Modelling of DNA Complexes with Distamycin Analogues Using an ab initio Continuum Solvent Model

2000 ◽  
Vol 65 (5) ◽  
pp. 631-643 ◽  
Author(s):  
Petr Bouř ◽  
Vladimír Král
Keyword(s):  
Complex Formation ◽  
Ab Initio ◽  
Polar Solvent ◽  
Molecular Shape ◽  
Conformational Flexibility ◽  
Model Systems ◽  
Dna Complexes ◽  
Solvent Model ◽  
Dna Complex

Model systems related to non-covalent minor groove DNA complexes with distamycin analogues were investigated using the Turbomole and Gaussian quantum chemical packages. The role of molecular shape, electrostatic field and conformer energies in the complex formation was discussed. The ab initio calculations included the COSMO solvent model. If compared to vacuum computations, polar solvent significantly destabilizes such complexes and increases conformational flexibility of distamycin. The DNA complex formation appears to be driven mainly by entropy lowering and complementarity of molecular shapes. The NH moiety of the amide group preferably points to the base pair according to the computations, in agreement with experimental data.

Determining the topology of stable protein–DNA complexes

2013 ◽  
Vol 41 (2) ◽  
pp. 601-605 ◽  
Author(s):  
Isabel K. Darcy ◽  
Mariel Vazquez
Keyword(s):  
Present Article ◽  
Experimental Technique ◽  
Topological Structure ◽  
Reaction Pathway ◽  
Dna Supercoiling ◽  
Dna Complexes ◽  
Nucleoprotein Complex ◽  
Mu Transpososome ◽  
Dna Complex

Difference topology is an experimental technique that can be used to unveil the topological structure adopted by two or more DNA segments in a stable protein–DNA complex. Difference topology has also been used to detect intermediates in a reaction pathway and to investigate the role of DNA supercoiling. In the present article, we review difference topology as applied to the Mu transpososome. The tools discussed can be applied to any stable nucleoprotein complex.

scholarly journals Cryo-EM structure ofEscherichia coliσ70RNA polymerase and promoter DNA complex revealed a role of σ non-conserved region during the open complex formation

2018 ◽  
Vol 293 (19) ◽  
pp. 7367-7375 ◽  
Author(s):  
Anoop Narayanan ◽  
Frank S. Vago ◽  
Kunpeng Li ◽  
M. Zuhaib Qayyum ◽  
Dinesh Yernool ◽  
...  
Keyword(s):  
Complex Formation ◽  
Conserved Region ◽  
Open Complex Formation ◽  
Promoter Dna ◽  
Dna Complex

Multicomponent Cationic Lipid−DNA Complex Formation:  Role of Lipid Mixing

Langmuir ◽  
2005 ◽  
Vol 21 (25) ◽  
pp. 11582-11587 ◽  
Author(s):  
Giulio Caracciolo ◽  
Daniela Pozzi ◽  
Heinz Amenitsch ◽  
Ruggero Caminiti
Keyword(s):  
Complex Formation ◽  
Cationic Lipid ◽  
Dna Complex

Regulation of microRNAs in Inflammation-Associated Colorectal Cancer: A Mechanistic Approach

2020 ◽  
Vol 20 ◽  
Author(s):  
Sridhar Muthusami ◽  
Ilangovan Ramachandran ◽  
Sneha Krishnamoorthy ◽  
Yuvaraj Sambandam ◽  
Satish Ramalingam ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Molecular Mechanisms ◽  
Colorectal Carcinogenesis ◽  
Model Systems ◽  
Necrosis Factor Alpha ◽  
Multi Stage ◽  
Mechanistic Approach ◽  
Tnf Α ◽  
Factor Alpha

: The development of colorectal cancer (CRC) is a multi-stage process. The inflammation of the colon as in inflammatory bowel disease (IBD) such as ulcerative colitis (UC) or Crohn’s disease (CD) is often regarded as the initial trigger for the development of CRC. Many cytokines such as tumor necrosis factor alpha (TNF-α) and several interleukins (ILs) are known to exert proinflammatory actions, and inflammation initiates or promotes tumorigenesis of various cancers, including CRC through differential regulation of microRNAs (miRNAs/miRs). miRNAs can be oncogenic miRNAs (oncomiRs) or anti-oncomiRs/tumor suppressor miRNAs, and they play key roles during colorectal carcinogenesis. However, the functions and molecular mechanisms of regulation of miRNAs involved in inflammation-associated CRC are still anecdotal and largely unknown. Consolidating the published results and offering perspective solutions to circumvent CRC, the current review is focused on the role of miRNAs and their regulation in the development of CRC. We have also discussed the model systems adapted by researchers to delineate the role of miRNAs in inflammation-associated CRC.

Role of inflammation in the development of colorectal cancer

2020 ◽  
Vol 20 ◽  
Author(s):  
Sridhar Muthusami ◽  
R. Ileng Kumaran ◽  
Kokelavani Nampalli Babu ◽  
Sneha Krishnamoorthy ◽  
Akash Guruswamy ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Chronic Inflammation ◽  
Interleukin 1 ◽  
Cell Types ◽  
Model Systems ◽  
Cytokine Gene Expression ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Proinflammatory Molecules

: Chronic inflammation can lead to the development of many diseases including cancer. Inflammatory bowel disease (IBD) that includes both ulcerative colitis (UC) and Crohn's disease (CD) are risk factors for the development of colorectal cancer (CRC). Many cytokines produced primarily by the gut immune cells either during or in response to localized inflammation in the colon and rectum are known to stimulate the complex interactions between the different cell types in the gut environment resulting in acute inflammation. Subsequently, chronic inflammation together with genetic and epigenetic changes has been shown to lead to the development and progression of CRC. Various cell types present in the colon such as enterocytes, Paneth cells, goblet cells and macrophages express receptors for inflammatory cytokines and respond to tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6 and other cytokines. Among the several cytokines produced, TNF-α and IL-1β are the key proinflammatory molecules that play critical roles in the development of CRC. The current review is intended to consolidate the published findings to focus on the role of proinflammatory cytokines, namely TNF-α and IL-1β, on inflammation (and the altered immune response) in the gut, to better understand the development of CRC in IBD, using various experimental model systems, preclinical and clinical studies. Moreover, this review also highlights the current therapeutic strategies available (monotherapy and combination therapy), to alleviate the symptoms or treat inflammationassociated CRC by using monoclonal antibodies or aptamers to block proinflammatory molecules, inhibitors of tyrosine kinases in inflammatory signaling cascade, competitive inhibitors of proinflammatory molecules, and the nucleic acid drugs like small activating RNAs (saRNAs) or microRNA (miRNA) mimics to activate tumor suppressor or repress oncogene/proinflammatory cytokine gene expression.

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