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Malinge Jean-Marc


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2016   Références trouvées : 1

Thibault T., Degrouard J., Baril P., Pichon C., Midoux P. and Malinge J.-M.  (2016)

Production of DNA minicircles less than 250 base pairs through a novel concentrated DNA circularization assay enabling minicircle design with NF-kappaB inhibition activity

Nucleic acids research (2016) - doi : 10.1093/nar/gkw1034
Double-stranded DNA minicircles of less than 1000 bp in length have great interest in both fundamental research and therapeutic applications. Although minicircles have shown promising activity in gene therapy thanks to their good biostability and better intracellular trafficking, minicircles down to 250 bp in size have not yet been investigated from the test tube to the cell for lack of an efficient production method. Herein, we report a novel versatile plasmid-free method for the production of DNA minicircles comprising fewer than 250 bp. We designed a linear nicked DNA double-stranded oligonucleotide blunt-ended substrate for efficient minicircle production in a ligase-mediated and bending protein-assisted circularization reaction at high DNA concentration of 2 muM. This one pot multi-step reaction based-method yields hundreds of micrograms of minicircle with sequences of any base composition and position and containing or not a variety of site-specifically chemical modifications or physiological supercoiling. Biochemical and cellular studies were then conducted to design a 95 bp minicircle capable of binding in vitro two NF-kappaB transcription factors per minicircle and to efficiently inhibiting NF-kappaB-dependent transcriptional activity in human cells. Therefore, our production method could pave the way for the design of minicircles as new decoy nucleic acids.

Double-stranded DNA minicircles of less than 1000 bp in length have great interest in both fundamental research and therapeutic applications. Although minicircles have shown promising activity in gene therapy thanks to their good biostability and better intracellular trafficking, minicircles down to 250 bp in size have not yet been investigated from the test tube to the cell for lack of an efficient production method. Herein, we report a novel versatile plasmid-free method for the production of DNA minicircles comprising fewer than 250 bp. We designed a linear nicked DNA double-stranded oligonucleotide blunt-ended substrate for efficient minicircle production in a ligase-mediated and bending protein-assisted circularization reaction at high DNA concentration of 2 muM. This one pot multi-step reaction based-method yields hundreds of micrograms of minicircle with sequences of any base composition and position and containing or not a variety of site-specifically chemical modifications or physiological supercoiling. Biochemical and cellular studies were then conducted to design a 95 bp minicircle capable of binding in vitro two NF-kappaB transcription factors per minicircle and to efficiently inhibiting NF-kappaB-dependent transcriptional activity in human cells. Therefore, our production method could pave the way for the design of minicircles as new decoy nucleic acids.


2014   Références trouvées : 1

Kasparkova, J. Thibault, T.Kostrhunova, H., Stepankova, J., Vojtiskova, M., Muchova, T., Midoux, P., Malinge, J.M. and Brabec, V.  (2014)

Different affinity of nuclear factor-kappa B proteins to DNA modified by antitumor cisplatin and its clinically ineffective trans isomer

Febs Journal (2014) 281 (5) 1393-1408 - doi : 10.1111/febs.12711
Nuclear factor-kappa B (NF-kB) comprises a family of protein transcription factors that have a regulatory function in numerous cellular processes and are implicated in the cancer cell response to antineoplastic drugs, including cisplatin. We characterized the effects of DNA adducts of cisplatin and ineffective transplatin on the affinity of NF-kB proteins to their consensus DNA sequence (kB site). Although the kB site-NF-B protein interaction was significantly perturbed by DNA adducts of cisplatin, transplatin adducts were markedly less effective both in cell-free media and in cellulo using a decoy strategy derivatized-approach. Moreover, NF-B inhibitor JSH-23 [4-methyl-N-1-(3-phenylpropyl)benzene-1,2-diamine] augmented cisplatin cytotoxicity in ovarian cancer cells and the data showed strong synergy with JSH-23 for cisplatin. The distinctive structural features of DNA adducts of the two platinum complexes suggest a unique role for conformational distortions induced in DNA by the adducts of cisplatin with respect to inhibition of the binding of NF-kB to the platinated kB sites. Because thousands of B sites are present in the DNA, the mechanisms underlying the antitumor efficiency of cisplatin in some tumor cells may involve downstream processes after inhibition of the binding of NF-B to B site(s) by DNA adducts of cisplatin, including enhanced programmed cell death in response to drug treatment.

