Bioinformation (Bioinformation )

Description

  • Impact factor
    0.50
  • 5-year impact
    0.00
  • Cited half-life
    0.00
  • Immediacy index
    0.00
  • Eigenfactor
    0.00
  • Article influence
    0.00
  • Other titles
    Bioinformation, Beyond informatics, Bioinformation journal for beyond bioinformatics
  • ISSN
    0973-2063
  • OCLC
    61658917
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract: Cell cycle is maintained almost all the times and is controlled by various regulatory proteins and their complexes (Cdk+Cyclin) in different phases of interphase (G1, S and G2) and mitosis of cell cycle. A number of mechanisms have been proposed for the initiation and progression of carcinogenesis by abruption in cell cycle process. One of the important features of cancer/carcinogenesis is functional loss of these cell cycle regulatory proteins particularly in CDKs and cyclins. We hypothesize that there is a direct involvement of these cell cycle regulatory proteins not only at the genetic level but also proteins level, during the initiation of carcinogenesis. Therefore, it becomes significant to determine inconsistency in the functioning of regulatory proteins due to interaction with carcinogen 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Hence, we investigated the interaction efficiency of NNK, against cell cycle regulatory proteins. We found a different value of ∆G (free energy of binding) among the studied proteins ranging between -3.29 to -7.25 kcal/mol was observed. To validate the results, we considered Human Oxy-Hemoglobin at 1.25 Å Resolution, [PDB_ID:1HHO] as a +ve control, (binding energy -6.06 kcal/mol). Finally, the CDK8 (PDB_ID:3RGF) and CDK2 (PDB_ID:3DDP) regulatory proteins showing significantly strong molecular interaction with NNK -7.25 kcal/mol, -6.19 kcal/mol respectively were analyzed in details. In this study we predicted that CDK8 protein fails to form functional complex with its complementary partner cyclin C in presence of NNK. Consequently, inconsistency of functioning in regulatory proteins might lead to the abruption in cell cycle progression; contribute to the loss of cell cycle control and subsequently increasing the possibility of carcinogenesis. Keywords: Cell cycle, Carcinogen NNK, Check points, CDKs, Oncoinformatics and Z-Dock.
    Bioinformation 08/2014; 10(8):474-479.
  • Source
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    ABSTRACT: Molecular modelling and structural study of 12-mer immobile four-way DNA junction model is reported here. The DNA junction which was built and investigated, consisted of the following sequences 5'd(GGAAGGGGCTGG), 5'd(CCAGCCTGAGCC), 5'd(GGCTCAACTCGG) and 5'd(CCGAGTCCTTCC). The model was made in such a way that the junction may lack two-fold sequence symmetry at the crossover point. A new version of the AMBER force field has been used, in addition to the Particle Mesh Ewald (PME) method which deals with the refinement treatment of the long range interaction potentials, the well known limitation in MD protocol. After molecular dynamics simulation the backbone parameters and helical parameters of the DNA junction model is calculated and its dynamical pathway is discussed in detail. A close observation near the junction point reveals the shifting in the orientation of some of the P-O bonds from the usual π3 turn for A- and B- DNA to either π1 or π2 type of turn in order to achieve conformational stability. With this study it seems possible to derivatize synthetic DNA molecules with special functional groups both on the bases and at the backbones as in the case of some natural processes by which drugs, particular proteins etc. recognizes and binds to the specific sites of DNA
    Bioinformation 07/2014; 10(7).