
ELK Biotechnology GluR-2 (Phospho-Tyr876) rabbit pAb
GluR-2 (Phospho-Tyr876) rabbit pAb는 인간, 마우스, 랫트 시료에 반응하는 다클론 항체입니다. IHC, IF, WB에 사용 가능하며, 세포막 및 시냅스 후막 단백질 검출에 적합합니다. 인산화 GluR-2 타깃으로 신경생리학 연구에 유용합니다.
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GluR-2 (Phospho-Tyr876) rabbit pAb
제품 정보
| 항목 | 내용 |
|---|---|
| Product name | GluR-2 (Phospho-Tyr876) rabbit pAb |
| Alternative Names | Glutamate receptor 2 (GluR-2; AMPA-selective glutamate receptor 2; GluR-B; GluR-K2; Glutamate receptor ionotropic, AMPA 2; GluA2) |
| Applications | IHC; IF; WB |
| Recommended Dilutions | IHC-p 1:50-200, WB 1:500-2000 |
| Immunogen | Synthesized peptide derived from human GluR-2 (Phospho-Tyr876) |
| Host | Rabbit |
| Storage | -20°C / 1 year |
| Clonality | Polyclonal |
| Isotype | IgG |
| Concentration | 1 mg/ml |
| Observed Band | 99 kD |
| 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 sensitive to alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) and functions as a ligand-activated cation channel.
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⁺.
Human and animal studies suggest that pre-mRNA editing is essential for brain function, and defective GRIA2 RNA editing at the Q/R site may be relevant to amyotrophic lateral sclerosis (ALS) etiology.
Alternative splicing results in transcript variants encoding different isoforms.
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