Nuclear factor-kappa B (NF-kB) comprises a family of protein transcription factors that have a regulatory function in numerous cellular processes and are implicated in the cancer cell response to antineoplastic drugs, including cisplatin. We characterized the effects of DNA adducts of cisplatin and ineffective transplatin on the affinity of NF-kB proteins to their consensus DNA sequence (kB site). Although the kB site-NF-B protein interaction was significantly perturbed by DNA adducts of cisplatin, transplatin adducts were markedly less effective both in cell-free media and in cellulo using a decoy strategy derivatized-approach. Moreover, NF-B inhibitor JSH-23 [4-methyl-N-1-(3-phenylpropyl)benzene-1,2-diamine] augmented cisplatin cytotoxicity in ovarian cancer cells and the data showed strong synergy with JSH-23 for cisplatin. The distinctive structural features of DNA adducts of the two platinum complexes suggest a unique role for conformational distortions induced in DNA by the adducts of cisplatin with respect to inhibition of the binding of NF-kB to the platinated kB sites. Because thousands of B sites are present in the DNA, the mechanisms underlying the antitumor efficiency of cisplatin in some tumor cells may involve downstream processes after inhibition of the binding of NF-B to B site(s) by DNA adducts of cisplatin, including enhanced programmed cell death in response to drug treatment.


2013   Références trouvées : 2

Sedletska, Y. Culard, F. Midoux, P.and Malinge, J. M.  (2013)

Interaction studies of muts and mutl with DNA containing the major cisplatin lesion and its mismatched counterpart under equilibrium and nonequilibrium conditions

Biopolymers 99 (9) 636-647
The DNA mismatch repair (MMR) system participates in cis-diamminedichloroplatinum (II) (cisplatin) cytotoxicity through signaling of cisplatin DNA lesions by yet unknown molecular mechanisms. It is thus of great interest to determine whether specialized function of MMR proteins could be associated with cisplatin DNA damage. The major cisplatin 1,2-d(GpG) intrastrand crosslink and compound lesions arising from misincorporation of a mispaired base opposite either platinated guanine of the 1,2-d(GpG) adduct are thought to be critical lesions for MMR signaling. Previously, we have shown that cisplatin compound lesion with a mispaired thymine opposite the 3 platinated guanine triggers new Escherichia coli MutS ATP-dependent biochemical activities distinguishable from those encountered with DNA mismatch consistent with a role of this lesion in MMR-dependent signaling mechanism. In this report, we show that the major cisplatin 1,2-d(GpG) intrastrand crosslink does not confer novel MutS postrecognition biochemical activity as studied by surface plasmon resonance spectroscopy. A fast rate of MutS ATP-dependent dissociation prevents MutL recruitment to the major cisplatin lesion in contrast to cisplatin compound lesion which authorized MutS-dependent recruitment of MutL with a dynamic of ternary complex formation distinguishable from that encountered with DNA mismatch substrate. We conclude that the mode of cisplatin DNA damage recognition by MutS and the nature of MMR post-recognition events are lesion-dependent and suggest that MMR signaling through the major cisplatin lesion is unlikely to occur.

