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Accueil > Départements > Biochimie, Biophysique et Biologie Structurale > Jean-Baptiste CHARBONNIER, Marie-Hélène LE DU, Sophie ZINN-JUSTIN : Enveloppe Nucléaire, Télomères et Réparation de l’ADN

Publications de l’équipe

2019


  • M. Bakail, A. Gaubert, J. Andreani, G. Moal, G. Pinna, E. Boyarchuk, M. - C. Gaillard, R. Courbeyrette, C. Mann, J. - Y. Thuret, B. Guichard, B. Murciano, N. Richet, A. Poitou, C. Frederic, M. - H. Le Du, M. Agez, C. Roelants, Z. A. Gurard-Levin, G. Almouzni, N. Cherradi, R. Guerois, et F. Ochsenbein, « Design on a Rational Basis of High-Affinity Peptides Inhibiting the Histone Chaperone ASF1 », Cell Chemical Biology, sept. 2019.
    Résumé : Anti-silencing function 1 (ASF1) is a conserved H3-H4 histone chaperone involved in histone dynamics during replication, transcription, and DNA repair. Overexpressed in proliferating tissues including many tumors, ASF1 has emerged as a promising therapeutic target. Here, we combine structural, computational, and biochemical approaches to design peptides that inhibit the ASF1-histone interaction. Starting from the structure of the human ASF1-histone complex, we developed a rational design strategy combining epitope tethering and optimization of interface contacts to identify a potent peptide inhibitor with a dissociation constant of 3 nM. When introduced into cultured cells, the inhibitors impair cell proliferation, perturb cell-cycle progression, and reduce cell migration and invasion in a manner commensurate with their affinity for ASF1. Finally, we find that direct injection of the most potent ASF1 peptide inhibitor in mouse allografts reduces tumor growth. Our results open new avenues to use ASF1 inhibitors as promising leads for cancer therapy.
    Mots-clés : AMIG, B3S, Cancer, Cell Penetrating Peptide, Chromatin, DBG, Drug Design, Epigenetics, INTGEN, PARI, Peptide Inhibitor, PF, Protein Binding, Protein-Protein Interaction, Rosetta Design, SEN, X-Ray Crystallography.

  • N. Essawy, C. Samson, A. Petitalot, S. Moog, A. Bigot, I. Herrada, A. Marcelot, A. - A. Arteni, C. Coirault, et S. Zinn-Justin, « An Emerin LEM-Domain Mutation Impairs Cell Response to Mechanical Stress », Cells, vol. 8, nᵒ 6, juin 2019.
    Résumé : Emerin is a nuclear envelope protein that contributes to genome organization and cell mechanics. Through its N-terminal LAP2-emerin-MAN1 (LEM)-domain, emerin interacts with the DNA-binding protein barrier-to-autointegration (BAF). Emerin also binds to members of the linker of the nucleoskeleton and cytoskeleton (LINC) complex. Mutations in the gene encoding emerin are responsible for the majority of cases of X-linked Emery-Dreifuss muscular dystrophy (X-EDMD). Most of these mutations lead to an absence of emerin. A few missense and short deletion mutations in the disordered region of emerin are also associated with X-EDMD. More recently, missense and short deletion mutations P22L, ∆K37 and T43I were discovered in emerin LEM-domain, associated with isolated atrial cardiac defects (ACD). Here we reveal which defects, at both the molecular and cellular levels, are elicited by these LEM-domain mutations. Whereas K37 mutation impaired the correct folding of the LEM-domain, P22L and T43I had no impact on the 3D structure of emerin. Surprisingly, all three mutants bound to BAF, albeit with a weaker affinity in the case of K37. In human myofibroblasts derived from a patient's fibroblasts, emerin ∆K37 was correctly localized at the inner nuclear membrane, but was present at a significantly lower level, indicating that this mutant is abnormally degraded. Moreover, SUN2 was reduced, and these cells were defective in producing actin stress fibers when grown on a stiff substrate and after cyclic stretches. Altogether, our data suggest that the main effect of mutation K37 is to perturb emerin function within the LINC complex in response to mechanical stress.
    Mots-clés : actin, atrial cardiac defects, B3S, BAF, CRYOEM, emerin, INTGEN, mechano-transduction, PF.

  • P. Frit, V. Ropars, M. Modesti, J. - B. Charbonnier, et P. Calsou, « Plugged into the Ku-DNA hub: The NHEJ network », Progress in Biophysics and Molecular Biology, mars 2019.
    Résumé : In vertebrates, double-strand breaks in DNA are primarily repaired by Non-Homologous End-Joining (NHEJ). The ring-shaped Ku heterodimer rapidly senses and threads onto broken DNA ends forming a recruiting hub. Through protein-protein contacts eventually reinforced by protein-DNA interactions, the Ku-DNA hub attracts a series of specialized proteins with scaffolding and/or enzymatic properties. To shed light on these dynamic interplays, we review here current knowledge on proteins directly interacting with Ku and on the contact points involved, with a particular accent on the different classes of Ku-binding motifs identified in several Ku partners. An integrated structural model of the core NHEJ network at the synapsis step is proposed.
    Mots-clés : B3S, Conserved binding motifs, DNA damage, DNA repair machineries, Double-strand breaks, INTGEN, Ku, NHEJ, Protein interactions network.

  • J. Lisboa, L. Celmal, D. Sanchez, M. Marquis, J. Andreani, R. Guerois, F. Ochsenbein, D. Durand, S. Marsin, P. Cuniasse, J. P. Radicella, et S. Queyillon-Cheruel, « The C-terminal domain of HpDprA is a DNA-binding winged helix domain that does not bind double-stranded DNA », Febs Journal, vol. 286, nᵒ 10, p. 1941-1958, mai 2019.
    Résumé : DNA-processing protein A, a ubiquitous multidomain DNA-binding protein, plays a crucial role during natural transformation in bacteria. Here, we carried out the structural analysis of DprA from the human pathogen Helicobacter pylori by combining data issued from the 1.8-angstrom resolution X-ray structure of the Pfam02481 domain dimer (RF), the NMR structure of the carboxy terminal domain (CTD), and the low-resolution structure of the full-length DprA dimer obtained in solution by SAXS. In particular, we sought a molecular function for the CTD, a domain that we show here is essential for transformation in H.pylori. Albeit its structural homology to winged helix DNA-binding motifs, we confirmed that the isolated CTD does not interact with ssDNA nor with dsDNA. The key R52 and K137 residues of RF are crucial for these two interactions. Search for sequences harboring homology to either HpDprA or Rhodopseudomonas palustris DprA CTDs led to the identification of conserved patches in the two CTD. Our structural study revealed the similarity of the structures adopted by these residues in RpDprA CTD and HpDprA CTD. This argues for a conserved, but yet to be defined, CTD function, distinct from DNA binding.
    Mots-clés : AMIG, B3S, bacillus-subtilis dpra, DprA, FAAM, Helicobacter pylori, helicobacter-pylori, INTGEN, natural transformation, nmr structure determination, protein, reca, recognition, recombination, sequence, WH DNA binding motif, WH DNA-binding motif, xplor-nih.

