Recombinant Mouse Bestrophin-1 (Best1)

1. Data suggest that the ion channels CaV1.3, bestrophin-1 and maxiK were identified as players in the regulation of photoreceptor outer segments (POS) phagocytosis by the retinal pigment epithelium (RPE). PMID: 26427483
2. Best1-mediated astrocytic glutamate activates the synaptic N-methyl-D-aspartate receptor (NMDAR) and modulates NMDAR-dependent synaptic plasticity. PMID: 25645137
3. Bestrophin-1 functions as an intracellular Cl channel which helps to accumulate and to release Ca(2+) from stores by conducting the counterion for Ca(2+). PMID: 24664688
4. Best1, located at the microdomains near the synaptic junctions, has a significantly high permeability to glutamate in vivo. PMID: 24321245
5. Results show that different mutations in Best1 cause differential effects on its localization and that this effect varies with the presence or absence of wild-type (WT) Best1. PMID: 23825107
6. Astrocytic glutamate via Best1 channel targets and activates synaptic NMDA receptors. PMID: 23324492
7. Upon activation of protease activated receptor 1 (PAR1), an increase in intracellular Ca2+ concentration leads to an opening of Best1 channels and subsequent release of glutamate in cultured astrocytes. PMID: 23062602
8. Ultrastructural analyses demonstrate that TREK-1 is preferentially localized at cell body and processes, whereas Best1 is mostly found in microdomains of astrocytes near synapses. PMID: 23021213
9. study reports that tonic inhibition in the cerebellum is due to GABA being released from glial cells by permeation through the Bestrophin 1 anion channel PMID: 20929730
10. Retinal pigment bestrophin-1 possibly conducts Cl(-) as counter ion for Ca(2+) uptake into cytosolic Ca(2+) stores. PMID: 20411394
11. Data demonstrate that bestrophin 1 is localized in the endoplasmic reticulum (ER), where it interacts with the ER-Ca(2+) sensor and can enhance Ca(2+) signaling and activation of Ca(2+)-dependent Cl(-) (TMEM16A) and K(+) (SK4) channels. PMID: 19823864
12. cloning and characterization by combining biocomputational analyses and molecular genetic approaches PMID: 15218265
13. We suggest the loss of vision associated with Best vitelliform macular dystrophy is not caused by the same pathologic process as the diminished light peak, but is caused by an unidentified effect of best-1 [VMD2] on other cellular processes. PMID: 16636205
14. BEST1 may form the Ca2+-activated Cl(-) current, or it may be a component of a Cl(-) channel complex in epithelial tissues. PMID: 17003041
15. suggest a role of bestrophin 1 and 2 for Ca(2+) dependent Cl(-) secretion in mouse airways PMID: 18652850
16. This study provides the first characterization of the biophysical properties of mBest1 and a framework for the elucidation of the physiological role of bestrophins. PMID: 19426717
17. Repression of cell proliferation, induction of Ca(2+)-dependent Cl(-) conductance, and expression of Best1 occurs during mesenchymal-to-epithelial transition once renal collecting duct cells polarize and terminally differentiate. PMID: 19470678
18. Our data suggest that Best1 belongs to a group of genes upregulated by nerve injury and supports functional Ca(2+)-activated chloride current expression in injured sensory neurons PMID: 19675239
19. The data of this study provided molecular evidence that the Bestrophin-1 channel is responsible for Ca2+-activated anion channel function in astrocytes. PMID: 19828819

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KEGG: mmu:24115

STRING: 10090.ENSMUSP00000113053

UniGene: Mm.31577