The DNA mismatch repair (MMR) system participates in cis-diamminedichloroplatinum (II) (cisplatin) cytotoxicity through signaling of cisplatin DNA lesions by yet unknown molecular mechanisms. It is thus of great interest to determine whether specialized function of MMR proteins could be associated with cisplatin DNA damage. The major cisplatin 1,2-d(GpG) intrastrand crosslink and compound lesions arising from misincorporation of a mispaired base opposite either platinated guanine of the 1,2-d(GpG) adduct are thought to be critical lesions for MMR signaling. Previously, we have shown that cisplatin compound lesion with a mispaired thymine opposite the 3 platinated guanine triggers new Escherichia coli MutS ATP-dependent biochemical activities distinguishable from those encountered with DNA mismatch consistent with a role of this lesion in MMR-dependent signaling mechanism. In this report, we show that the major cisplatin 1,2-d(GpG) intrastrand crosslink does not confer novel MutS postrecognition biochemical activity as studied by surface plasmon resonance spectroscopy. A fast rate of MutS ATP-dependent dissociation prevents MutL recruitment to the major cisplatin lesion in contrast to cisplatin compound lesion which authorized MutS-dependent recruitment of MutL with a dynamic of ternary complex formation distinguishable from that encountered with DNA mismatch substrate. We conclude that the mode of cisplatin DNA damage recognition by MutS and the nature of MMR post-recognition events are lesion-dependent and suggest that MMR signaling through the major cisplatin lesion is unlikely to occur.

Ezzine, S., Vassaux, G., Pitard, B., Barteau, B., Malinge, J. M., Midoux, P., Pichon, C. and Baril, P.  (2013)

RILES, a novel method for temporal analysis of the in vivo regulation of miRNA expression

Nucleic Acids Res - 1-14 - doi : 10.1093/nar/gkt797
Novel methods are required to investigate the complexity of microRNA (miRNA) biology and particularly their dynamic regulation under physiopathological conditions. Herein, a novel plasmid-based RNAi-Inducible Luciferase Expression System (RILES) was engineered to monitor the activity of endogenous RNAi machinery. When RILES is transfected in a target cell, the miRNA of interest suppresses the expression of a transcriptional repressor and consequently switch-ON the expression of the luciferase reporter gene. Hence, miRNA expression in cells is signed by the emission of bioluminescence signals that can be monitored using standard bioluminescence equipment. We validated this approach by monitoring in mice the expression of myomiRs-133, -206 and -1 in skeletal muscles and miRNA-122 in liver. Bioluminescence experiments demonstrated robust qualitative and quantitative data that correlate with the miRNA expression pattern detected by quantitative RT-PCR (qPCR). We further demonstrated that the regulation of miRNA-206 expression during the development of muscular atrophy is individual-dependent, time-regulated and more complex than the information generated by qPCR. As RILES is simple and versatile, we believe that this methodology will contribute to a better understanding of miRNA biology and could serve as a rationale for the development of a novel generation of regulatable gene expression systems with potential therapeutic applications.

Novel methods are required to investigate the complexity of microRNA (miRNA) biology and particularly their dynamic regulation under physiopathological conditions. Herein, a novel plasmid-based RNAi-Inducible Luciferase Expression System (RILES) was engineered to monitor the activity of endogenous RNAi machinery. When RILES is transfected in a target cell, the miRNA of interest suppresses the expression of a transcriptional repressor and consequently switch-ON the expression of the luciferase reporter gene. Hence, miRNA expression in cells is signed by the emission of bioluminescence signals that can be monitored using standard bioluminescence equipment. We validated this approach by monitoring in mice the expression of myomiRs-133, -206 and -1 in skeletal muscles and miRNA-122 in liver. Bioluminescence experiments demonstrated robust qualitative and quantitative data that correlate with the miRNA expression pattern detected by quantitative RT-PCR (qPCR). We further demonstrated that the regulation of miRNA-206 expression during the development of muscular atrophy is individual-dependent, time-regulated and more complex than the information generated by qPCR. As RILES is simple and versatile, we believe that this methodology will contribute to a better understanding of miRNA biology and could serve as a rationale for the development of a novel generation of regulatable gene expression systems with potential therapeutic applications.


2008   Références trouvées : 2

Lopez-Crapez, E., Malinge, J.M., Gatchitch, F., Casano, L., Langlois, T., Pugniere, M., Roquet, F., Mathis, G. & Bazin, H.  (2008)

A homogeneous resonance energy transfer-based assay to monitor MutS/DNA interactions.

Anal. Biochem. 383, 301-306.

Castellano-Castillo, M., Kostrhunova, H., Marini, V., Kasparkova, J., Sadler, P.J., Malinge, J.M. & Brabec, V.  (2008)

Binding of mismatch repair protein MutS to mispaired DNA adducts of intercalating ruthenium(II) arene complexes.