  • A. Petitalot, E. Dardillac, E. Jacquet, N. Nhiri, J. Guirouilh-Barbat, P. Julien, I. Bouazzaoui, D. Bonte, J. Feunteun, J. A. Schnell, P. Lafitte, J. - C. Aude, C. Nogues, E. Rouleau, R. Lidereau, B. S. Lopez, S. Zinn-Justin, S. M. Caputo, F. Bonnet, N. Jones, V. Bubien, M. Longy, N. Sevenet, S. Krieger, L. Casters, D. Vaur, N. Uhrhammer, Y. J. Bignon, S. Lizard, A. Dumont, F. Revillion, M. Leone, N. Boutry-Kryza, O. Sinilnikova, A. Remenieras, V. Bourdon, T. Noguchi, H. Sobol, P. - O. Harmand, P. Vilquin, P. Pujol, P. Jonveaux, M. Bronner, J. Sokolowska, C. Delnatte, V. Guibert, C. Garrec, S. Bezieau, F. Soubrier, E. Guillerm, F. Coulet, C. Lefol, V. Caux-Moncoutier, L. Golmard, C. Houdayer, D. Stoppa-Lyonnet, C. Delvincoun, O. Beaudoux, D. Muller, C. Toulas, M. Guillaud-Bataille, et B. Bressac-De Paillerets, « Combining Homologous Recombination and Phosphopeptide-binding Data to Predict the Impact of BRCA1 BRCT Variants on Cancer Risk », Molecular Cancer Research, vol. 17, nᵒ 1, p. 54-69, janv. 2019.
    Résumé : BRCA1 mutations have been identified that increase the risk of developing hereditary breast and ovarian cancers. Genetic screening is now offered to patients with a family history of cancer, to adapt their treatment and the management of their relatives. However, a large number of BRCA1 variants of uncertain significance (VUS) are detected. To better understand the significance of these variants, a high-throughput structural and functional analysis was performed on a large set of BRCA1 VUS. Information on both cellular localization and homology-directed DNA repair (HR) capacity was obtained for 78 BRCT missense variants in the UMD-BRCA1 database and measurement of the structural stability and phosphopeptide-binding capacities was performed for 42 mutated BRCT domains. This extensive and systematic analysis revealed that most characterized causal variants affect BRCT-domain solubility in bacteria and all impair BRCA1 HR activity in cells. Furthermore, binding to a set of 5 different phosphopeptides was tested: all causal variants showed phosphopeptide-binding defects and no neutral variant showed such defects. A classification is presented on the basis of mutated BRCT domain solubility, phosphopeptide-binding properties, and VUS HR capacity. These data suggest that HR-defective variants, which present, in addition, BRCT domains either insoluble in bacteria or defective for phosphopeptide binding, lead to an increased cancer risk. Furthermore, the data suggest that variants with a WT HR activity and whose BRCT domains bind with a WT affinity to the 5 phosphopeptides are neutral. The case of variants with WT HR activity and defective phosphopeptide binding should be further characterized, as this last functional defect might be sufficient per se to lead to tumorigenesis. Implications: The analysis of the current study on BRCA1 structural and functional defects on cancer risk and classification presented may improve clinical interpretation and therapeutic selection.
    Mots-clés : B3S, bach1 phosphopeptide, BIM, classification, DBG, dna-damage, domain, functional-analysis, hereditary breast, INTGEN, missense variants, ovarian, repair, structural basis.

  • F. Real, V. Vallet, et M. Masella, « Improving the Description of Solvent Pairwise Interactions Using Local Solute/Solvent Three-Body Functions. The Case of Halides and Carboxylates in Aqueous Environment », Journal of Computational Chemistry, vol. 40, nᵒ 11, p. 1209-1218, avr. 2019.
    Résumé : We propose a general strategy to remediate force-field artifacts in describing pairwise interactions among similar molecules M in the vicinity of another chemical species, C, like water molecules interacting at short distance from a monoatomic ion. This strategy is based on introducing a three-body potential energy term that alters the pairwise interactions among M-type molecules when they lie at short range from the species C. In other words the species C is the center of a space domain where the pairwise interactions among the molecules M is altered. Here, we apply it to improve the description of the water interactions provided by the polarizable water model TCPE/2013 in the vicinity of halides, from F- to At-, and of the prototypical carboxylate anion CH3COO-. We show the accuracy and the transferability of such an approach to investigate not only the hydration process of single anions but also of a salt solution NH4+/Cl- in aqueous phase. This strategy can be used to remediate the drawbacks of any kind of force fields. (C) 2019 Wiley Periodicals, Inc.
    Mots-clés : anion hydration, B3S, basis-sets, binding, convergence, dimer, energies, force field, interface, INTGEN, ion, potential functions, salt solution, simulated solvation, water model.

