CACNB3 Membrane Protein Introduction

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
Gene Name	CACNB3
Aliases	CACNLB3
Organism	Homo sapiens (Human)
UniProt ID	P54284
Transmembrane Times	Peripheral membrane protein
Length (aa)	484
Sequence	MYDDSYVPGFEDSEAGSADSYTSRPSLDSDVSLEEDRESARREVESQAQQQLERAKHKPVAFAVRTNVSYCGVLDEECPVQGSGVNFEAKDFLHIKEKYSNDWWIGRLVKEGGDIAFIPSPQRLESIRLKQEQKARRSGNPSSLSDIGNRRSPPPSLAKQKQKQAEHVPPYDVVPSMRPVVLVGPSLKGYEVTDMMQKALFDFLKHRFDGRISITRVTADLSLAKRSVLNNPGKRTIIERSSARSSIAEVQSEIERIFELAKSLQLVVLDADTINHPAQLAKTSLAPIIVFVKVSSPKVLQRLIRSRGKSQMKHLTVQMMAYDKLVQCPPESFDVILDENQLEDACEHLAEYLEVYWRATHHPAPGPGLLGPPSAIPGLQNQQLLGERGEEHSPLERDSLMPSDEASESSRQAWTGSSQRSSRHLEEDYADAYQDLYQPHRQHTSGLPSANGHDPQDRLLAQDSEHNHSDRNWQRNRPWPKDSY

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

Mustafá E.R., et al. Constitutive activity of the Ghrelin receptor reduces surface expression of voltage-gated Ca²⁺ channels in a CaVβ-dependent manner. J Cell Sci. 2017, 130(22): 3907-3917. PubMed ID: 29038230

This article reports that the growth hormone secretagogue receptor type 1a (GHSR), a GPCR, can inhibit the forwarding trafficking of several Ca_V subtypes, even in the absence of agonist.
Zahir F.R., et al. Comprehensive whole genome sequence analyses yield novel genetic and structural insights for Intellectual Disability. BMC Genomics. 2017, 18(1): 403. PubMed ID: 28539120

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.
van Hulzen K.J.E., et al. Genetic Overlap Between Attention-Deficit/Hyperactivity Disorder and Bipolar Disorder: Evidence From Genome-wide Association Study Meta-analysis. Biol Psychiatry. 2017: 82(9): 634-641. PubMed ID: 27890468

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.
Ferdous Z., et al. Different Profile of mRNA Expression in Sinoatrial Node from Streptozotocin-Induced Diabetic Rat. PLoS One. 2016, 11(4): e0153934. PubMed ID: 27096430

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.
McCarthy M.J., et al. Calcium channel genes associated with bipolar disorder modulate lithium's amplification of circadian rhythms. Neuropharmacology. 2016, 101: 439-48. PubMed ID: 26476274

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

To obtain the soluble and functional target protein, the versatile Magic™ membrane protein production platform in Creative Biolabs enables many flexible options, from which you can always find a better match for your particular project. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-CACNB3 antibody development services.

As a forward-looking research institute as well as a leading custom service provider in the field of membrane protein, Creative Biolabs has won good reputation among our worldwide customers for successfully accomplishing numerous challenging projects including generation of many functional membrane proteins. Please feel free to contact us for more information.

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