Cartron, Pierre-François, 19..-....
![Sudoc [ABES], France](/viaf/images/flags/SUDOC.png "Sudoc [ABES], France")
Pierre-Francois Cartron
VIAF ID: 117147093782225002276 (Personal)
Permalink: http://viaf.org/viaf/117147093782225002276
Preferred Forms
4xx's: Alternate Name Forms (2)
Works
| Title | Sources |
|---|---|
| Activation of Bax by BH3 domains during apoptosis: the unfolding of a deadly plot |
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| Caractérisation d'un facteur épigénétique impliqué dans la régulation des cellules souches embryonnaires murines |
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| Caspase 3 activation is controlled by a sequence located in the N-terminus of its large subunit. |
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| Characterization of a novel candidate epigenetic regulator of pluripotency. |
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| Characterization of circulating tumor cells as a reflection of the tumor heterogeneity: myth or reality? |
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| Control of Bax homodimerization by its carboxyl terminus. |
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| Control of glioma cell death and differentiation by PKM2-Oct4 interaction |
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| Développement de stratégies innovantes pour cibler la méthylation de l'ADN dans les cancers |
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| Distinct domains control the addressing and the insertion of Bax into mitochondria. |
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| DNA methylation and apoptosis resistance in cancer cells |
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| The DNMT1/PCNA/UHRF1 disruption induces tumorigenesis characterized by similar genetic and epigenetic signatures |
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| Dnmt3/transcription factor interactions as crucial players in targeted DNA methylation. |
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| Epigenetic of Primary Bone Tumors' Progression and Chemoresistance. |
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| Epigenetic regulation of estrogen signaling in breast cancer |
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| Etude du rôle de la protéine autophagique ATG9A dans les cancers du sein |
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| The expression of a new variant of the pro-apoptotic molecule Bax, Baxpsi, is correlated with an increased survival of glioblastoma multiforme patients |
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| Expression of bcl-2, bax and bcl-xl in human gliomas: a re-appraisal. |
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| The first alpha helix of Bax plays a necessary role in its ligand-induced activation by the BH3-only proteins Bid and PUMA. |
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| Folate supplementation limits the tumourigenesis in rodent models of gliomagenesis. |
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| Glioblastome multiforme et épigénétique : de la prévention au développement de nouveaux traitements |
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| HDAC1-mSin3a-NCOR1, Dnmt3b-HDAC1-Egr1 and Dnmt1-PCNA-UHRF1-G9a regulate the NY-ESO1 gene expression. |
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| Hétérogénéité et plasticité de l'intégrine α5 dans les cellules souches de glioblastome |
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| High hydrostatic pressure induces immunogenic cell death in human tumor cells |
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| Histone H3 phosphorylation in GBM: a new rational to guide the use of kinase inhibitors in anti-GBM therapy. |
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| Identification of TET1 Partners That Control Its DNA-Demethylating Function. |
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| Impact of pH on Bax alpha conformation, oligomerisation and mitochondrial integration |
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| Impact of the DNA methyltransferases expression on the methylation status of apoptosis-associated genes in glioblastoma multiforme. |
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| Inhibition of UHRF1 protein by epigenetic partners and epi-drugs. |
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| The interplay between the lysine demethylase KDM1A and DNA methyltransferases in cancer cells is cell cycle dependent |
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| Involvement of the N-terminus of Bax in its intracellular localization and function. |
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| Kinetics of DNA methylation inheritance by the Dnmt1-including complexes during the cell cycle. |
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| Mécanismes épigénétiques associés à la progression et à la chimiorésistance des sarcomes osseux |
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| Mécanismes épigénétiques et influence du micro-environnement tumoral |
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| Metaxins 1 and 2, two proteins of the mitochondrial protein sorting and assembly machinery, are essential for Bak activation during TNF alpha triggered apoptosis |
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| Minimal BH3 peptides promote cell death by antagonizing anti-apoptotic proteins. |
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| miR-370-3p Is a Therapeutic Tool in Anti-glioblastoma Therapy but Is Not an Intratumoral or Cell-free Circulating Biomarker |
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| The N-terminal end of Bax contains a mitochondrial-targeting signal. |
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| New histone deacetylase inhibitors improve cisplatin antitumor properties against thoracic cancer cells. |
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| The phosphorylation of Metaxin 1 controls Bak activation during TNFα induced cell death |
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| Prostaglandins antagonistically control Bax activation during apoptosis |
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| Proximity ligation in situ assay for monitoring the global DNA methylation in cells |
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| The small organic compound HA14-1 prevents Bcl-2 interaction with Bax to sensitize malignant glioma cells to induction of cell death. |
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| Specific inhibition of DNMT1/CFP1 reduces cancer phenotypes and enhances chemotherapy effectiveness. |
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| Specific Inhibition of DNMT3A/ISGF3γ Interaction Increases the Temozolomide Efficiency to Reduce Tumor Growth |
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| Specific inhibition of one DNMT1-including complex influences tumor initiation and progression. |
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| Specific or not specific recruitment of DNMTs for DNA methylation, an epigenetic dilemma |
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| Study of epigenetic and epitranscriptomic mechanisms involved in acquiring resistance to cell cycle inhibitors (CDK4/6) in homono-dependant breast cancers. |
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| Study of mechanisms and epigenetics dynamics in glioblastoma multiforme during the acquisition of temozolomide resistance. |
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| Study of the role of ATG9A, an autophagic protein, in breast cancer. |
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| Tandem virtual screening targeting the SRA domain of UHRF1 identifies a novel chemical tool modulating DNA methylation. |
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| Telomeric maintenance : interest in the diagnosis of gliomas related to mitochondrial metabolism. |
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| TOM22, a core component of the mitochondria outer membrane protein translocation pore, is a mitochondrial receptor for the proapoptotic protein Bax. |
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