J. Biol. Inorg. Chem. 13, 993-999.


2007   Références trouvées : 1

Sedletska, Y ; Fourrier, L ; Malinge, JM  (2007)

Modulation of MutS ATP-dependent functional activities by DNA containing a cisplatin compound lesion (base damage and mismatch)

Journal of Molecular Biology 369 (1) 27-40
DNA damage-dependent signaling by the DNA mismatch repair (MMR) system is thought to mediate cytotoxicity of the anti-tumor drug cisplatin through molecular mechanisms that could differ from those required for normal mismatch repair. The present study investigated whether ATP-dependent biochemical properties of Escherichia coli MutS protein differ when the protein interacts with a DNA oligonucleotide containing a GT mismatch versits a unique site specifically placed cisplatin compound lesion, a cisplatin 1,2-d(GpG) intrastrand cross-link with a mispaired thymine opposite the 3' platinated guanine.

DNA damage-dependent signaling by the DNA mismatch repair (MMR) system is thought to mediate cytotoxicity of the anti-tumor drug cisplatin through molecular mechanisms that could differ from those required for normal mismatch repair. The present study investigated whether ATP-dependent biochemical properties of Escherichia coli MutS protein differ when the protein interacts with a DNA oligonucleotide containing a GT mismatch versits a unique site specifically placed cisplatin compound lesion, a cisplatin 1,2-d(GpG) intrastrand cross-link with a mispaired thymine opposite the 3’ platinated guanine.


2005   Références trouvées : 1

Malinge, JM   (2005)

Cisplatin is a DNA-damaging antitumour compound triggering multifactorial biochemical responses in cancer cells : importance of apoptotic pathways

Current Medicinal Chemistry- Anti-Cancer Agents 5 (3) 251-265


2003   Références trouvées : 1

Fourrier, L ; Brooks, P ; Malinge, JM  (2003)

Binding discrimination of MutS to a set of lesions and compound lesions (base damage and mismatch) reveals its potential role as a cisplatin-damaged DNA sensing protein

Journal of Biological Chemistry 278 (23) 21267-21275
The DNA mismatch repair (MMR) system plays a critical role in sensitizing both prokaryotic and eukaryotic cells to the clinically potent anticancer drug cisplatin. It is thought to mediate cytotoxicity through recognition of cisplatin DNA lesions. This drug generates a range of lesions that may also give rise to compound lesions resulting from the misincorporation of a base during translesion synthesis. Using gel mobility shift competition assays and surface plasmon resonance, we have analyzed the interaction of Escherichia coli MutS protein with site-specifically modified DNA oligonucleotides containing each of the four cisplatin cross-links or a set of compound lesions. The major 1,2-d(GpG) cisplatin intrastrand cross-link was recognized with only a 1.5-fold specificity, whereas a 47-fold specificity was found with a natural G/T containing DNA substrate.

The DNA mismatch repair (MMR) system plays a critical role in sensitizing both prokaryotic and eukaryotic cells to the clinically potent anticancer drug cisplatin. It is thought to mediate cytotoxicity through recognition of cisplatin DNA lesions. This drug generates a range of lesions that may also give rise to compound lesions resulting from the misincorporation of a base during translesion synthesis. Using gel mobility shift competition assays and surface plasmon resonance, we have analyzed the interaction of Escherichia coli MutS protein with site-specifically modified DNA oligonucleotides containing each of the four cisplatin cross-links or a set of compound lesions. The major 1,2-d(GpG) cisplatin intrastrand cross-link was recognized with only a 1.5-fold specificity, whereas a 47-fold specificity was found with a natural G/T containing DNA substrate.