  • D. Roos-Weil, C. Decaudin, M. Armand, V. Della-Valle, M. K. Diop, H. Ghamlouch, V. Ropars, C. Herate, D. Lara, E. Durot, R. Haddad, E. Mylonas, F. Damm, F. Pflumio, B. Stoilova, M. Metzner, O. Elemento, P. Dessen, V. Camara-Clayette, F. - L. Cosset, E. Verhoeyen, V. Leblond, V. Ribrag, P. Cornillet-Lefebvre, P. Rameau, N. Azars, F. Charlottes, P. More, J. - B. Charbonnier, P. Vyas, T. Mercher, S. Aoufouchi, N. Droin, C. Guillouf, F. Nguyen-Khac, et O. A. Bernard, « A Recurrent Activating Missense Mutation in Waldenstrom Macroglobulinemia Affects the DNA Binding of the ETS Transcription Factor SPI1 and Enhances Proliferation », Cancer Discovery, vol. 9, nᵒ 6, p. 796-811, juin 2019.
    Résumé : The ETS-domain transcription factors divide into subfamilies based on protein sim- ilarities, DNA-binding sequences, and interaction with cofactors. They are regulated by extracellular clues and contribute to cellular processes, including proliferation and transformation. ETS genes are targeted through genomic rearrangements in oncogenesis. The PU.1/SPI1 gene is inactivated by point mutations in human myeloid malignancies. We identified a recurrent somatic mutation (Q226E) in PU.1/SPI1 in Waldenstrom macroglobulinemia, a B-cell lymphoproliferative disorder. It affects the DNA-binding affinity of the protein and allows the mutant protein to more frequently bind and activate promoter regions with respect to wild-type protein. Mutant SPI1 binding at promoters activates gene sets typically promoted by other ETS factors, resulting in enhanced proliferation and decreased terminal B-cell differentiation in model cell lines and primary samples. In summary, we describe oncogenic subversion of transcription factor function through subtle alteration of DNA binding leading to cellular proliferation and differentiation arrest. SIGNIFICANCE: The demonstration that a somatic point mutation tips the balance of genome-binding pattern provides a mechanistic paradigm for how missense mutations in transcription factor genes may be oncogenic in human tumors.
    Mots-clés : acute myeloid-leukemia, B3S, cell differentiation, cll, INTGEN, lymphoma, mouse, pu.1, somatic mutation, spi-1/pu.1.

2018


  • F. Celli, A. Petitalot, C. Samson, F. - X. Theillet, et S. Zinn-Justin, « H-1, C-13 and N-15 backbone resonance assignment of the lamin C-terminal region specific to prelamin A », Biomolecular Nmr Assignments, vol. 12, nᵒ 2, p. 225-229, oct. 2018.
    Résumé : Lamins are the main components of the nucleoskeleton. They form a protein meshwork that underlies the inner nuclear membrane. Mutations in the LMNA gene coding for A-type lamins (lamins A and C) cause a large panel of human diseases, referred to as laminopathies. These diseases include muscular dystrophies, lipodystrophies and premature aging diseases. Lamin A exhibits a C-terminal region that is different from lamin C and is post-translationally modified. It is produced as prelamin A and it is then farnesylated, cleaved, carboxymethylated and cleaved again in order to become mature lamin A. In patients with the severe Hutchinson-Gilford progeria syndrome, a specific single point mutation in LMNA leads to an aberrant splicing of the LMNA gene preventing the post-translational processing of prelamin A. This leads to the accumulation of a permanently farnesylated lamin A mutant lacking 50 amino acids named progerin. We here report the NMR H-1, N-15, (CO)-C-13, C-13 and C-13 chemical shift assignment of the C-terminal region that is specific to prelamin A, from amino acid 567 to amino acid 664. We also report the NMR H-1, N-15, (CO)-C-13, C-13 and C-13 chemical shift assignment of the C-terminal region of the progerin variant, from amino acid 567 to amino acid 614. Analysis of these chemical shift data confirms that both prelamin A and progerin C-terminal domains are largely disordered and identifies a common partially populated -helix from amino acid 576 to amino acid 585. This helix is well conserved from fishes to mammals.
    Mots-clés : B3S, INTGEN, Intrinsically disordered protein, mutations, networks, NMR spectroscopy, NMR spectroscopy, Nuclear envelope, Nucleoskeleton.

  • L. Celma, P. Cuniasse, D. Durand, J. Lisboa, D. Sanchez, S. Marsin, S. Quevillon-Cheruel, et P. Radicella, « HpDprA domains involved in interaction with DNA », Acta Crystallographica a-Foundation and Advances, vol. 74, p. E201-E201, août 2018.
    Mots-clés : B3S, dna, FAAM, HpDprA, INTGEN, Transformation.

  • W. Jalby, D. Kuck, A. D. Malony, M. Masella, A. Mazouz, et M. Popov, « The Long and Winding Road Toward Efficient High-Performance Computing », Proceedings of the Ieee, vol. 106, nᵒ 11, p. 1985-2003, nov. 2018.
    Résumé : The major challenge to Exaflop computing, and more generally, efficient high-end computing, is in finding the best "matches" between advanced hardware capabilities and the software used to program applications, so that top performance will be achieved. Several benchmarks show very disappointing performance progress over the last decade, clearly indicating a mismatch between hardware and software. To remedy this problem, it is important that key performance enablers at the software level-autotuning, performance analysis tools, full application optimization-are understood. For each area, we highlight major limitations and most promising approaches to reaching better performance and energy levels. Finally, we conclude by analyzing hardware and software design, trying to pave the way for more tightly integrated hardware and software codesign.
    Mots-clés : Autotuning, B3S, benchmarking, code, design, hardware design, implementation, INTGEN, molecular dynamics, molecular-dynamics, performance evaluation tools.

  • F. Lallemand, A. Petitalot, S. Vacher, L. de Koning, K. Taouis, B. S. Lopez, S. Zinn-Justin, N. Dalla-Venezia, W. Chemlali, A. Schnitzler, R. Lidereau, I. Bieche, et S. M. Caputo, « Involvement of the FOXO6 transcriptional factor in breast carcinogenesis », Oncotarget, vol. 9, nᵒ 7, p. 7464-7475, janv. 2018.
    Résumé : In mammals, FOXO transcriptional factors form a family of four members (FOXO1, 3, 4, and 6) involved in the modulation proliferation, apoptosis, and carcinogenesis. The role of the FOXO family in breast cancer remains poorly elucidated. According to the cellular context and the stage of the disease, FOXOs can have opposite effects on carcinogenesis. To study the role of FOXOs in breast carcinogenesis in more detail, we examined their expression in normal tissues, breast cell lines, and a large series of breast tumours of human origin. We found a very low physiological level ofFOXO6expression in normal adult tissues and high levels of expression in foetal brain.FOXOgene expressions fluctuate specifically in breast cancer cells compared to normal cells, suggesting that these genes may have different roles in breast carcinogenesis. For the first time, we have shown that, among the variousFOXOgenes, onlyFOXO6was frequently highly overexpressed in breast cell lines and tumours. We also found that inhibition of the endogenous expression of FOXO6 by a specific siRNA inhibited the growth of the human breast cell lines MDA-MB-468 and HCC-38. FACS and Western blot analysis showed that inhibition of endogenous expression of FOXO6 induced accumulation of cells in G0/G1 phase of the cell cycle, but not apoptosis. These results tend to demonstrate that the overexpression of the humanFOXO6gene that we highlighted in the breast tumors stimulates breast carcinogenesis by activating breast cancer cell proliferation.
    Mots-clés : B3S, cervical squamous cell carcinoma, endometrial adenocarcinoma, gynecological cancers, INTGEN, prognosis, uc.189.

