KCNMB1: A Protein Regulating Voltage-Dependent Ion Channels (G3779)

Target Name: KCNMB1

NCBI ID: G3779

KCNMB1

KCNMB1: A Protein Regulating Voltage-Dependent Ion Channels

KCNMB1 (k(VCA)beta-1) is a protein that is expressed in a variety of tissues, including the brain, heart, and kidneys. It is a key regulator of the voltage-dependent ion channels, which are responsible for the rapid flow of electrical signals through the cell. In recent years, researchers have become increasingly interested in studying the role of these channels in various physiological processes, including neurotransmission and muscle contractions.

One of the unique features of KCNMB1 is its ability to modulate the activity of other proteins. This is accomplished through a process called interaction, which involves the protein binding to a specific target protein and altering its activity. This interaction between proteins is often accompanied by changes in the structure and function of the target protein.

One of the most promising aspects of KCNMB1 is its potential as a drug target. Researchers have identified several potential binding sites on the protein that could be targeted by small molecules. These sites are located in the region between the N-terminus and the C- terminus of the protein, which is known as the alpha-helix region.

One of the most promising potential drug targets for KCNMB1 is its role in neurotransmission. The voltage-dependent ion channels that KCNMB1 regulates are involved in the rapid flow of electrical signals through the cell, which is critical for the transmission of neural signals. Alterations in the activity of these channels can have a profound impact on neurotransmission, including changes in the strength and duration of neural signals.

Research has shown that alterations in the activity of voltage-dependent ion channels, including those regulated by KCNMB1, can have a negative impact on neurotransmission. For example, studies have shown that blockers of the potassium channels, which are regulated by KCNMB1, can cause a decrease in the number of action potentials generated by neurons. This decrease in the number of action potentials can have a profound impact on the transmission of neural signals, including changes in the speed and reliability of neural communication.

Another potential drug target for KCNMB1 is its role in muscle contractions. The voltage-dependent ion channels that KCNMB1 regulates are also involved in the rapid flow of electrical signals through the muscle fibers, which is critical for muscle contractions. Alterations in the activity of these channels can have a profound impact on muscle contractions, including changes in the strength and duration of muscle fibers.

Research has shown that alterations in the activity of voltage-dependent ion channels, including those regulated by KCNMB1, can have a positive impact on muscle contractions. For example, studies have shown that activation of the sodium channels, which are regulated by KCNMB1, can cause an increase in the number of muscle fibers that contract during muscle contraction. This increase in the number of muscle fibers that contract can have a profound impact on muscle strength and endurance.

In addition to its potential as a drug target, KCNMB1 is also a potential biomarker for various diseases. Its ability to modulate the activity of other proteins makes it an attractive tool for the study of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease. These Conditions are characterized by the progressive loss of brain cells and the accumulation of neurofibrillary tangles, which are thought to contribute to the development and progression of these diseases.

Research has shown that altered levels of KCNMB1 are associated with the development and progression of neurodegenerative diseases. For example, studies have shown that individuals with Alzheimer's disease have lower levels of KCNMB1 compared to individuals without the disease. Similarly, research has shown that individuals with Parkinson's disease have higher levels of KCNMB1 compared to individuals without the disease.

In conclusion, KCNMB1 is a protein that is expressed in a variety of tissues and is involved in the regulation of voltage-dependent ion channels. Its ability to

Protein Name: Potassium Calcium-activated Channel Subfamily M Regulatory Beta Subunit 1

Functions: Regulatory subunit of the calcium activated potassium KCNMA1 (maxiK) channel. Modulates the calcium sensitivity and gating kinetics of KCNMA1, thereby contributing to KCNMA1 channel diversity. Increases the apparent Ca(2+)/voltage sensitivity of the KCNMA1 channel. It also modifies KCNMA1 channel kinetics and alters its pharmacological properties. It slows down the activation and the deactivation kinetics of the channel. Acts as a negative regulator of smooth muscle contraction by enhancing the calcium sensitivity to KCNMA1. Its presence is also a requirement for internal binding of the KCNMA1 channel opener dehydrosoyasaponin I (DHS-1) triterpene glycoside and for external binding of the agonist hormone 17-beta-estradiol (E2). Increases the binding activity of charybdotoxin (CTX) toxin to KCNMA1 peptide blocker by increasing the CTX association rate and decreasing the dissociation rate

The "KCNMB1 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about KCNMB1 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
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•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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