2002   Références trouvées : 1

Montero, EI ; Perez, JM ; Schwartz, A ; Fuertes, MA ; Malinge, JM ; Alonso, C ; Leng, M ; Navarro-Ranninger, C  (2002)

Apoptosis induction and DNA interstrand cross-link formation by cytotoxic trans-[PtCl2(NH(CH3)(2))(NHCH(CH3)(2))] : Cross-linking between d(G) and complementary d(C) within oligonucleotide duplexes

Chembiochem 3 (1) 61-67
We have investigated the cytotoxic activity, the induction of apoptosis, and the interstrand cross-linking efficiency in the A2780cisR ovarian tumor cell line, after replacement of the two NH3 nonleaving groups in trans-[PtCl2(NH3)(2)] (trans-DDP) by dimethylamine and isopropylamine. The data show that trans-[PtCl2(NH(CH3)(2))(NHCH(CH3)(2))] is able to circumvent resistance to cis-[PtCl2(NH3)(2)] (cis-DDP, cisplatin) in A2780cisR cells.

We have investigated the cytotoxic activity, the induction of apoptosis, and the interstrand cross-linking efficiency in the A2780cisR ovarian tumor cell line, after replacement of the two NH3 nonleaving groups in trans-[PtCl2(NH3)(2)] (trans-DDP) by dimethylamine and isopropylamine. The data show that trans-[PtCl2(NH(CH3)(2))(NHCH(CH3)(2))] is able to circumvent resistance to cis-[PtCl2(NH3)(2)] (cis-DDP, cisplatin) in A2780cisR cells.


2001   Références trouvées : 1

Fourrier, L ; Malinge, JM ; Brooks, P  (2001)

Analysis of the binding of MutS to cisplatin-modified DNA

Journal of Inorganic Biochemistry 86 (1) 220-220


2000   Références trouvées : 3

Malinge, JM   (2000)

Obituary : Remembering Marc Leng

Metal-Based Drugs 7 (3) 165-166

Malinge, JM ; Giraud-Panis, MJ ; Leng, M  (2000)

Interstrand cross-links of cisplatin induce striking distortions in DNA (vol 77, pg 23, 1999)

Journal of Inorganic Biochemistry 81 (1-2) 119-119

Malinge, JM ; Schwartz, A ; Leng, M  (2000)

Gel electrophoresis and bending in cisplatin-modified linear DNA

Dna-Protein Interactions 25-35 - Editor(s) : Travers, A ; Buckle, M ; Travers, A ; Buckle, M


1999   Références trouvées : 3

Malinge, JM ; Leng, M   (1999)

Interstrand cross-links in cisplatin-or transplatin- modified DNA

Cisplatin - Chemistry and Biochemistry of A Leading Anticancer Drug 159-180 - Editor(s) : Lippert, B

Malinge, JM ; Giraud-Panis, MJ ; Leng, M  (1999)

Interstrand cross-links of cisplatin induce striking distortions in DNA

Journal of Inorganic Biochemistry 77 (1-2) 23-29
In the reaction between cellular DNA and cisplatin, different bifunctional adducts are formed including intrastrand and interstrand crosslinks. The respective role of these lesions in the cytotoxicity of the drug is not yet elucidated. This paper deals with the current knowledge on cisplatin interstrand cross-links and presents results on the formation, stability and structure of these adducts. A key step in the studies of these lesions is the recent determination of solution and crystallographic structures of double-stranded oligonucleotides containing a unique interstrand cross-link.

In the reaction between cellular DNA and cisplatin, different bifunctional adducts are formed including intrastrand and interstrand crosslinks. The respective role of these lesions in the cytotoxicity of the drug is not yet elucidated. This paper deals with the current knowledge on cisplatin interstrand cross-links and presents results on the formation, stability and structure of these adducts. A key step in the studies of these lesions is the recent determination of solution and crystallographic structures of double-stranded oligonucleotides containing a unique interstrand cross-link.

Coste, F ; Malinge, JM ; Serre, L ; Shepard, W ; Roth, M ; Leng, M ; Zelwer, C  (1999)

Crystal structure of a double-stranded DNA containing a cisplatin interstrand cross-link at 1.63 angstrom resolution : hydration at the platinated site

Nucleic Acids Research 27 (8) 1837-1846
cis-diamminedichloroplatinum (II) (cisplatin) is a powerful anti-tumor drug whose target is cellular DNA, In the reaction between DNA and cisplatin, covalent intrastrand and interstrand cross-links (ICL) are formed. Two solution structures of the ICL have been published recently. In both models the double-helix is bent and unwound but with significantly different angle values. We solved the crystal structure at 100K of a double-stranded DNA decamer containing a single cisplatin ICL, using the anomalous scattering (MAD) of platinum as a unique source of phase information.

