INSERM U1242 OSS - SPECIAL SEMINAR - Dr. Fatima SMAGULOVA - CR INSERM – U1242 - OSS - ASTER TEAM
"Role of epigenetic and chromatin compactization factors in DNA repair"
Dienstag 6 Oktober, 11:00
200
Role of epigenetic and chromatin compactization factors in DNA repair
Dr. Fatima SMAGULOVA
CR INSERM – U1242 - Oncogenesis Stress Signaling
ASTER TEAM
Abstract
DNA repair is vital for maintaining cellular homeostasis and genomic integrity. Among all forms of genomic instability, DNA double-strand breaks (DSBs) are the most deleterious; a failure to resolve these lesions directly triggers apoptosis or cell death. Mammalian cells rely on two primary pathways to repair DSBs: homologous recombination (HR) and non-homologous end joining (NHEJ). The pathway choice is tightly regulated by the cell cycle, and emerging evidence suggests that the surrounding epigenetic landscape predisposes this repair pathway selection. In this presentation, Fatima Smagulova will show how histone deacetylase (HDAC) inhibition alters the chromatin microenvironment and influences DSB repair pathway choice in a C57BL/6J mouse testis tissue, where is the physiological abundance of programmed DSBs during mammalian meiosis. In a second part, she will describe her new project in which she propose that that chromatin compactization and a transesion biosynthesis proteins play essential role in chemoresistence in small cell lung cancer. She will talk about objectives, strategy, methods, first results, and future directions and perspectives.
INSERM U1242 OSS - SPECIAL SEMINAR - Dr. Fatima SMAGULOVA - CR INSERM – U1242 - OSS - ASTER TEAM
"Role of epigenetic and chromatin compactization factors in DNA repair"
Dienstag 6 Oktober, 11:00
200
Role of epigenetic and chromatin compactization factors in DNA repair
Dr. Fatima SMAGULOVA
CR INSERM – U1242 - Oncogenesis Stress Signaling
ASTER TEAM
Abstract
DNA repair is vital for maintaining cellular homeostasis and genomic integrity. Among all forms of genomic instability, DNA double-strand breaks (DSBs) are the most deleterious; a failure to resolve these lesions directly triggers apoptosis or cell death. Mammalian cells rely on two primary pathways to repair DSBs: homologous recombination (HR) and non-homologous end joining (NHEJ). The pathway choice is tightly regulated by the cell cycle, and emerging evidence suggests that the surrounding epigenetic landscape predisposes this repair pathway selection. In this presentation, Fatima Smagulova will show how histone deacetylase (HDAC) inhibition alters the chromatin microenvironment and influences DSB repair pathway choice in a C57BL/6J mouse testis tissue, where is the physiological abundance of programmed DSBs during mammalian meiosis. In a second part, she will describe her new project in which she propose that that chromatin compactization and a transesion biosynthesis proteins play essential role in chemoresistence in small cell lung cancer. She will talk about objectives, strategy, methods, first results, and future directions and perspectives.
