Anne‐Laure Pauleau

ORCID: 0000-0002-0242-6756
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About
Contact & Profiles
Research Areas
  • Genomics and Chromatin Dynamics
  • Microtubule and mitosis dynamics
  • Cell death mechanisms and regulation
  • Toxoplasma gondii Research Studies
  • Chromosomal and Genetic Variations
  • DNA Repair Mechanisms
  • Cytomegalovirus and herpesvirus research
  • Animal Virus Infections Studies
  • Cytokine Signaling Pathways and Interactions
  • Viral gastroenteritis research and epidemiology
  • Immune Response and Inflammation
  • Mitochondrial Function and Pathology
  • S100 Proteins and Annexins
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Plant Molecular Biology Research
  • Virus-based gene therapy research
  • Hepatitis B Virus Studies
  • Immune cells in cancer
  • Redox biology and oxidative stress
  • Endoplasmic Reticulum Stress and Disease
  • Helicobacter pylori-related gastroenterology studies
  • Neuroendocrine regulation and behavior
  • Sulfur Compounds in Biology
  • IL-33, ST2, and ILC Pathways
  • Protein Kinase Regulation and GTPase Signaling

Heidelberg University
2011-2019

DKFZ-ZMBH Alliance
2011-2019

University of Copenhagen
2018

Institut Gustave Roussy
2004-2012

Université Paris-Sud
2007-2012

Université Paris-Saclay
2007-2012

Inserm
2007-2012

German Cancer Research Center
2008

Centre National de la Recherche Scientifique
2003-2005

St. Jude Children's Research Hospital
2003-2004

Autophagic cell death is morphologically characterized by an accumulation of autophagic vacuoles. Here, we show that inactivation LAMP2 RNA interference or homologous recombination leads to vacuolization in nutrient-depleted cells. Cells lack expression showed enhanced vacuoles carrying the marker LC3, yet a decreased colocalization LC3 and lysosomes, suggesting fusion between lysosomes was inhibited. While fraction mitochondria from starved LAMP2-expressing cells colocalized with lysosomal...

10.1242/jcs.02447 article EN Journal of Cell Science 2005-06-29

Nod2 (CARD15) is a macrophage-specific protein containing two CARD domains, large nucleotide binding domain and leucine-rich repeats. Human genetic studies have linked mutations in NOD2/CARD15 with Crohn's disease, although the mechanisms involved are unknown. However, has been proposed to directly bind bacterial lipopolysaccharide (LPS) subsequently act as an activator of NF-κB via association domains Rip2/RICK/CARDIAK. This hypothesized constitute pathogen recognition pathway distinct from...

10.1128/mcb.23.21.7531-7539.2003 article EN Molecular and Cellular Biology 2003-10-15

Abstract Arginase I expression in the liver must remain constant throughout life to eliminate excess nitrogen via urea cycle. In contrast, arginase macrophages is silent until signals from Th2 cytokines such as IL-4 and IL-13 are received mRNA then induced four five orders of magnitude. hypothesized play a regulatory potentially pathogenic role diseases asthma, parasitic, bacterial, worm infections by modulating NO levels promoting fibrosis. We show that Th2-inducible mouse controlled an...

10.4049/jimmunol.172.12.7565 article EN The Journal of Immunology 2004-06-15

The viral mitochondria-localized inhibitor of apoptosis (vMIA), encoded by the UL37 gene human cytomegalovirus, inhibits apoptosis-associated mitochondrial membrane permeabilization a mechanism different from that Bcl-2. Here we show vMIA induces several changes in Bax resemble those found apoptotic cells yet take place unstimulated, non-apoptotic vMIA-expressing cells. These include constitutive localization at mitochondria, where it associates tightly with membrane, forming high molecular...

10.1074/jbc.m308408200 article EN cc-by Journal of Biological Chemistry 2004-05-01

Replication of human cytomegalovirus (CMV) requires the expression viral mitochondria–localized inhibitor apoptosis (vMIA). vMIA inhibits by recruiting Bax to mitochondria, resulting in its neutralization. We show that decreases cell size, reduces actin polymerization, and induces rounding. As compared with vMIA-expressing CMV, vMIA-deficient which replicates fibroblasts expressing adenoviral suppressor E1B19K, less cytopathic effects. These effects can be separated from death–inhibitory...

10.1083/jcb.200604069 article EN The Journal of Cell Biology 2006-09-18

Chromatin reorganization and the incorporation of specific histone modifications during DNA damage response are essential steps for successful repair any lesion. Here, we show that histone-fold protein CHRAC14 plays an role in to Drosophila. Chrac14 mutants hypersensitive genotoxic stress do not activate G2/M cell-cycle checkpoint after induction. Even though process is activated absence CHRAC14, lesions repaired efficiently. In centromere-specific H3 variant CENP-A localizes sites damage,...

10.1016/j.celrep.2014.03.008 article EN cc-by-nc-nd Cell Reports 2014-04-01

Article11 December 2018Open Access Transparent process TIAR marks nuclear G2/M transition granules and restricts CDK1 activity under replication stress Vanesa Lafarga Corresponding Author [email protected] German Cancer Research Center (DKFZ), Heidelberg, Germany for Molecular Biology of Heidelberg University (ZMBH), DKFZ-ZMBH Alliance, Spanish National Centre (CNIO), Madrid, Spain Search more papers by this author Hsu-Min Sung orcid.org/0000-0001-6498-4254 Division Biochemistry, Biomedicine...

10.15252/embr.201846224 article EN cc-by EMBO Reports 2018-12-11

A defining feature of centromeres is the presence histone H3 variant CENP-A that replaces in a subset centromeric nucleosomes. In Drosophila cultured cells deposition at takes place during metaphase stage cell cycle and strictly depends on its specific chaperone CAL1. How loading restricted to mitosis unknown. We found overexpression CAL1 associated with increased levels uncouples from mitosis. Moreover, inversely correlate duration suggesting crosstalk regulatory machinery Mitosis length...

10.1371/journal.pgen.1008380 article EN cc-by PLoS Genetics 2019-09-25

Abstract A defining feature of centromeres is the presence histone H3 variant CENP-A that replaces in a subset centromeric nucleosomes. In Drosophila cultured cells deposition at takes place during metaphase stage cell cycle and strictly depends on its specific chaperone CAL1. How loading restricted to mitosis unknown. We found overexpression CAL1 associated with increased levels completely uncouples from mitosis. Moreover, inversely correlate duration. interacts spindle assembly checkpoint...

10.1101/394981 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2018-08-17
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