Rat Gamma-aminobutyric acid receptor subunit gamma-2 (GABRG2) ELISA kit; CAE2; ECA2; GEFSP3; gamma-aminobutyric acid A receptor; gamma 2; gamma-aminobutyric acid (GABA) A receptor; gamma 2

For Research Use Only. Not for use in diagnostic procedures.

No significant cross-reactivity or interference between Rat GABRG2 and analogues was observed.

Store all reagents at 2-8 degree C

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Small volumes of GABRG2 elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

MBS9336526 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the gamma-aminobutyric acid (GABA) A receptor, gamma 2 (GABRG2) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing GABRG2. The ELISA analytical biochemical technique of the MBS9336526 kit is based on GABRG2 antibody-GABRG2 antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect GABRG2 antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, GABRG2. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

Background: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! It is intended to be determinated GABRG2 concentrations in Rat serum, plasma and other body fluids. Using Purified Rat GABRG2 antibody to coat Microelisa Stripplate wells to make solid-phase antibody, then add GABRG2 and GABRG2 antibody which has been labeled with HRP to wells, then the reactants become antibody-antigen-antibody-enzyme complex, after washing completely, add TMB substrate solution, TMB substrate becomes blue color under HRP enzyme-catalyzed, reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. The concentration of GABRG2 in the samples is then determined by comparing the O.D. of the samples to the standard curve.

54,077 Da

gamma-aminobutyric acid (GABA) A receptor, gamma 2

gamma-aminobutyric acid receptor subunit gamma-2; GABA(A) receptor subunit gamma-2; gamma-aminobutyric acid A receptor, gamma 2; gamma-aminobutyric acid A receptor, gamma 2; gamma-aminobutyric acid (GABA-A) receptor, subunit gamma 2

Gamma-aminobutyric acid receptor subunit gamma-2

GBRG2_RAT

subunit of GABA receptors, which bind benzodiazepines and act as inhibitory ion channels in the brain [RGD, Feb 2006]

GABRG2 iso2: GABA, the major inhibitory neurotransmitter in the vertebrate brain, mediates neuronal inhibition by binding to the GABA/benzodiazepine receptor and opening an integral chloride channel. Defects in GABRG2 are the cause of childhood absence epilepsy type 2 (ECA2). ECA2 is a subtype of idiopathic generalized epilepsy (IGE) characterized by an onset at age 6-7 years, frequent absence seizures (several per day) and bilateral, synchronous, symmetric 3-Hz spike waves on EEG. During adolescence, tonic-clonic and myoclonic seizures develop. Some individuals manifest ECA2 occurring in combination with febrile convulsions. Defects in GABRG2 are the cause of familial febrile convulsions type 8 (FEB8). A febrile convulsion is defined as a seizure event in infancy or childhood, usually occurring between 6 months and 6 years of age, associated with fever but without any evidence of intracranial infection or defined pathologic or traumatic cause. Febrile convulsions affect 5-12% of infants and children up to 6 years of age. There is epidemiological evidence that febrile seizures are associated with subsequent afebrile and unprovoked seizures in 2% to 7% of patients. Defects in GABRG2 are the cause of generalized epilepsy with febrile seizures plus type 3 (GEFS+3). Generalized epilepsy with febrile seizures-plus refers to a rare autosomal dominant, familial condition with incomplete penetrance and large intrafamilial variability. Patients display febrile seizures persisting sometimes beyond the age of 6 years and/or a variety of afebrile seizure types. GEFS+ is a disease combining febrile seizures, generalized seizures often precipitated by fever at age 6 years or more, and partial seizures, with a variable degree of severity. Defects in GABRG2 are a cause of severe myoclonic epilepsy in infancy (SMEI); also called Dravet syndrome. SMEI is a rare disorder characterized by generalized tonic, clonic, and tonic-clonic seizures that are initially induced by fever and begin during the first year of life. Later, patients also manifest other seizure types, including absence, myoclonic, and simple and complex partial seizures. Psychomotor development delay is observed around the second year of life. SMEI is considered to be the most severe phenotype within the spectrum of generalized epilepsies with febrile seizures-plus. Belongs to the ligand-gated ion channel (TC 1.A.9) family. Gamma-aminobutyric acid receptor (TC 1.A.9.5) subfamily. GABRG2 sub-subfamily. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Channel, chloride; Membrane protein, multi-pass; Membrane protein, integral; Transporter, ion channel; Transporter; Channel, ligand-gated

Cellular Component: postsynaptic membrane; axon; integral to plasma membrane; cytoplasm; cell junction

Molecular Function: chloride channel activity; protein binding; GABA-A receptor activity; GABA receptor activity; inhibitory extracellular ligand-gated ion channel activity

Biological Process: synaptic transmission; ***** behavior; synaptic transmission, GABAergic; chloride transport; signal transduction; gamma-aminobutyric acid signaling pathway; post-embryonic development

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