cis-diamminedichloroplatinum (II) (cisplatin) is a powerful anti-tumor drug whose target is cellular DNA, In the reaction between DNA and cisplatin, covalent intrastrand and interstrand cross-links (ICL) are formed. Two solution structures of the ICL have been published recently. In both models the double-helix is bent and unwound but with significantly different angle values. We solved the crystal structure at 100K of a double-stranded DNA decamer containing a single cisplatin ICL, using the anomalous scattering (MAD) of platinum as a unique source of phase information.


1997   Références trouvées : 1

Perez, C ; Leng, M ; Malinge, JM  (1997)

Rearrangement of interstrand cross-links into intrastrand cross-links in cis-diamminedichloroplatinum(II)-modified DNA

Nucleic Acids Research 25 (4) 896-903
In the reaction of the anticancer drug cis diamminedichloroplatinum(II) (cis-DDP) with DNA, bifunctional intrastrand and interstrand cross-links are formed, In this work, we show that at 37 degrees C interstrand cross-links (ICL) are labile and rearrange into intrastrand cross-links, The ICL instability was first studied with a 10 base pairs (bp) double-stranded oligonucleotide containing a unique site-specific ICL resulting from chelation of the N7 position of two guanine residues on the opposite strands of DNA at the d(GC/GC) site by a cis-diammineplatinum(II) residue.

In the reaction of the anticancer drug cis diamminedichloroplatinum(II) (cis-DDP) with DNA, bifunctional intrastrand and interstrand cross-links are formed, In this work, we show that at 37 degrees C interstrand cross-links (ICL) are labile and rearrange into intrastrand cross-links, The ICL instability was first studied with a 10 base pairs (bp) double-stranded oligonucleotide containing a unique site-specific ICL resulting from chelation of the N7 position of two guanine residues on the opposite strands of DNA at the d(GC/GC) site by a cis-diammineplatinum(II) residue.


1996   Références trouvées : 1

Paquet, F ; Perez, C ; Leng, M ; Lancelot, G ; Malinge, JM  (1996)

NMR solution structure of a DNA decamer containing an interstrand cross-link of the antitumor drug cis-diamminedichloroplatinum(II)

Journal of Biomolecular Structure & Dynamics 14 (1) 67-77
A 10 base pairs double-stranded oligonucleotide with the sequence d(CCTCG*CTCTC). d(GAGAG*CGAGG) containing a single interstrand cross-link resulting from chelation of the N7 position of two guanine residues on the opposite strands of DNA at the d(G*C/G*C) site by a cis-diammineplatinum(II) residue was analyzed by H-1 NMR spectroscopy. All the exchangeable and nonexchangeable protons resonance lines (except some H5'-H5 '') were assigned. NOESY spectra and chemical shifts indicated that the cross-linkage of the guanines of G*5 and G*6 induced extrahelicity of C5 and C6.

A 10 base pairs double-stranded oligonucleotide with the sequence d(CCTCG*CTCTC). d(GAGAG*CGAGG) containing a single interstrand cross-link resulting from chelation of the N7 position of two guanine residues on the opposite strands of DNA at the d(G*C/G*C) site by a cis-diammineplatinum(II) residue was analyzed by H-1 NMR spectroscopy. All the exchangeable and nonexchangeable protons resonance lines (except some H5’-H5 ’’) were assigned. NOESY spectra and chemical shifts indicated that the cross-linkage of the guanines of G*5 and G*6 induced extrahelicity of C5 and C6.


1994   Références trouvées : 1

Malinge, JM ; Perez, C ; Leng, M  (1994)

Base sequence-independent distorsions induced by interstrand cross-links in cis-diaminedichloroplatinum (II)-modified DNA

Nucleic Acids Research 22 (19) 3834-3839
Physico-chemical and immunological studies have been done in order to further characterize the distorsions induced in DNA by the interstrand crosslinks formed between the antitumor diamminedichloroplatinum (II) (cis-DDP) guanines on the opposite strands of DNA at the d(GC/GC) sites. Bending (45 degrees) and unwinding(79 4 degrees) were determined from the electrophoretic mobility of multimers of 21- 24-base pairs double-stranded oligonucleotides containing an interstrand cross-link in the central sequence d(TGCT/AGCA).

