Mara Sannai

ORCID: 0000-0001-9634-004X
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • DNA Repair Mechanisms
  • Epigenetics and DNA Methylation
  • Genomics and Chromatin Dynamics
  • PARP inhibition in cancer therapy
  • Endoplasmic Reticulum Stress and Disease
  • Genetics and Neurodevelopmental Disorders
  • Pluripotent Stem Cells Research
  • RNA regulation and disease
  • CRISPR and Genetic Engineering
  • Cellular transport and secretion
  • Genetic factors in colorectal cancer
  • Marine Ecology and Invasive Species
  • Nuclear Structure and Function
  • Planarian Biology and Electrostimulation
  • Microtubule and mitosis dynamics
  • Integrated Circuits and Semiconductor Failure Analysis

Leibniz Institute on Aging - Fritz Lipmann Institute (FLI)
2020-2023

Fox Chase Cancer Center
2011-2019

Leibniz Association
2011

COPII and COPI mediate the formation of membrane vesicles translocating in opposite directions within secretory pathway. Live-cell electron microscopy revealed a novel mode function for during cargo export from ER. is recruited to membranes defining boundary between ER exit sites, facilitating selective concentration. Using direct observation living cells, we monitored selection processes, accumulation, fission COPII-free ERES membranes. CRISPR/Cas12a tagging, RUSH system, pharmaceutical...

10.1083/jcb.201907224 article EN cc-by-nc-sa The Journal of Cell Biology 2021-04-14

Article10 December 2020Open Access Transparent process Tnfaip2/exoc3-driven lipid metabolism is essential for stem cell differentiation and organ homeostasis Sarmistha Deb orcid.org/0000-0002-2702-3881 Leibniz Institute on Aging – Fritz Lipmann e.V., Jena, Germany Search more papers by this author Daniel A Felix Philipp Koch orcid.org/0000-0003-2825-7943 Maharshi Krishna orcid.org/0000-0003-0026-6194 Karol Szafranski orcid.org/0000-0001-6391-1766 Katrin Buder Mara Sannai Marco Groth...

10.15252/embr.201949328 article EN cc-by EMBO Reports 2020-12-10

Abstract MCPH1 is a causal gene for the neurodevelopmental disorder, human primary microcephaly (MCPH1, OMIM251200). Most pathogenic mutations are located in N-terminal region of gene, which encodes BRCT domain, suggesting an important function this domain brain size determination. To investigate specific vivo, we generated mouse model lacking N’-BRCT (referred as Mcph1 -ΔBR1). These mutant mice viable, but exhibit reduced size, with thinner cortex due to reduction neuroprogenitor...

10.1038/s41419-021-03406-3 article EN cc-by Cell Death and Disease 2021-02-01

Poly(ADP-ribose) polymerase-1 (PARP1) binds DNA lesions to catalyse poly(ADP-ribosyl)ation (PARylation) using NAD+ as a substrate. PARP1 plays multiple roles in cellular activities, including repair, transcription, cell death, and chromatin remodelling. However, whether these functions are governed by the enzymatic activity or scaffolding function of remains elusive. In this study, we inactivated mice truncating its C-terminus that is essential for ART catalysis (PARP1ΔC/ΔC, designated...

10.3390/cells12162078 article EN cc-by Cells 2023-08-16

Abstract Exit from the endoplasmic reticulum is mediated by Sar1/COPII machinery and a number of accessory factors. How initial steps cargo recruitment upstream are remains unclear, but dihydropyridine FLI-06 inhibits into ER exit sites. Here, we used chemical genetics screening approaches in conjunction with treatment identified membrane proteins YIPF5 GOT1A/B as putative components early export processes. Surprisingly, two homologous GOT1A GOT1B, coded GOLT1A GOLT1B , respectively,...

10.1101/2023.12.12.569033 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-12-12
Coming Soon ...