대학원 공지

— 세미나 시리즈 –

건국대학교 생명과학특성학과/대학원 생명과학과

4단계 BK21 미래통합형 생명과학 인재양성 사업단

Roles of translation initiation factor eIF2a phosphorylation

In response to various environmental stresses, a family of protein kinases phosphorylate the alpha subunit of eukaryotic translation initiation factor 2 (eIF2alpha) at Ser51 to alleviate cellular injury. Previous our reports elucidating the physiological role of eIF2alpha phosphorylation showed that mice with a homozygous mutation at the eIF2alpha phosphorylation site (Ser51Ala) died postnatally due to hypoglycemia associated with defective gluconeogenesis. In addition, homozygous mutant embryos and neonates displayed a deficiency in pancreatic beta cells. Moreover, the absence of eIF2alpha phosphorylation in fully differentiated pancreatic beta cells causes a severe diabetic phenotype due to unregulated proinsulin translation and deficiency of gene expression to effectively manage endoplasmic reticulum (ER) stress conditions. We concluded that regulation of translation through eIF2alpha phosphorylation is essential for the ER stress response and in vivo glucose homeostasis. Now we extended our study to other eIF2alpha phosphorylation-deficient differentiated cells. We have analyzed mice with hepatocyte-specific eIF2alpha phosphorylation deficiency. The analysis of eIF2alpha phosphorylation-deficient liver sections revealed hepatic cell death and development of liver fibrosis at 12 months of age. Furthermore, high fructose diet-feeding accelerated the hepatocyte cell death and liver fibrosis. We will discuss about possible mechanisms of the cell death in eIF2alpha phosphorylation-deficient hepatocytes.

연사: 백승훈 교수 (생명과학부, 울산대학교)

일시: 2021년 06월 01일 화요일. 오후 5시~6시

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