  • C. Nemoz, V. Ropars, P. Frit, A. Gontier, P. Drevet, J. Yu, R. Guerois, A. Pitois, A. Comte, C. Delteil, N. Barboule, P. Legrand, S. Baconnais, Y. Yin, S. Tadi, E. Barbet-Massin, I. Berger, E. Le Cams, M. Modesti, E. Rothenberg, P. Calsou, et J. B. Charbonnier, « XLF and APLF bind Ku80 at two remote sites to ensure DNA repair by non-homologous end joining », Nature Structural & Molecular Biology, vol. 25, nᵒ 10, p. 971-980, oct. 2018.
    Résumé : The Ku70-Ku80 (Ku) heterodimer binds rapidly and tightly to the ends of DNA double-strand breaks and recruits factors of the non-homologous end-joining (NHEJ) repair pathway through molecular interactions that remain unclear. We have determined crystal structures of the Ku-binding motifs (KBM) of the NHEJ proteins APLF (A-KBM) and XLF (X-KBM) bound to a Ku-DNA complex. The two KBM motifs bind remote sites of the Ku80 alpha/beta domain. The X-KBM occupies an internal pocket formed by an unprecedented large outward rotation of the Ku80 alpha/beta domain. We observe independent recruitment of the APLF-interacting protein XRCC4 and of XLF to laser-irradiated sites via binding of A- and X-KBMs, respectively, to Ku80. Finally, we show that mutation of the X-KBM and A-KBM binding sites in Ku80 compromises both the efficiency and accuracy of end joining and cellular radiosensitivity. A- and X-KBMs may represent two initial anchor points to build the intricate interaction network required for NHEJ.
    Mots-clés : AMIG, B3S, c2orf13, complex, dependent protein-kinase, heterodimer, INTGEN, ligase-iv, pathway, stimulation, strand break repair, x-ray, xrcc4.

  • M. Parlato, F. Charbit-Henrion, J. Pan, C. Romano, R. Duclaux-Loras, M. - H. Le Du, N. Warner, P. Francalanci, J. Bruneau, M. Bras, M. Zarhrate, B. Bègue, N. Guegan, S. Rakotobe, N. Kapel, P. De Angelis, A. M. Griffiths, K. Fiedler, E. Crowley, F. Ruemmele, A. M. Muise, et N. Cerf-Bensussan, « Human ALPI deficiency causes inflammatory bowel disease and highlights a key mechanism of gut homeostasis », EMBO molecular medicine, mars 2018.
    Résumé : Herein, we report the first identification of biallelic-inherited mutations inALPIas a Mendelian cause of inflammatory bowel disease in two unrelated patients.ALPIencodes for intestinal phosphatase alkaline, a brush border metalloenzyme that hydrolyses phosphate from the lipid A moiety of lipopolysaccharides and thereby drastically reduces Toll-like receptor 4 agonist activity. Prediction tools and structural modelling indicate that all mutations affect critical residues or inter-subunit interactions, and heterologous expression in HEK293T cells demonstrated that allALPImutations were loss of function.ALPImutations impaired either stability or catalytic activity of ALPI and rendered it unable to detoxify lipopolysaccharide-dependent signalling. Furthermore, ALPI expression was reduced in patients' biopsies, and ALPI activity was undetectable in ALPI-deficient patient's stool. Our findings highlight the crucial role of ALPI in regulating host-microbiota interactions and restraining host inflammatory responses. These results indicate thatALPImutations should be included in screening for monogenic causes of inflammatory bowel diseases and lay the groundwork for ALPI-based treatments in intestinal inflammatory disorders.
    Mots-clés : B3S, inflammatory bowel diseases, intestinal phosphatase alkaline, INTGEN, monogenic disease.

  • C. Samson, A. Petitalot, F. Celli, I. Herrada, V. Ropars, M. - H. Le Du, N. Nhiri, E. Jacquet, A. - A. Arteni, B. Buendia, et S. Zinn-Justin, « Structural analysis of the ternary complex between lamin A/C, BAF and emerin identifies an interface disrupted in autosomal recessive progeroid diseases », Nucleic Acids Research, vol. 46, nᵒ 19, p. 10460-10473, nov. 2018.
    Résumé : Lamins are the main components of the nucleoskeleton. Whereas their 3D organization was recently described using cryoelectron tomography, no structural data highlights how they interact with their partners at the interface between the inner nuclear envelope and chromatin. A large number of mutations causing rare genetic disorders called laminopathies were identified in the C-terminal globular Igfold domain of lamins A and C. We here present a first structural description of the interaction between the lamin A/C immunoglobulin-like domain and emerin, a nuclear envelope protein. We reveal that this lamin A/C domain both directly binds self-assembled emerin and interacts with monomeric emerin LEM domain through the dimeric chromatin-associated Barrier-to-Autointegration Factor (BAF) protein. Mutations causing autosomal recessive progeroid syndromes specifically impair proper binding of lamin A/C domain to BAF, thus destabilizing the link between lamin A/C and BAF in cells. Recent data revealed that, during nuclear assembly, BAF's ability to bridge distant DNA sites is essential for guiding membranes to form a single nucleus around the mitotic chromosome ensemble. Our results suggest that BAF interaction with lamin A/C also plays an essential role, and that mutations associated with progeroid syndromes leads to a dysregulation of BAF-mediated chromatin organization and gene expression.
    Mots-clés : B3S, barrier, binding, c-terminal domain, CRYOEM, hutchinson-gilford-progeria, INTGEN, lmna mutation, localization, mandibuloacral dysplasia, nuclear-envelope, organization, PF, to-autointegration factor.

  • C. Tellier-Lebegue, E. Dizet, E. Ma, X. Veaute, E. Coïc, J. - B. Charbonnier, et L. Maloisel, « Correction: The translesion DNA polymerases Pol ζ and Rev1 are activated independently of PCNA ubiquitination upon UV radiation in mutants of DNA polymerase δ », PLoS genetics, vol. 14, nᵒ 2, p. e1007236, févr. 2018.
    Résumé : [This corrects the article DOI: 10.1371/journal.pgen.1007119.].
    Mots-clés : B3S, INTGEN.

