Anti-GABA A Receptor α 5 Antibody
Brand: MM
Price: 637 USD

Chemicon^®, from rabbit

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100 μL

$637.00

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About This Item

UNSPSC Code:

12352203

eCl@ss:

32160702

NACRES:

NA.41

Key Documents

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biological source

rabbit

Quality Level

100

conjugate

unconjugated

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.

NM_000810.2

UniProt accession no.

P31644

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

human ... GABRA5(2558)

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Show Differences

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This Item	SAB2100878	SAB5202248	SAB5202242
Sigma-Aldrich AB9678 Anti-GABA A Receptor α 5 Antibody	Sigma-Aldrich SAB2100878 Anti-GABRA5 (ab2) antibody produced in rabbit	Sigma-Aldrich SAB5202248 Monoclonal Anti-GABA A Receptor-Allophycocyanin antibody produced in mouse	Sigma-Aldrich SAB5202242 Monoclonal Anti-GABA A Receptor-Atto 594 antibody produced in mouse
Quality Level 100	Quality Level 100	Quality Level -	Quality Level -
antibody form affinity purified immunoglobulin	antibody form affinity isolated antibody	antibody form purified immunoglobulin	antibody form purified immunoglobulin
biological source rabbit	biological source rabbit	biological source mouse	biological source mouse
UniProt accession no. P31644	UniProt accession no. P31644	UniProt accession no. -	UniProt accession no. -
species reactivity rat, mouse	species reactivity mouse, guinea pig, rabbit, rat, human	species reactivity human, mouse	species reactivity human, mouse
Gene Information human ... GABRA5(2558)	Gene Information human ... GABRA5(2558)	Gene Information human ... GABRA5(2558)	Gene Information human ... GABRA5(2558)

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.

Biochem/physiol Actions

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.

Legal Information

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

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Storage Class

10 - Combustible liquids

wgk_germany

WGK 2

Certificates of Analysis (COA)

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Venlafaxine Attenuated the Cognitive and Memory Deficit in Mice Exposed to Isoflurane Alone.

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

Chronic inflammatory pain induced GABAergic synaptic plasticity in the adult mouse anterior cingulate cortex.

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

Reciprocal control of obesity and anxiety-depressive disorder via a GABA and serotonin neural circuit.

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

Gene expression changes in GABA(A) receptors and cognition following chronic ketamine administration in mice.

Tan, S; Rudd, JA; Yew, DT

Testing null

Altered GABAA Receptor Expression in the Primary Somatosensory Cortex of a Mouse Model of Genetic Absence Epilepsy.

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

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