
ELK Biotechnology GluR-2 rabbit pAb
GluR-2 단백질을 인식하는 토끼 다클론 항체로, WB, IHC, IF, ELISA에 사용 가능. 인간 GluR2 유래 합성 펩타이드로 면역화됨. 신경세포막 단백질 연구 및 AMPA 수용체 관련 연구에 적합. -20°C에서 1년 보관 가능.
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ELK Biotechnology GluR-2 rabbit pAb
제품 정보
| 항목 | 내용 |
|---|---|
| Product name | GluR-2 rabbit pAb |
| Alternative Names | GRIA2; GLUR2; Glutamate receptor 2; GluR-2; AMPA-selective glutamate receptor 2; GluR-B; GluR-K2; Glutamate receptor ionotropic; AMPA 2; GluA2 |
| Applications | WB; IHC; IF; ELISA |
| Recommended Dilutions | Western Blot: 1/500–1/2000 Immunohistochemistry: 1/100–1/300 Immunofluorescence: 1/200–1/1000 ELISA: 1/20000 Not yet tested in other applications |
| Immunogen | Synthesized peptide derived from human GluR2 (AA range: 834–883) |
| Host | Rabbit |
| Storage | -20°C / 1 year |
| Clonality | Polyclonal |
| Isotype | IgG |
| Concentration | 1 mg/ml |
| Observed Band | 99 kDa |
| Gene ID (Human) | 2891 |
| Human Swiss-Prot No. | P42262 |
| Species Reactivity | Human; Mouse; Rat |
세포 내 위치 (Cellular Localization)
Cell membrane; Multi-pass membrane protein.
Endoplasmic reticulum membrane; Multi-pass membrane protein.
Cell junction, synapse, postsynaptic cell membrane; Multi-pass membrane protein.
Cell junction, synapse, postsynaptic density membrane; Multi-pass membrane protein.
Interaction with CACNG2, CNIH2, and CNIH3 promotes cell surface expression (By similarity).
Displays a somatodendritic localization and is excluded from axons in neurons (By similarity).
Background
Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes.
This gene product belongs to a family of glutamate receptors that are sensitive to alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), and function as ligand-activated cation channels.
These channels are assembled from four related subunits, GRIA1–4.
The subunit encoded by this gene (GRIA2) undergoes RNA editing (CAG→CGG; Q→R) within the second transmembrane domain, rendering the channel impermeable to Ca²⁺.
Defective GRIA2 RNA editing at the Q/R site may be relevant to amyotrophic lateral sclerosis (ALS) etiology.
Alternative splicing results in multiple transcript variants.
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