Biological signals and cell signaling pathways – A computational approach.
Type I interferons are used effectively in the treatment of Hepatitis C by activating a cascade of interferon-stimulated genes with antiviral properties. The signaling cascade involves the binding of IFN to the two subunits of the IFN receptor, IFNAR1 (R1) and IFNAR2 (R2), to form a ternary complex. The kinases – Jak’s and Tyk’s – bound to the cytoplasmic domains of receptor subunits become phosphorylated, which further phosphorylates STAT (p-STAT). Dimers of p-STAT migrate to the nucleus to initiate the transcription of a large number of genes. The subtypes of type I interferons can exhibit differential response even though they bind to the same receptor subunits and initiate similar signaling pathways. Type I interferons is also known to exhibit a reduced response (refractoriness) to prolonged or multiple doses of IFN. It has been shown that despite binding to the same receptor, the subtype IFN-α is more refractory than IFN-β. The talk focusses on explaining the differential behavior of the subtypes of type I interferon by using computational and analytic tools.
The second part of the talk will highlight the use of nonlinear time series analysis and nonlinear parameters to classify and differentiate ECG signals of normal versus clinical conditions.
After the presentation Prof. Nayak will be meeting with any interested students to continue discussion.