Olivier Lohez

ORCID: 0000-0001-9446-9915
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About
Contact & Profiles
Research Areas
  • Cancer-related Molecular Pathways
  • Microtubule and mitosis dynamics
  • Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • Autophagy in Disease and Therapy
  • Ubiquitin and proteasome pathways
  • Hormonal Regulation and Hypertension
  • Mitochondrial Function and Pathology
  • Endoplasmic Reticulum Stress and Disease
  • 14-3-3 protein interactions
  • Cell death mechanisms and regulation
  • RNA Interference and Gene Delivery
  • RNA and protein synthesis mechanisms
  • Advanced biosensing and bioanalysis techniques
  • Gene expression and cancer classification
  • Cancer Genomics and Diagnostics
  • Eicosanoids and Hypertension Pharmacology
  • Adrenal Hormones and Disorders
  • Cancer Research and Treatments
  • Bioinformatics and Genomic Networks
  • Renin-Angiotensin System Studies
  • Genomic variations and chromosomal abnormalities

Inserm
2012-2024

Université Claude Bernard Lyon 1
2006-2024

Centre National de la Recherche Scientifique
2002-2024

Centre Léon Bérard
2021-2024

Centre de Recherche en Cancérologie de Lyon
2021-2024

Hôpital Nord
2014-2015

Institut de Biologie et de Chimie des Protéines
2006

École Normale Supérieure de Lyon
2006

Université Joseph Fourier
2003

Université Grenoble Alpes
2001-2003

A “spindle assembly” checkpoint has been described that arrests cells in G1 following inappropriate exit from mitosis the presence of microtubule inhibitors. We have here addressed question whether resulting tetraploid state itself, rather than failure spindle function or induction damage, acts as a to arrest G1. Dihydrocytochalasin B induces cleavage where and chromatid segregation are both normal. Notably, we show nontransformed REF-52 indefinitely failure. The assembly tetraploidization...

10.1091/mbc.12.5.1315 article EN Molecular Biology of the Cell 2001-05-01

A high degree of aneuploidy characterizes the majority human tumors. Aneuploid status can arise through mitotic or cleavage failure coupled with tetraploid G 1 checkpoint control, deregulation centrosome number, thus altering number spindle poles. p53 and RB pocket proteins are important to control progression, has previously been suggested as duplication. We demonstrate here that neither suppression nor protein family directly generates altered numbers in any several mammalian primary cell...

10.1073/pnas.152205299 article EN Proceedings of the National Academy of Sciences 2002-07-15

Abstract Apoptosis plays a role in cell homeostasis both normal development and disease. Bcl-xL, member of the Bcl-2 family proteins, regulates intrinsic mitochondrial pathway apoptosis. It is overexpressed several cancers. Bcl-xL has dual subcellular localisation found at mitochondria as well endoplasmic reticulum (ER). However, biological significance its ER unclear. In order to decipher functional contributions reticular pools we generated genetically modified mice expressing exclusively...

10.1038/s41420-024-02112-1 article EN cc-by Cell Death Discovery 2024-08-01

p53 and the retinoblastoma (RB) pocket proteins are central to control of progression through G1 phase cell cycle. The RB protein family is downstream controls S-phase entry. Disruption actin assembly arrests nontransformed mammalian fibroblasts in G1. We show that this arrest requires intact function, but surprisingly does not require p53. Thus, with normal function reversibly on exposure inhibitors regardless their status. By contrast, triple knockout mouse embryo T antigen–transformed rat...

10.1083/jcb.200208140 article EN The Journal of Cell Biology 2003-04-07

Abstract High cortisol and aldosterone levels increase cardiovascular risk, but the respective roles of each hormone within arterial wall remain controversial. We tested hypothesis that production may contribute to atherosclerotic remodeling act through illicit activation mineralocorticoid receptor ( MR ). Gene expression studies corticoid system components marker genes process in human carotid atheroma plaque nearby macroscopically intact tissue MIT ) were considered together with clinical...

10.1111/j.1472-8206.2012.01064.x article EN Fundamental and Clinical Pharmacology 2012-07-20

Non-lethal caspase activation (NLCA) has been linked to neurodevelopmental processes. However, how neurons control NLCA remains elusive. Here, we focused on Bcl-xL, a Bcl-2 homolog regulating through the mitochondria. We generated mouse model, referred as ER-xL, in which Bcl-xL is absent mitochondria, yet present endoplasmic reticulum. Unlike

10.1016/j.isci.2023.106674 article EN cc-by-nc-nd iScience 2023-04-14

We will summarize the data we have obtained in human carotid artery concerning organization of an extended local renin angiotensin aldosterone system and its variations at different stages atheroma. In a view, propose model where concomitant increase glucocorticoid signaling is induced amplified VSMC while vascular smooth muscle cells transdifferentiate toward lipid storing phenotype.

10.1155/2015/593086 article EN cc-by Conference Papers in Science 2015-05-18

Abstract Apoptosis plays a role in cell homeostasis both normal development and disease. Bcl-xL, member of the Bcl-2 family proteins, regulates intrinsic mitochondrial pathway apoptosis. It is overexpressed several cancers. Bcl-xL has dual subcellular localization found at mitochondria as well endoplasmic reticulum (ER). However, biological significance its ER unclear. In order to decipher functional contributions reticular pools we generated genetically modified mice expressing exclusively...

10.1101/2021.01.27.428229 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-01-28

Objective: During atherogenesis, vascular smooth muscle cells (VSMCs) undergo a phenotypic modulation leading to migration and loss of contractility. Here we propose gene regulatory network specific the contractile phenotype carotid VSMCs from transcriptomic data. Design method: Human atheroma plaque (ATH, Stary>4) nearby macroscopically intact tissue (MIT, Stary<3) 32 patients were analysed by microarrays (Affymetrix HuGene-1.0ST). Histological analysis ensured large predominance in MIT....

10.1097/01.hjh.0000467353.66660.d4 article EN Journal of Hypertension 2015-06-01
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