CACNB3: A Calcium-Regulated Voltage-Gated Channel Subunit for Drug Targets and Biomarkers

Target Name: CACNB3

NCBI ID: G784

CACNB3: A Calcium-Regulated Voltage-Gated Channel Subunit for Drug Targets and Biomarkers

Introduction

CACNB3, also known as calcium-regulated voltage-gated channel auxiliary subunit beta 3, is a highly conserved gene that is expressed in various tissues and cell types in the human body. It is a member of the voltage-gated channel subfamily, which is a crucial group of transmembrane proteins that play a central role in electrical signaling. The尾3 subunit is involved in the regulation of intracellular calcium (Ca2+) levels, which is a critical signaling molecule that plays a pivotal role in various cellular processes, including muscle contractions, neurotransmitter release, and chromatin regulation.

CACNB3 is a G protein-coupled receptor (GPCR), which means that it is a transmembrane protein that uses a protein called G protein to communicate with intracellular signaling pathways. GPCR signaling pathways are involved in a wide range of physiological processes, including cell growth , differentiation, and survival. The CACNB3 gene has been well-studied, and numerous studies have identified its involvement in various physiological processes, including neuronal excitability and synaptic plasticity.

Drug Targets and Biomarkers

The CACNB3 gene is an attractive drug target due to its involvement in multiple signaling pathways. The CACNB3 gene has been shown to play a role in neuronal excitability and synaptic plasticity, which makes it an attractive target for drugs that aim to modulate these processes. One of the main classes of drugs that are known to modulate CACNB3 function is the beta-adrenergic antagonists, which are commonly used to treat hypertension and heart failure. These drugs work by blocking the activity of the beta1 adrenergic receptor, which is a GPCR that is involved in cardiovascular and respiratory signaling. By blocking the activity of this receptor, beta-adrenergic antagonists can reduce the contractile activity of smooth muscle cells and decrease the levels of intracellular Ca2+.

Another class of drugs that are known to modulate CACNB3 function are the inhibitors of the voltage-gated K channels, which are involved in the regulation of action potentials. These drugs work by blocking the ability of these channels to regulate the flow of Ca2+ into the cell, which can lead to increased levels of intracellular Ca2+ and increased muscle contractions.

Biomarkers

The CACNB3 gene has been shown to play a role in various biological processes, including neuronal excitability and synaptic plasticity. One of the main biomarkers for CACNB3 function is the level of intracellular Ca2+. Using techniques such as immunofluorescence and biochemical assays, researchers have shown that the levels of Ca2+ in the cells can be modulated by various factors, including the levels of Ca2+ in the diet, exercise, and environmental factors. These changes in Ca2+ levels can have a significant impact on cellular processes, including muscle contractions, neurotransmitter release, and chromatin regulation.

Another biomarker for CACNB3 function is the expression of the CACNB3 gene. Researchers have used techniques such as qRT-PCR and RNA sequencing to show that the expression of the CACNB3 gene is highly correlated with the levels of intracellular Ca2+. These studies have identified a positive correlation between the levels of Ca2+ and the expression of the CACNB3 gene.

Conclusion

CACNB3 is a well-conserved gene that is involved in the regulation of various physiological processes, including neuronal excitability and synaptic plasticity. Its function is closely tied to the regulation of intracellular Ca2+ levels, which is a critical signaling molecule that plays a central role in

Protein Name: Calcium Voltage-gated Channel Auxiliary Subunit Beta 3

Functions: Regulatory subunit of the voltage-gated calcium channel that gives rise to L-type calcium currents (PubMed:8119293). Increases CACNA1B peak calcium current and shifts the voltage dependencies of channel activation and inactivation (By similarity). Increases CACNA1C peak calcium current and shifts the voltage dependencies of channel activation and inactivation (By similarity)

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