[BK21 Plus Seminar]
              
                
             ▶Subject: Genetic Interrogation of Cellular Senescence
                        
             ▶Speaker: Chanhee Kang, Ph.D.
                       (Department of Genetics Brigham and Women’s Hospital, Harvard Medical School)
                                     
             ▶Date: 4:00PM/Aug. 24(Mon.)/2015
                     
             ▶Place: Life Science Bldg. #104
                      
                    *Abctract
              Cellular senescence is a terminal stress-activated program controlled by the p53 and p16INK4a tumor suppressor pathways that prevent abnormal cells from further proliferation. While a potent tumor suppressive mechanism, cellular senescence has been implicated in several pathological processes including aging and, counterintuitively, tumorigenesis. One potential mechanism through which senescent cells exert such pleiotropic effects is the expression and secretion of many proinflammatory cytokines, chemokines, growth factors, and proteases, a feature termed the senescence-associated secretory phenotype (SASP).
SASP factors can either reinforce senescence growth arrest in an autocrine manner or relay the senescence phenotype to surrounding cells in a paracrine manner. SASP factors can also stimulate adjacent premalignant and malignant cells to proliferate and form tumors. On the other hand, SASP factors can stimulate the immune system to both suppress tumorigenesis and promote optimal repair of damaged tissues. Lastly, SASP factors may directly or indirectly promote chronic inflammation that is thought to be a major factor in many, if not all, age-related diseases.
Despite the wide range of biological activities attributed to the SASP, little is known about how it is regulated beyond the classical regulators of inflammation. In contrast to senescence growth arrest in which the p53 and p16INK4a tumor suppressor pathways have a crucial role, the SASP does not depend on either p53 or p16INK4a, suggesting the existence of an independent senescence regulatory network that controls the SASP.
Moreover, in contrast to normal inflammatory responses that develop acutely, the SASP develops relatively slowly, normally taking several days after initiation of the senescence growth arrest to manifest, suggesting a senescence specific mechanism of activation.
Here, I will discuss the mechanism by which the SASP is initiated and maintained, including DNA damage response, selective autophagy, and a new branch of transcriptional circuit underlying cellular senescence.

            ▶Inquiry: Prof. Park, Sang Ki (279-2349)
                    
             * This seminar will be given in English.
     please refrain from taking photos during seminars. *