CEP152: A Potential Drug Target and Biomarker for Chronic Obstructive Pulmonary Disease

Target Name: CEP152

NCBI ID: G22995

CEP152

CEP152: A Potential Drug Target and Biomarker for Chronic Obstructive Pulmonary Disease

Abstract:

Chronic Obstructive Pulmonary Disease (COPD) is a leading cause of morbidity and mortality worldwide, characterized by progressive lung airflow obstruction and decline in lung function. The most common genetic variant associated with COPD is the CEP152 variant, which has been shown to increase the risk of COPD development in individuals with a family history of the disease. This variant has also been associated with increased airway resistance and decreased lung expansion, leading to reduced lung function and increased morbidity. The aim of this article is to provide an overview of CEP152, its association with COPD, and its potential as a drug target and biomarker.

Introduction:

COPD is a progressive lung disease that is caused by the chronic obstruction of airflow to the lungs, leading to progressive lung airflow obstruction and decline in lung function. It is a leading cause of morbidity and mortality worldwide, with an estimated 15 million people worldwide diagnosed with COPD. COPD is a complex disease that is associated with various genetic and environmental factors, including smoking, air pollution, and genetics. The most common genetic variant associated with COPD is the CEP152 variant, which has been shown to increase the risk of COPD development in individuals with a family history of the disease.

The CEP152 variant is a single nucleotide polymorphism (SNP) in the exon 22 of the B33 gene, which encodes for the proteinase-activated receptor 1 (PAR-1). PAR-1 is a G protein-coupled receptor (GPCR) that plays a critical role in airway regulation and is expressed in the airways of the lungs. The CEP152 variant has been shown to increase the expression of PAR-1, leading to increased airway resistance and decreased lung expansion, leading to reduced lung function and increased morbidity.

CEP152 and COPD:

The CEP152 variant has been shown to increase the risk of COPD development in individuals with a family history of the disease. Studies have shown that individuals with a family history of COPD are more likely to have the CEP152 variant than those without a family history of the disease. The CEP152 variant has also been associated with increased airway resistance and decreased lung expansion, leading to reduced lung function and increased morbidity.

The impact of CEP152 on COPD severity:

The severity of COPD is determined by various factors, including spirometry results, lung function tests, and symptoms. Studies have shown that individuals with the CEP152 variant have more severe COPD than those without the variant. This is thought to be due to the increased airway resistance and decreased lung expansion, which can lead to reduced lung expansion and decreased oxygenation of the lungs.

The potential role of CEP152 as a drug target:

The CEP152 variant has been shown to increase the expression of PAR-1, leading to increased airway resistance and decreased lung expansion, leading to reduced lung function and increased morbidity. The potential role of CEP152 as a drug target is to target the PAR-1 protein and prevent its increased expression, leading to decreased airway resistance and increased lung expansion, leading to improved lung function and reduced morbidity.

The potential role of CEP152 as a biomarker:

The CEP152 variant has been shown to increase the risk of COPD development in individuals with a family history of the disease. The potential role of CEP152 as a biomarker for COPD is to

Protein Name: Centrosomal Protein 152

Functions: Necessary for centrosome duplication; the function seems also to involve CEP63, CDK5RAP2 and WDR62 through a stepwise assembled complex at the centrosome that recruits CDK2 required for centriole duplication (PubMed:26297806). Acts as a molecular scaffold facilitating the interaction of PLK4 and CENPJ, 2 molecules involved in centriole formation (PubMed:21059844, PubMed:20852615). Proposed to snatch PLK4 away from PLK4:CEP92 complexes in early G1 daughter centriole and to reposition PLK4 at the outer boundary of a newly forming CEP152 ring structure (PubMed:24997597). Also plays a key role in deuterosome-mediated centriole amplification in multiciliated that can generate more than 100 centrioles (By similarity). Overexpression of CEP152 can drive amplification of centrioles (PubMed:20852615)

The "CEP152 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 CEP152 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;
•   related patent analysis;
•   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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