  • S. V. Vartak, H. A. Swarup, V. Gopalakrishnan, V. K. Gopinatha, V. Ropars, M. Nambiar, F. John, S. K. S. Kothanahally, R. Kumari, N. Kumari, U. Ray, G. Radha, D. Dinesh, M. Pandey, H. Ananda, S. S. Karki, M. Srivastava, J. B. Charbonnier, B. Choudhary, K. Mantelingu, et S. C. Raghavan, « Autocyclized and oxidized forms of SCR7 induce cancer cell death by inhibiting nonhomologous DNA end joining in a Ligase IV dependent manner », Febs Journal, vol. 285, nᵒ 21, p. 3959-3976, nov. 2018.
    Résumé : Nonhomologous DNA end joining (NHEJ) is the major DNA double-strand break (DSB) repair pathway in mammals. Previously, we have described a small molecule inhibitor, SCR7, which can inhibit NHEJ in a Ligase IV-dependent manner. Administration of SCR7 within the cells resulted in the accumulation of DNA breaks, cell death, and inhibition of tumor growth in mice. In the present study, we report that parental SCR7, which is unstable, can be autocyclized into a stable form. Both parental SCR7 and cyclized SCR7 possess the same molecular weight (334.09) and molecular formula (C18H14N4OS), whereas its oxidized form, SCR7-pyrazine, possesses a different molecular formula (C18H12N4OS), molecular weight (332.07), and structure. While cyclized form of SCR7 showed robust inhibition of NHEJ in vitro, both forms exhibited efficient cytotoxicity. Cyclized and oxidized forms of SCR7 inhibited DNA end joining catalyzed by Ligase IV, whereas their impact was minimal on Ligase III, Ligase I, and T4 DNA Ligase-mediated joining. Importantly, both forms inhibited V(D)J recombination, although the effect was more pronounced for SCR7-cyclized. Both forms blocked NHEJ in a Ligase IV-dependent manner leading to the accumulation of DSBs within the cells. Although cytotoxicity due to SCR7-cyclized was Ligase IV specific, the pyrazine form exhibited nonspecific cytotoxicity at higher concentrations in Ligase IV-null cells. Finally, we demonstrate that both forms can potentiate the effect of radiation. Thus, we report that cyclized and oxidized forms of SCR7 can inhibit NHEJ in a Ligase IV-dependent manner, although SCR7-pyrazine is less specific to Ligase IV inside the cell.
    Mots-clés : B3S, chromosomal translocations, CRISPR, DNA Ligase, Double-strand break, End-joining, Genome editing, Homologous recombination, Inhibitor of DNA repair, INTGEN, NHEJ, V(D)J recombination.

  • M. Zinke, P. Fricke, S. Lange, S. Zinn-Justin, et A. Lange, « Protein-Protein Interfaces Probed by Methyl Labeling and Proton-Detected Solid-State NMR Spectroscopy », Chemphyschem, vol. 19, nᵒ 19, p. 2457-2460, oct. 2018.
    Résumé : Proton detection and fast magic-angle spinning have advanced biological solid-state NMR, allowing for the backbone assignment of complex protein assemblies with high sensitivity and resolution. However, so far no method has been proposed to detect intermolecular interfaces in these assemblies by proton detection. Herein, we introduce a concept based on methyl labeling that allows for the assignment of these moieties and for the study of protein-protein interfaces at atomic resolution.
    Mots-clés : angle-spinning nmr, B3S, backbone assignment, c-13, dynamics, fibrils, gp17.1, h-1-h-1 distance restraints, interfaces, INTGEN, isoleucine, methyl labeling, methyl-labeling, multidimensional nmr, protein structures, Proteins, Solid-State NMR, SPP1.

2017



  • P. Cuniasse, P. Tavares, E. V. Orlova, et S. Zinn-Justin, « Structures of biomolecular complexes by combination of NMR and cryoEM methods », Current Opinion in Structural Biology, vol. 43, p. 104-113, 2017.


  • Y. Duroc, R. Kumar, L. Ranjha, C. Adam, R. Guérois, K. Md Muntaz, M. - C. Marsolier-Kergoat, F. Dingli, R. Laureau, D. Loew, B. Llorente, J. - B. Charbonnier, P. Cejka, et V. Borde, « Concerted action of the MutLβ heterodimer and Mer3 helicase regulates the global extent of meiotic gene conversion », eLife, vol. 6, janv. 2017.
    Mots-clés : AMIG, B3S, biochemistry, Chromosomes, genes, INTGEN, Meiosis, mismatch repair, Recombination, S. cerevisiae.

  • C. Houriez, M. Meot-Ner Mautner, et M. Masella, « Solvation of the Guanidinium Ion in Pure Aqueous Environments: A Theoretical Study from an "Ab Initio"-Based Polarizable Force Field », The Journal of Physical Chemistry. B, vol. 121, nᵒ 50, p. 11219-11228, déc. 2017.
    Résumé : We report simulation results regarding the hydration process of the guanidinium cation in water droplets and in bulk liquid water, at a low concentration of 0.03 M, performed using a polarizable approach to model both water/water and ion/water interactions. In line with earlier theoretical studies, our simulations show a preferential orientation of guanidinium at water-vacuum interfaces, i.e., a parallel orientation of the guanidinium plane to the aqueous surface. In an apparent contradiction with earlier simulation studies, we show also that guanidinium has a stronger propensity for the cores of aqueous systems than the ammonium cation. However, our bulk simulation conditions correspond to weaker cation concentrations than in earlier studies, by 2 orders of magnitude, and that the same simulations performed using a standard nonpolarizable force field leads to the same conclusion. From droplet data, we extrapolate the guanidinium single hydration enthalpy value to be -82.9 ± 2.2 kcal mol-1. That is about half as large as the sole experimental estimate reported to date, about -144 kcal mol-1. Our result yields a guanidinium absolute bulk hydration free energy at ambiant conditions to be -78.4 ± 2.6 kcal mol-1, a value smaller by 3 kcal mol-1 compared to ammonium. The relatively large magnitude of our guanidinium hydration free energy estimate suggests the Gdm+ protein denaturing properties to result from a competition between the cation hydration effects and the cation/protein interactions, a competition that can be modulated by weak differences in the protein or in the cation chemical environment.
    Mots-clés : B3S, INTGEN.

