Introduction of CACNB3
CACNB3, also known as voltage-dependent L-type calcium channel subunit beta-3, is encoded by the CACNB3 gene. It belongs to the calcium channel beta subunit family which has been deeply studied during the past few years because it offers numerous possibilities for therapeutic applications. Recent studies show that mutations in the CACNB3 gene are associated with various diseases, such as attention-deficit, hyperactivity disorder, and bipolar disorder.
|Basic Information of CACNB3|
|Protein Name||Voltage-dependent L-type calcium channel subunit beta-3|
|Organism||Homo sapiens (Human)|
|Transmembrane Times||Peripheral membrane protein|
Function of CACNB3 Membrane Protein
As a voltage-dependent L-type calcium channel, CACNB3 plays a role in the regulation of transcription factors and calcium transport, as well as regulation of the expression and gating of calcium channels. It is one of the four homologous genes coding for the auxiliary Cavβ subunits, which are important modulators of the Ca2+ channel activity. Studies conducted on CACNB3 suggest it can be a potential biomarker for various diseases and provide new ideas for clinical therapy. By an extensive analysis of whole genome sequencing (WGS) in the context of intellectual disability (ID), scientists identify some de novo single nucleotide variants (SNVs) in CACNB3, such as c.1289G > A, which is associated with ID, providing the potential to diagnose idiopathic patients.
Fig.1 Structure of CACNB3 membrane protein.
Application of CACNB3 Membrane Protein in Literature
This article reports that the growth hormone secretagogue receptor type 1a (GHSR), a GPCR, can inhibit the forwarding trafficking of several CaV subtypes, even in the absence of agonist.
This article conducts a whole genome sequencing (WGS) on eight children with idiopathic Intellectual Disability (ID). The result shows that several SNP loci can be targets for ID diagnoses.
Authors in this group conduct a Genome-wide Association Study on Attention-deficit/hyperactivity disorder (ADHD) and bipolar disorder patients. These results indicate that a significant single nucleotide polymorphism-based genetic correlation between ADHD and BPD in the full and age-restricted samples.
This article evaluates the expression level of a variety of intercellular proteins, and try to identify the association between proteins and diseases. The data demonstrate that differences in the profile of mRNA encoding a variety of proteins are associated with the generation, conduction and regulation of electrical signals in the sinoatrial node of streptozotocin-induced diabetic rat heart.
This article examines whether loss of function in L-type calcium channels accounts for the attenuated response to lithium in BD cells. The results suggest that calcium signaling is abnormal, and that LTCCs underlie the failure of lithium to amplify circadian rhythms in bipolar disorder patients.
CACNB3 Preparation Options
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