BEGIN:VCALENDAR

VERSION:2.0

PRODID:-//wp-events-plugin.com//7.2.2.1//EN

TZID:Asia/Jerusalem

X-WR-TIMEZONE:Asia/Jerusalem
BEGIN:VEVENT

UID:1280@biology.technion.ac.il

DTSTART;TZID=Asia/Jerusalem:20250513T130000

DTEND;TZID=Asia/Jerusalem:20250513T140000

DTSTAMP:20250427T083743Z

URL:https://biology.technion.ac.il/en/seminars/phd-graduate-seminar-laila-
 bishara/

SUMMARY:PhD Graduate Seminar-Laila Bishara [No Categories]
DESCRIPTION:Location: Biology auditorium\, https:https://technion.zoom.us/j
 /95485558065   Laila Bishara\n Affiliation: \n Host: Prof. Nabieh Ayoub\n 
 C8orf33: A novel regulator of DNA double strand break repair choice\n\nLiv
 ing organisms are continuously exposed to exogenous and endogenous DNA-dam
 aging agents that form DNA lesions. One of the most cytotoxic types of DNA
  lesions is double strand break (DSB) and its defective repair triggers ge
 nomic instability and carcinogenesis. DSBs are repaired through two main r
 epair pathways: homologous recombination (HR) and non-homologous end joini
 ng (NHEJ). While HR ensures accurate repair\, NHEJ is a rapid but mostly m
 utagenic repair pathway. Maintaining the balance between HR and NHEJ is cr
 ucial for preserving genomic stability. Consequently\, there is increasing
  interest in elucidating the molecular mechanisms that govern DSB repair p
 athway selection. Here\, we identify the uncharacterized C8orf33 protein a
 s a novel regulator of DSB repair choice. Our data reveal that C8orf33 is 
 a nuclear protein localized predominantly to the nucleolus and accumulates
  at DSB sites within both nuclear and nucleolar regions. We demonstrate th
 at C8orf33 promotes NHEJ and suppresses HR repair of DSBs. Mechanistically
 \, we show that C8orf33 alters the epigenetic mark histone 4 lysine 16 ace
 tylation (H4K16ac)\, which controls the recruitment of NHEJ and HR factors
  to DSB sites. Accordingly\, C8orf33 deficiency elevates HR repair which r
 esults in genomic instability\, as evidenced by the loss of nucleolar DNA 
 content and increased cell lethality. Collectively\, our findings establi
 sh C8orf33 as a critical regulator of DSB repair pathway choice\, safeguar
 ding genomic integrity. 
LOCATION:Biology auditorium\, https:https://technion.zoom.us/j/95485558065

END:VEVENT

BEGIN:VTIMEZONE

TZID:Asia/Jerusalem

X-LIC-LOCATION:Asia/Jerusalem

BEGIN:DAYLIGHT

DTSTART:20250328T030000

TZOFFSETFROM:+0200

TZOFFSETTO:+0300

TZNAME:IDT

END:DAYLIGHT

END:VTIMEZONE
END:VCALENDAR