  • C. Houriez, V. Vallet, F. Réal, M. Meot-Ner Mautner, et M. Masella, « Organic ion association in aqueous phase and ab initio-based force fields: The case of carboxylate/ammonium salts », The Journal of Chemical Physics, vol. 147, nᵒ 16, p. 161720, oct. 2017.
    Résumé : We performed molecular dynamics simulations of carboxylate/methylated ammonium ion pairs solvated in bulk water and of carboxylate/methylated ammonium salt solutions at ambient conditions using an ab initio-based polarizable force field whose parameters are assigned to reproduce only high end quantum computations, at the Møller-Plesset second-order perturbation theory/complete basis set limit level, regarding single ions and ion pairs as isolated and micro-hydrated in gas phase. Our results agree with the available experimental results regarding carboxylate/ammonium salt solutions. For instance, our force field approach predicts the percentage of acetate associated with ammonium ions in CH3COO(-)/CH3NH3(+) solutions at the 0.2-0.8M concentration scale to range from 14% to 35%, in line with the estimates computed from the experimental ion association constant in liquid water. Moreover our simulations predict the number of water molecules released from the ion first hydration shell to the bulk upon ion association to be about 2.0 ± 0.6 molecules for acetate/protonated amine ion pairs, 3.1 ± 1.5 molecules for the HCOO(-)/NH4(+) pair and 3.3 ± 1.2 molecules for the CH3COO(-)/(CH3)4N(+) pair. For protonated amine-based ion pairs, these values are in line with experiment for alkali/halide pairs solvated in bulk water. All these results demonstrate the promising feature of ab initio-based force fields, i.e., their capacity in accurately modeling chemical systems that cannot be readily investigated using available experimental techniques.
    Mots-clés : B3S, INTGEN.

  • S. Mohr, M. Masella, L. E. Ratcliff, et L. Genovese, « Complexity Reduction in Large Quantum Systems: Fragment Identification and Population Analysis via a Local Optimized Minimal Basis », Journal of Chemical Theory and Computation, août 2017.
    Résumé : We present, within Kohn-Sham density functional theory calculations, a quantitative method to identify and assess the partitioning of a large quantum-mechanical system into fragments. We then show how within this framework simple generalizations of other well-known population analyses can be used to extract, from first-principles, reliable electrostatic multipoles for the identified fragments. Our approach reduces arbitrariness in the fragmentation procedure and enables the possibility to assess quantitatively whether the corresponding fragment multipoles can be interpreted as observable quantities associated with a system moiety. By applying our formalism within the code BigDFT, we show that the use of a minimal set of in situ-optimized basis functions allows at the same time a proper fragment definition and an accurate description of the electronic structure.
    Mots-clés : B3S, INTGEN.

  • C. Pattamadilok, V. Chanoine, C. Pallier, J. - L. Anton, B. Nazarian, P. Belin, et J. C. Ziegler, « Automaticity of phonological and semantic processing during visual word recognition », NeuroImage, vol. 149, p. 244-255, févr. 2017.
    Résumé : Reading involves activation of phonological and semantic knowledge. Yet, the automaticity of the activation of these representations remains subject to debate. The present study addressed this issue by examining how different brain areas involved in language processing responded to a manipulation of bottom-up (level of visibility) and top-down information (task demands) applied to written words. The analyses showed that the same brain areas were activated in response to written words whether the task was symbol detection, rime detection, or semantic judgment. This network included posterior, temporal and prefrontal regions, which clearly suggests the involvement of orthographic, semantic and phonological/articulatory processing in all tasks. However, we also found interactions between task and stimulus visibility, which reflected the fact that the strength of the neural responses to written words in several high-level language areas varied across tasks. Together, our findings suggest that the involvement of phonological and semantic processing in reading is supported by two complementary mechanisms. First, an automatic mechanism that results from a task-independent spread of activation throughout a network in which orthography is linked to phonology and semantics. Second, a mechanism that further fine-tunes the sensitivity of high-level language areas to the sensory input in a task-dependent manner.
    Mots-clés : Automatic activation, B3S, Bottom-up process, INTGEN, Stimulus-driven, Task-dependent, Top-down process.


  • L. E. Ratcliff, S. Mohr, G. Huhs, T. Deutsch, M. Masella, et L. Genovese, « Challenges in large scale quantum mechanical calculations: Challenges in large scale quantum mechanical calculations », Wiley Interdisciplinary Reviews: Computational Molecular Science, vol. 7, nᵒ 1, p. e1290, 2017.


  • C. Samson, F. Celli, K. Hendriks, M. Zinke, N. Essawy, I. Herrada, A. - A. Arteni, F. - X. Theillet, B. Alpha-Bazin, J. Armengaud, C. Coirault, A. Lange, et S. Zinn-Justin, « Emerin self-assembly mechanism: role of the LEM domain », The FEBS Journal, vol. 284, nᵒ 2, p. 338-352, 2017.
    Mots-clés : B3S, CRYOEM, INTGEN, PF.


  • C. Tellier-Lebegue, E. Dizet, E. Ma, X. Veaute, E. Coïc, J. - B. Charbonnier, et L. Maloisel, « The translesion DNA polymerases Pol ζ and Rev1 are activated independently of PCNA ubiquitination upon UV radiation in mutants of DNA polymerase δ », PLOS Genetics, vol. 13, nᵒ 12, p. e1007119, déc. 2017.

  • E. Vernhes, M. Renouard, B. Gilquin, P. Cuniasse, D. Durand, P. England, S. Hoos, A. Huet, J. F. Conway, A. Glukhov, V. Ksenzenko, E. Jacquet, N. Nhiri, S. Zinn-Justin, et P. Boulanger, « Erratum: High affinity anchoring of the decoration protein pb10 onto the bacteriophage T5 capsid », Scientific Reports, vol. 7, p. 43977, avr. 2017.


  • E. Vernhes, M. Renouard, B. Gilquin, P. Cuniasse, D. Durand, P. England, S. Hoos, A. Huet, J. F. Conway, A. Glukhov, V. Ksenzenko, E. Jacquet, N. Nhiri, S. Zinn-Justin, et P. Boulanger, « High affinity anchoring of the decoration protein pb10 onto the bacteriophage T5 capsid », Scientific Reports, vol. 7, p. 41662, févr. 2017.

