|開催日時：||2018年4月3日 16：00 〜 17：00|
|講師：||Mounira K Chelbi-Alix|
|所属：||Université Paris Descartes, Mechanism of interferon action / Director of Research at the CNRS|
|演題：||Role of PML and SUMO on intrinsic and innate immunity|
The tumor suppressor protein, promyelocytic leukemia protein (PML), was originally identified in acute promyelocytic leukemia (APL) due to a chromosomal translocation between chromosomes 15 and 17. Treatment of APL patients with arsenic trioxide (As2O3) reverses the disease phenotype by a process involving the degradation of the fusion protein via its PML moiety. PML is the organizer of nuclear structures named PML nuclear bodies (NBs). Several PML isoforms are generated from a single PML gene by alternative splicing. They share the same N-terminal region containing the RBCC/tripartite motif but differ in their C-terminal sequences. Recent studies of all the PML isoforms reveal the specific functions of each isoform. PML plays important roles in interferon (IFN) response and antiviral defense. PML confers viral resistance directly in an IFN-independent manner and also specifically enhances IFN production via a higher activation of IFN Regulatory Factor 3, thus implicating PML in both intrinsic and innate immunity.
|世話人：||〇高橋 理貴 （RNA医科学社会連携研究部門）