KCNN1: A Potassium Intermediate/Small Conductance Calcium-Activated Channel Subfamily N Member 1

Target Name: KCNN1

NCBI ID: G3780

KCNN1

KCNN1: A Potassium Intermediate/Small Conductance Calcium-Activated Channel Subfamily N Member 1

Characterizing KCNN1: A Potassium Intermediate/Small Conductance Calcium-Activated Channel Subfamily N Member 1 and Its Potential as a Drug Target

Introduction

Potassium intermediate/small conductance calcium-activated channels (KCNNs) play a crucial role in various physiological processes, including neurotransmission, muscle contractions, and sensory perception. These channels are involved in the regulation of intracellular calcium levels and have been implicated in various neurological and psychiatric disorders. While several small molecule inhibitors have been identified as potential drug targets for KCNNs, the precise molecular mechanisms underlying their function remain poorly understood.

In this article, we will focus on the characterization of KCNN1, a member of the N-type KCNN channel subfamily. We will review its structure, function, and potential drug targets.

Structure and Function

KCNN1 is a single-channel, voltage-dependent potassium channel, which is expressed in various tissues, including brain, heart, and skeletal muscles. It is a member of the N-type KCNN channel subfamily, which is characterized by the presence of a single voltage-dependent ion channel and a unique selectivity for calcium ions.

KCNN1 is expressed in the brain and plays a crucial role in neurotransmission, particularly in the regulation of action potentials. It has been shown to be involved in the regulation of synaptic plasticity, learning, and memory.

In addition to its role in neurotransmission, KCNN1 is also involved in the regulation of muscle contractions. It has been shown to play a role in the regulation of muscle fibers, including the rapid regulation of muscle contractions that is critical for muscle performance.

KCNN1 is also involved in the regulation of pain perception. It has been shown to play a role in the regulation of pain modulation, particularly in the regulation of neuropeptides that mediate pain modulation.

Potential Drug Targets

Several small molecules have been identified as potential drug targets for KCNNs. These molecules act by modulating the activity of KCNN1, leading to changes in cellular behavior.

One of the most well-known small molecules is amiloride, which is a known inhibitor of sodium channels. Amiloride has been shown to inhibit the activity of KCNN1, reducing its ability to regulate calcium ions in the brain.

Another small molecule that has been shown to be a potential drug target for KCNNs is nifedipine, which is an inhibitor of angiotensin II, a potent regulator of blood pressure. Nifedipine has been shown to inhibit the activity of KCNN1, reducing its ability to regulate calcium ions in the body.

In addition to these drugs, several other small molecules have also been shown to be potential drug targets for KCNNs. These molecules include verapamil, diltiazem, and flecainide.

Conclusion

In conclusion, KCNN1 is a member of the N-type KCNN channel subfamily that plays a crucial role in various physiological processes. Its function is regulated by small molecules, including amiloride and nifedipine. These molecules have been shown to inhibit the activity of KCNN1, reducing its ability to regulate calcium ions in the brain and body.

While further studies are needed to fully understand the precise molecular mechanisms underlying the function of KCNN1 and its potential as a drug target, the characterization of this channel provides new insights into the complex physiological processes that are involved in its regulation.

Protein Name: Potassium Calcium-activated Channel Subfamily N Member 1

Functions: Forms a voltage-independent potassium channel activated by intracellular calcium (PubMed:8781233, PubMed:9287325, PubMed:17142458). Activation is followed by membrane hyperpolarization (By similarity). Thought to regulate neuronal excitability by contributing to the slow component of synaptic afterhyperpolarization (By similarity)

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