  • M. Zinke, P. Fricke, C. Samson, S. Hwang, J. Wall, S. Lange, S. Zinn-Justin, et A. Lange, « Bacteriophage Tail Tube Assembly Studied by Proton-Detected 4D Solid-State NMR », Angewandte Chemie (International Ed. in English), juin 2017.
    Résumé : Obtaining unambiguous resonance assignments remains a major bottleneck in solid-state NMR studies of protein structure and dynamics. Particularly for supramolecular assemblies with large subunits (>150 residues), the analysis of crowded spectral data presents a challenge, even if three-dimensional (3D) spectra are used. Here, we present a proton-detected 4D solid-state NMR assignment procedure that is tailored for large assemblies. The key to recording 4D spectra with three indirect carbon or nitrogen dimensions with their inherently large chemical shift dispersion lies in the use of sparse non-uniform sampling (as low as 2%). As a proof-of-principle we acquired 4D (H)COCANH, (H)CACONH and (H)CBCANH spectra of the 20 kDa bacteriophage tail tube protein gp17.1 in a total time of two and a half weeks. These spectra were sufficient to obtain complete resonance assignments in a straightforward manner without use of previous solution NMR data.
    Mots-clés : B3S, gp17.1, INTGEN, non-uniform sampling, Proteins, Solid-state NMR, SPP1.

2016



  • A. Araye, A. Goudet, J. Barbier, S. Pichard, B. Baron, P. England, J. Pérez, S. Zinn-Justin, A. Chenal, et D. Gillet, « Correction: The Translocation Domain of Botulinum Neurotoxin A Moderates the Propensity of the Catalytic Domain to Interact with Membranes at Acidic pH », PLOS ONE, vol. 11, nᵒ 8, p. e0161743, août 2016.


  • A. Araye, A. Goudet, J. Barbier, S. Pichard, B. Baron, P. England, J. Pérez, S. Zinn-Justin, A. Chenal, et D. Gillet, « The Translocation Domain of Botulinum Neurotoxin A Moderates the Propensity of the Catalytic Domain to Interact with Membranes at Acidic pH », PLOS ONE, vol. 11, nᵒ 4, p. e0153401, avr. 2016.


  • D. Benarroch-Popivker, S. Pisano, A. Mendez-Bermudez, L. Lototska, P. Kaur, S. Bauwens, N. Djerbi, C.  M. Latrick, V. Fraisier, B. Pei, A. Gay, E. Jaune, K. Foucher, J. Cherfils-Vicini, E. Aeby, S. Miron, A. Londoño-Vallejo, J. Ye, M. - H. Le Du, H. Wang, E. Gilson, et M. - J. Giraud-Panis, « TRF2-Mediated Control of Telomere DNA Topology as a Mechanism for Chromosome-End Protection », Molecular Cell, vol. 61, nᵒ 2, p. 274-286, 2016.


  • J. P. Coles, C. Houriez, M. Meot-Ner (Mautner), et M. Masella, « Extrapolating Single Organic Ion Solvation Thermochemistry from Simulated Water Nanodroplets », The Journal of Physical Chemistry B, vol. 120, nᵒ 35, p. 9402-9409, sept. 2016.


  • G. Gaullier, S. Miron, S. Pisano, R. Buisson, Y. - V. Le Bihan, C. Tellier-Lebègue, W. Messaoud, P. Roblin, B. G. Guimarães, R. Thai, M. - J. Giraud-Panis, E. Gilson, et M. - H. Le Du, « A higher-order entity formed by the flexible assembly of RAP1 with TRF2 », Nucleic Acids Research, vol. 44, nᵒ 4, p. 1962-1976, févr. 2016.
    Mots-clés : B3S, DNA Damage, DNA-Binding Proteins, Genomic Instability, Humans, INTGEN, Multiprotein Complexes, Protein Binding, Telomere, Telomere-Binding Proteins, Telomeric Repeat Binding Protein 2.


  • I. Herrada, B. Bourgeois, C. Samson, B. Buendia, H. J. Worman, et S. Zinn-Justin, « Purification and Structural Analysis of LEM-Domain Proteins », in Methods in Enzymology, vol. 569, Elsevier, 2016, p. 43-61.

  • S. McGovern, S. Baconnais, P. Roblin, P. Nicolas, P. Drevet, H. Simonson, O. Piétrement, J. - B. Charbonnier, E. Le Cam, P. Noirot, et F. Lecointe, « C-terminal region of bacterial Ku controls DNA bridging, DNA threading and recruitment of DNA ligase D for double strand breaks repair », Nucleic Acids Research, mars 2016.
    Résumé : Non-homologous end joining is a ligation process repairing DNA double strand breaks in eukaryotes and many prokaryotes. The ring structured eukaryotic Ku binds DNA ends and recruits other factors which can access DNA ends through the threading of Ku inward the DNA, making this protein a key ingredient for the scaffolding of the NHEJ machinery. However, this threading ability seems unevenly conserved among bacterial Ku. As bacterial Ku differ mainly by their C-terminus, we evaluate the role of this region in the loading and the threading abilities of Bacillus subtilis Ku and the stimulation of the DNA ligase LigD. We identify two distinct sub-regions: a ubiquitous minimal C-terminal region and a frequent basic C-terminal extension. We show that truncation of one or both of these sub-regions in Bacillus subtilis Ku impairs the stimulation of the LigD end joining activity in vitro. We further demonstrate that the minimal C-terminus is required for the Ku-LigD interaction, whereas the basic extension controls the threading and DNA bridging abilities of Ku. We propose that the Ku basic C-terminal extension increases the concentration of Ku near DNA ends, favoring the recruitment of LigD at the break, thanks to the minimal C-terminal sub-region.
    Mots-clés : B3S, INTGEN.


  • E. Pompe, E. M. van Rikxoort, O. M. Mets, J. - P. Charbonnier, J. - M. Kuhnigk, H. J. de Koning, M. Oudkerk, R. Vliegenthart, P. Zanen, J. - W. J. Lammers, B. van Ginneken, P. A. de Jong, et F. A. A. Mohamed Hoesein, « Follow-up of CT-derived airway wall thickness: Correcting for changes in inspiration level improves reliability », European Journal of Radiology, vol. 85, nᵒ 11, p. 2008-2013, 2016.


  • F. Réal, A. Severo Pereira Gomes, Y. O. Guerrero Martínez, T. Ayed, N. Galland, M. Masella, et V. Vallet, « Structural, dynamical, and transport properties of the hydrated halides: How do At− bulk properties compare with those of the other halides, from F− to I−? », The Journal of Chemical Physics, vol. 144, nᵒ 12, p. 124513, mars 2016.
    Mots-clés : astatine,bromine,chlorine,fluorine,free energy,halides,hydrogen bonds,iodine,molecular force constants,perturbation theory,polarisability,solvation,spin-orbit interactions, B3S, INTGEN.

