By Ivan Mura (auth.), Luis F. Castillo, Marco Cristancho, Gustavo Isaza, Andrés Pinzón, Juan Manuel Corchado Rodríguez (eds.)
This quantity compiles permitted contributions for the second variation of the Colombian Computational Biology and Bioinformatics Congress CCBCOL, after a rigorous evaluation technique during which fifty four papers have been permitted for book from 119 submitted contributions. Bioinformatics and Computational Biology are parts of information that experience emerged because of advances that experience taken position within the organic Sciences and its integration with info Sciences. the growth of tasks concerning the research of genomes has led the best way within the construction of large quantities of series info which has to be prepared, analyzed and saved to appreciate phenomena linked to dwelling organisms on the topic of their evolution, habit in several ecosystems, and the advance of functions that may be derived from this analysis.
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Additional resources for Advances in Computational Biology: Proceedings of the 2nd Colombian Congress on Computational Biology and Bioinformatics (CCBCOL)
Cabezas et al. interacting regions of domaains I and III (fig. 3) has strong negative charges (+36. 813 kT/e) due to the positive charges in the interacting reggion with the EGFR (fig. 4). 4 Interacting Residuees The Protein-protein interacctions of the solved complex are mostly hydrophobic innteractions but present some hydrogen h bond interactions. The residues implicated in the complex PDGFB-EGFR arre: ASN 128, SER 127, LYS 86, ASP 155, ILE 13, L LEU Fig. 3. Structure of the dockin ng between PDGF-BB and the EGFR.
PDGFs act via two RTKs (PDGFR-α and PDGFR-β) which share common domain structures, including five extracellular immunoglobulin (Ig) loops and an intracellular tyrosine kinase (TK) domain. This structure is shared with other receptors like VEGFR, c-Fms, c-Kit, and Flt3 . Ligand binding promotes receptor dimerization, which initiates signaling through various pathways became activated including: Mitogen activated protein kinase (MAPK), PI3K phosphatidylinositol 3- kinase, PLCy, Src TK, and activation of transcription factors such as STATs, ELK-1, c-jun/c-fos and NFkB [34,36].
Natl. Cancer Inst. 97, 880–887 (2005) 8. : Intracellular transactivation of the insulin-like growth factor I receptor by an epidermal growth factor receptor. Exp. Cell Res. 223, 412–419 (1996) 9. : Receptor heterodimerization: essential mechanism for platelet-derived growth factor-induced epidermal growth factor receptor transactivation. Mol. Cell Biol. 21(19), 6387–6394 (2001) 10. : PDGF and PDGF receptors in glioma. Ups. J. Med. Sci. 117(2), 99–112 (2012) 11. : Glioblastoma subclasses can be defined by activity among signal transduction pathways and associated genomic alterations.