| ID | Sequence | Length | GC content |
|---|---|---|---|
| GCAUUGGCGCGGGGAGGAGCAGGGAUCUUGGCAGCGGGCGAGGAGGCUG… | 1841 nt | 0.5747 | |
| GCAUUGGCGCGGGGAGGAGCAGGGAUCUUGGCAGCGGGCGAGGAGGCUG… | 1647 nt | 0.5689 | |
| GCAUUGGCGCGGGGAGGAGCAGGGAUCUUGGCAGCGGGCGAGGAGGCUG… | 1814 nt | 0.5728 | |
| GCAUUGGCGCGGGGAGGAGCAGGGAUCUUGGCAGCGGGCGAGGAGGCUG… | 1769 nt | 0.5726 | |
| GCAUUGGCGCGGGGAGGAGCAGGGAUCUUGGCAGCGGGCGAGGAGGCUG… | 1702 nt | 0.5699 | |
| GCAUUGGCGCGGGGAGGAGCAGGGAUCUUGGCAGCGGGCGAGGAGGCUG… | 1778 nt | 0.5692 | |
| GCAUUGGCGCGGGGAGGAGCAGGGAUCUUGGCAGCGGGCGAGGAGGCUG… | 1733 nt | 0.5690 |
Members of arrestin/beta-arrestin protein family are thought to participate in agonist-mediated desensitization of G-protein-coupled receptors and cause specific dampening of cellular responses to stimuli such as hormones, neurotransmitters, or sensory signals. Arrestin beta 2, like arrestin beta 1, was shown to inhibit beta-adrenergic receptor function in vitro. It is expressed at high levels in the central nervous system and may play a role in the regulation of synaptic receptors. Besides the brain, a cDNA for arrestin beta 2 was isolated from thyroid gland, and thus it may also be involved in hormone-specific desensitization of TSH receptors. Multiple alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Mar 2012]
A study in porcine skin exposed to bromine vapor demonstrated that the ARRB2 gene was significantly upregulated, showing an approximate 2.4-fold increase in both 10-minute and 20-minute exposure groups at 48 hours post-exposure, identifying it as a component within the significantly altered signaling pathways [Rogers et al. DOI:10.1002/jbt.20383]. In a separate investigation of severe burn injury progression in a mouse model, the ARRB2 was identified by other researchers as a potential key gene involved in the treatment of major burn injuries and the prevention of complications [Wu et al. DOI:10.007/s10753-019-00984-5].