MedElevator Войти в исследования
← Поиск публикаций
Reproductive sciences (Thousand Oaks, Calif.) · 2026

Insilico Analysis of CYP17A1 in the Pathogenesis of Polycystic Ovarian Syndrome by Molecular Dynamics and Genotypic Characterization.

СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…

История · было → стало

Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.

Vetriselvan Yogesh, Murugan Manoranjani, Samantaray Mahesh, Ganesh Irisappan, Jayakumar Swetha, Samuel Melissa Shaelyn, Singh Sarman, Shanmugam Deepa, Ravikumar Sambandam

Аннотация

CYP17A1 gene (Cytochrome P45017A1) plays a significant role in the steroidogenic pathway that synthesizes sex steroids and glucocorticoids. In Cytochrome P45017A1, the heme-binding domain region is essential for its catalytic function to synthesize steroids. Mutations in the CYP17A1 gene have been associated with several pathological conditions, including congenital adrenal hyperplasia, Polycystic Ovary Syndrome (PCOS), now referred to as Polyendocrine Metabolic Ovarian Syndrome (PMOS), and certain types of cancers. This study aimed to identify deleterious missense mutations in CYP17A1 using in silico tools, molecular dynamics simulations, and genotyping to detect both rare and common variants. In silico analyses identified 22 pathogenic mutations using sequence- and structure-based tools. Furthermore, the mutations in the heme-binding domain (F453S, R449C) were characterized using molecular dynamics simulations. Results of Molecular dynamics simulations show that CYP17A1 mutants exhibit significant structural changes, particularly in the heme and steroid-binding regions, which weaken heme coordination and alter heme affinity. Based on the high minor allele frequency (MAF) of 0.04% in the South Indian population, the common variant rs743572 was genotyped in a cohort of (n = 100 PMOS cases and n = 90 healthy controls) to assess its population distribution and potential regulatory role in hormone-related disorders. These changes indicate functional impairments in steroidogenesis, informing the development of targeted therapies for related disorders. Thus, our findings offer valuable insights into the genetic basis of CYP17A1 dysregulation and highlight the need for precision medicine in targeting therapeutics for related disorders.