Výsledky vyhledávání - "Fatih Abdula"

Akademický článek

Integrating leiomyoma genetics, epigenomics, and single-cell transcriptomics reveals causal genetic variants, genes, and cell types

Autor: Kadir Buyukcelebi, Alexander J. Duval, Fatih Abdula, Hoda Elkafas, Fidan Seker-Polat, Mazhar Adli

Publikováno v: Nature Communications, Vol 15, Iss 1, Pp 1-14 (2024)

Abstract Uterine fibroids (UF), that can disrupt normal uterine function and cause significant physical and psychological health problems, are observed in nearly 70% of women of reproductive age. Although heritable genetics is a significant risk fact

Externí odkaz: https://doaj.org/article/cb4cff71b346416789a546546ce12594

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Akademický článek

Engineered MED12 mutations drive leiomyoma-like transcriptional and metabolic programs by altering the 3D genome compartmentalization

Autor: Kadir Buyukcelebi, Xintong Chen, Fatih Abdula, Hoda Elkafas, Alexander James Duval, Harun Ozturk, Fidan Seker-Polat, Qiushi Jin, Ping Yin, Yue Feng, Serdar E. Bulun, Jian Jun Wei, Feng Yue, Mazhar Adli

Publikováno v: Nature Communications, Vol 14, Iss 1, Pp 1-15 (2023)

Abstract Nearly 70% of Uterine fibroid (UF) tumors are driven by recurrent MED12 hotspot mutations. Unfortunately, no cellular models could be generated because the mutant cells have lower fitness in 2D culture conditions. To address this, we employ

Externí odkaz: https://doaj.org/article/f796869116f04aa3836b1d309cad5481

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Integrative analysis of uterine leiomyoma genetics, epigenomics, and single-cell transcriptomics reveals causal genetic variants, gene targets, and cell types

Autor: Kadir Buyukcelebi, Fidan Seker-Polat, Fatih Abdula, Meric Kinali, Mazhar Adli

Uterine fibroids (UF), also called leiomyomas, are observed in nearly 70% of women of reproductive age. These tumors disrupt normal uterine function and cause significant physical and psychological health problems. Although heritable genetics is a si

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::d623f5ef8d10b68b1dfc3836b714a26b
https://doi.org/10.21203/rs.3.rs-2548537/v1

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Engineered MED12 mutations drive uterine fibroid-like transcriptional and metabolic programs by altering the 3D genome compartmentalization

Autor: Kadir Buyukcelebi, Xintong Chen, Fatih Abdula, Alexander Duval, Harun Ozturk, Fidan Seker-Polat, Qiushi Jin, Ping Yin, Yue Feng, Jian-Jun Wei, Serdar Bulun, Feng Yue, Mazhar Adli

Uterine fibroid (UF) tumors originate from a mutated smooth muscle cell (SMC). Nearly 70% of these tumors are driven by hotspot recurrent somatic mutations in the MED12 gene; however, there are no tractable genetic models to study the biology of UF t

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::32b45cfbb44aeb215080c69e17dfed95
https://doi.org/10.21203/rs.3.rs-2537075/v1

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