| 货号 | ACS-003-25ul |
| 描述 | Each antibody ordered from Alomone Labs is supplied with its corresponding control peptide (antigen), free of charge. A Rabbit Polyclonal Antibody to Calcium-Binding Protein 2 |
| 反应种属 | H, M, R |
| 应用 | WB |
| 供应商 | Alomone |
| 背景 | Neuronal Ca2+-binding proteins (CaBP1-5) are a subclass of the calmodulin (CaM) superfamily that regulates specific Ca2+ channel targets in the brain and retina. Multiple isoforms of CaBPs are localized in different neuronal cell types and perform specialized roles in sensory transduction and disease processes1. CaBP1–5 proteins have four EF hands that form pairs within the N lobe (EF1 and 2) and C lobe (EF3 and 4). The two lobes are structurally independent and connected by a flexible linker. Whereas all four EF hands bind Ca2+ in CaM, EF2 in CaBP1 does not bind Ca2+, and EF1 has reduced selectivity for Ca2+ over Mg2+. EF3 and EF4 in the C lobe of CaBP1 exhibit canonical Ca2+-induced conformational changes2. CaBP-target interactions induce functional changes distinct from those caused by CaM and may diversify neuronal responses to Ca2+ signals. CaBPs interact with and reshape the functional properties of certain voltage-gated Ca2+ channels (CaVs)3. CaBP1 is the best characterized family member and has been shown to regulate inositol 1,4,5-triphosphate receptors (IP3Rs), P/Q-type voltage-gated Ca2+ channels, L-type Ca2+ channels, and the transient receptor potential channel (TRPC5)4. CaBP1 regulates the currents of CaV1 and CaV2 channels in neurons, photoreceptors, and auditory hair cells. CaBP interactions with CaV1 channels may be required for hearing and vision, as mutations that disrupt these interactions cause blindness and deafness5. |
| 运输条件 | Ambient |
| 存放说明 | -20 |
| 纯度 | Affinity purified on immobilized antigen. |
| 参考文献 | 1.Park, S. et al. (2011) Protein Sci. 20, 1356. 2.Li, C. et al. (2009) J. Biol. Chem. 284, 2472. 3.Findeisen, F. et al. (2010) Structure 18, 1617. 4.Kinoshita-Kawada, M. et al. (2005) Pflugers Arch. 450, 345. 5.Schrauwen, I. et al. (2012) Am. J. Hum. Genet. 91, 636. |
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