Physico-chemical and immunological studies have been done in order to further characterize the distorsions induced in DNA by the interstrand crosslinks formed between the antitumor diamminedichloroplatinum (II) (cis-DDP) guanines on the opposite strands of DNA at the d(GC/GC) sites. Bending (45 degrees) and unwinding(79 4 degrees) were determined from the electrophoretic mobility of multimers of 21- 24-base pairs double-stranded oligonucleotides containing an interstrand cross-link in the central sequence d(TGCT/AGCA).


1992   Références trouvées : 1

Gaucheron, F ; Lemaire, MA ; Malinge, JM ; Schwartz, A ; Leng, M.  (1992)

Reactivity of DNA and cisdiamminedichloroplatinum (II) in the presence of intercalatingagents

Platinum and Other Metal Coordination Compounds in Cancer Chemotherapy 73 - Editor(s) : Howell, SB ( Plenum Press, New York)


1990   Références trouvées : 1

Malinge, JM ; Sip, M ; Blacker, AJ ; Lehn, JM ; Leng, M  (1990)

Formation of a DNA monofunctional cis-platinum adduct cross-linking the intercalating drug n-methyl-2,7-diazapyrenium

Nucleic Acids Research 18 (13) 3887-3891


1988   Références trouvées : 2

Malinge, JM ; Leng, M  (1988)

Reactivity of monofunctional cis-platinum adducts as a function of DNA-sequence

Nucleic Acids Research 16 (15) 7663-7672

Malinge, JM ; Schwartz, A ; Leng, M  (1988)

Reaction of nucleic-acids with cis-dichlorodiammineplatinum(ii) in the presence of intercalating agents - characterization of new ternary complexes

Bulletin Du Cancer 75 (7) 668-668


1987   Références trouvées : 1

Malinge, JM ; Schwartz, A ; Leng, M  (1987)

Characterization of the ternary complexes formed in the reaction of cis-diamminedichloroplatinum-(II), ethidium-bromide and nucleic-acids

Nucleic Acids Research 15 (4) 1779-1797


1985   Références trouvées : 2

Leng, M ; Malinge, JM ; Ptak, M  (1985)

Importance of DNA conformation in the reaction with cisdichlorodiammine platinum(II)

Journal of Biosciences 8 (3-4) 721-729

Rahmouni, A ; Malinge, JM ; Schwartz, A ; Leng, M  (1985)

Comparison between poly(dg-dc).poly(dg-dc) and DNA modified by cis-diamminedichloroplatinum(II) - immunological and spectroscopic studies

Journal of Biomolecular Structure & Dynamics 3 (2) 363-375


1984   Références trouvées : 3

Malinge, JM ; Leng, M  (1984)

Reaction of cis-diamminedichloroplatinum(II) and DNA in b-conformation or z-conformation)

Embo Journal 3 (6) 1273-1279

Malinge, JM ; Ptak, M ; Leng, M  (1984)

Immunological and spectroscopic studies of poly(dg-dc).poly(dg-dc) modified by cis-diamminedichloroplatinum(II)

Nucleic Acids Research 12 (14) 5767-5778

Revet, B ; Malinge, JM ; Delain, E ; Lebret, M ; Leng, M  (1984)

Electron-microscopic measurement of chain flexibility of poly(dg-dc).poly(dg-dc) modified by cis-diamminedichloroplatinum(ii)

Nucleic Acids Research 12 (22) 8349-8362


1983   Références trouvées : 1

Leng, M ; Freund, A M ; Malfoy, B ; Malinge, JM ; Pilet, J ; Rio, P   (1983)

ZDNA : Implication for DNA damage and repair. Cellular responses to DNA damage

New Series 11 23-26 - Editor(s) : Liss, AR Inc. (NewYork)


Mots-clés

Chargé de recherche , Thérapies innovantes et nanomédecine