1. 수상자/강연자: 정재웅 박사
(美 남가주대 KECK 의대 교수, KAIST 생명과학과 겸임교수)
2. 일시: 2012. 5. 2 (수) 오후 4시
3. 장소: KAIST KI빌딩(E4) 1층 퓨전홀
4. 주최: KAIST 생명과학과, KI 바이오융합연구소, ISBC 글로벌프론티어 연구단, KAIST-USC 글로벌연구소, 호암재단
* 강연 제목 및 초록
Host-Pathogen Standoff: Roles of Pattern Recognizing Receptors and Intracellular Restriction Factors in Antiviral Immune Response
Understanding the host-viral interaction is an essential step in developing safe and effective anti-microbials against viruses. Since virus is most vulnerable at the early stage of lifecycle, this stage should therefore offer the best opportunity for therapeutic interventions. The early detection of invading viruses by the host depends on a limited number of Pattern Recognizing Receptors (PRRs) that serve as the primary intracellular sensors for viral specific genetic patterns and activate signal transduction cascades, thereby triggering interferon (IFN)-mediated antiviral defense mechanisms. Key virus-detecting PRRs include the nucleic acid-recognizing Toll-like receptors and the cytosolic RNA receptors RIG-I and MDA-5. Specifically, RIG-I has emerged as a key receptor in sensing viruses, including the influenza virus and hepatitis virus C (HCV), whereas MDA5 responds to the infection of picornaviruses and noroviruses. Upon viral infection, RIG-I undergoes the multiple step processes of ATP-dependent structural and functional activations to elicit IFN-mediated antiviral signal transduction. In addition, members of the tripartite motif (TRIM) proteins and the Linear Ubiquitination Assembly Complex (LUBAC) proteins also play major roles in the IFN-mediated inhibition of the lifecycles of viruses.
Following the PRR-mediated viral sensing, hosts subsequently elicit intracellular
(美 남가주대 KECK 의대 교수, KAIST 생명과학과 겸임교수)
2. 일시: 2012. 5. 2 (수) 오후 4시
3. 장소: KAIST KI빌딩(E4) 1층 퓨전홀
4. 주최: KAIST 생명과학과, KI 바이오융합연구소, ISBC 글로벌프론티어 연구단, KAIST-USC 글로벌연구소, 호암재단
* 강연 제목 및 초록
Host-Pathogen Standoff: Roles of Pattern Recognizing Receptors and Intracellular Restriction Factors in Antiviral Immune Response
Understanding the host-viral interaction is an essential step in developing safe and effective anti-microbials against viruses. Since virus is most vulnerable at the early stage of lifecycle, this stage should therefore offer the best opportunity for therapeutic interventions. The early detection of invading viruses by the host depends on a limited number of Pattern Recognizing Receptors (PRRs) that serve as the primary intracellular sensors for viral specific genetic patterns and activate signal transduction cascades, thereby triggering interferon (IFN)-mediated antiviral defense mechanisms. Key virus-detecting PRRs include the nucleic acid-recognizing Toll-like receptors and the cytosolic RNA receptors RIG-I and MDA-5. Specifically, RIG-I has emerged as a key receptor in sensing viruses, including the influenza virus and hepatitis virus C (HCV), whereas MDA5 responds to the infection of picornaviruses and noroviruses. Upon viral infection, RIG-I undergoes the multiple step processes of ATP-dependent structural and functional activations to elicit IFN-mediated antiviral signal transduction. In addition, members of the tripartite motif (TRIM) proteins and the Linear Ubiquitination Assembly Complex (LUBAC) proteins also play major roles in the IFN-mediated inhibition of the lifecycles of viruses.
Following the PRR-mediated viral sensing, hosts subsequently elicit intracellular