  • C. Samson, I. Herrada, F. Celli, F. - X. Theillet, et S. Zinn-Justin, « 1H, 13C and 15N backbone resonance assignment of the intrinsically disordered region of the nuclear envelope protein emerin », Biomolecular NMR assignments, vol. 10, nᵒ 1, p. 179-182, 2016.
    Résumé : Human emerin is an inner nuclear membrane protein involved in the response of the nucleus to mechanical stress. It contributes to the physical connection between the cytoskeleton and the nucleoskeleton. It is also involved in chromatin organization. Its N-terminal region is nucleoplasmic and comprises a globular LEM domain from residue 1 to residue 43. The three-dimensional structure of this LEM domain in complex with the chromatin BAF protein was solved from NMR data. Apart from the LEM domain, the nucleoplasmic region of emerin, from residue 44 to residue 221, is predicted to be intrinsically disordered. Mutations in this region impair binding to several emerin partners as lamin A, actin or HDAC3. However the molecular details of these recognition defects are unknown. Here we report (1)H, (15)N, (13)CO, (13)Cα and (13)Cβ NMR chemical shift assignments of the emerin fragment from residue 67 to residue 170, which is sufficient for nuclear localization and involved in lamin A binding. Chemical shift analysis confirms that this fragment is intrinsically disordered in 0 and 8 M urea.
    Mots-clés : B3S, Dose-Response Relationship, Drug, Emerin, Humans, INTGEN, intrinsically disordered protein, Lamin Type A, Membrane Proteins, Muscular dystrophy, NMR spectroscopy, Nuclear Envelope, Nuclear Magnetic Resonance, Biomolecular, Nuclear Proteins, Urea.


  • S.  K. Tadi, C. Tellier-Lebègue, C. Nemoz, P. Drevet, S. Audebert, S. Roy, K. Meek, J. - B. Charbonnier, et M. Modesti, « PAXX Is an Accessory c-NHEJ Factor that Associates with Ku70 and Has Overlapping Functions with XLF », Cell Reports, vol. 17, nᵒ 2, p. 541-555, 2016.

2015

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Publications avant 2015


2014

- Hug1 is an intrinsically disordered protein that inhibits ribonucleotide reductase activity by directly binding Rnr2 subunit.
Meurisse J, Bacquin A, Richet N, Charbonnier JB, Ochsenbein F, Peyroche A. (2014) Nucleic Acids Res., 42 : 13174-13185.

- Automated classification of tailed bacteriophages according to their neck organization.
Lopes A, Tavares P, Petit MA, Guérois R, Zinn-Justin S. (2014) BMC Genomics, 15 : 1027.

- Regulation of the catalytic activity of the human phosphatase PTPN4 by its PDZ domain.
Maisonneuve P, Caillet-Saguy C, Raynal B, Gilquin B, Chaffotte A, Pérez J, Zinn-Justin S, Delepierre M, Buc H, Cordier F, Wolff N. (2014) FEBS J., 281 : 4852-4865.

- Simulated solvation of organic ions : protonated methylamines in water nanodroplets. Convergence toward bulk properties and the absolute proton solvation enthalpy.
Houriez C, Meot-Ner Mautner M, Masella M. (2014) J. Phys. Chem. B, 118 : 6222-6233.


2013

- Grafting of functional motifs onto protein scaffolds identified by PDB screening—an efficient route to design optimizable protein binders.
Tlatli R, Nozach H, Collet G, Beau F, Vera L, Stura E, Dive V, Cuniasse P (2013) FEBS J. 280 : 139-159.

- The helicase FBH1 is tightly regulated by PCNA via CRL4(Cdt2)-mediated proteolysis in human cells.
Bacquin A, Pouvelle C, Siaud N, Perderiset M, Salomé-Desnoulez S, Tellier-Lebegue C, Lopez B, Charbonnier JB, Kannouche PL. (2013) Nucleic Acids Res., 41 : 6501-6513.

- Structure of the MutLα C-terminal domain reveals how Mlh1 contributes to Pms1 endonuclease site.
Gueneau E, Dherin C, Legrand P, Tellier-Lebegue C, Gilquin B, Bonnesoeur P, Londino F, Quemener C, Le Du MH, Marquez JE, Moutiez M, Gondry M, Boiteux S, Charbonnier, JB. (2013) Nat. Struct. Mol. Biol., 20 : 461-468.

- Substrate and reaction specificity of Mycobacterium tuberculosis cytochrome P450 CYP121 : insights from biochemical studies and crystal structures.
Fonvielle M, Le Du MH, Lequin O, Lecoq A, Jacquet M, Thai R, Dubois S, Grach G, Gondry M, Belin P. (2013) J. Biol. Chem., 288 : 17347-17359.

- Effect of Rap1 binding on DNA distortion and potassium permanganate hypersensitivity.
Le Bihan YV, Matot B, Pietrement O, Giraud-Panis MJ, Gasparini S, Le Cam E, Gilson E, Sclavi B, Miron S, Le Du MH. (2013) Acta Crystallogr. D Biol. Crystallogr., 69(Pt 3) : 409-419.

- One identity or more for telomeres ?
Giraud-Panis MJ, Pisano S, Benarroch-Popivker D, Pei B, Le Du MH, Gilson E. (2013) Front Oncol., 3 : 48.

- Revisiting a many-body model for water based on a single polarizable site : from gas phase clusters to liquid and air/liquid water systems.
Réal F, Vallet V, Flament JP, Masella M. (2013) J. Chem. Phys., 139 : 114502.

- A multiscale coarse-grained polarizable solvent model for handling long tail bulk electrostatics.
Masella M, Borgis D, Cuniasse P. (2013) J. Comput. Chem., 34:1112-1124.

- Further insights in the ability of classical nonadditive potentials to model actinide ion-water interactions.
Réal F, Trumm M, Schimmelpfennig B, Masella M, Vallet V. (2013) J. Comput. Chem., 34 : 707-719.

- Inhibitory signalling to the Arp2/3 complex steers cell migration.
Dang I, Gorelik R, ..., Herrada I, ..., Zinn-Justin S, Cherfils J, Bièche I, Alexandrova AY, David NB, Small JV, Faix J, Blanchoin L, Gautreau A. (2013) Nature, 503 : 281-284.

- Inhibition of TGF-β signaling at the nuclear envelope : characterization of interactions between MAN1, Smad2 and Smad3, and PPM1A.
Bourgeois B, Gilquin B, Tellier-Lebègue C, Östlund C, Wu W, Pérez J, El Hage P, Lallemand F, Worman HJ, Zinn-Justin S. (2013) Sci. Signal., 6 : ra49.

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