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Abstract
Apoptosis Inducing Factor protein has a dual role depending on its localization in mitochondrion (energy production) and nucleus (induces apoptosis). Cell damage transports this protein to nucleus which otherwise favors mitochondrion. The alteration of Nuclear Localisation Signal tags could aid nuclear translocation. In this study, apoptosis inducing factor protein (AIF) was conjugated with strong NLS tags and its binding affinity with Importin was studied using in silico approaches such as molecular modeling and docking. This aims to improve the docking affinity of the AIF-Importin complex thus allowing for nuclear translocation, in order to induce caspase-independent apoptosis of the cell.
Highlights
Cancer is the uncontrolled growth of abnormal cells that are invasive and destroy body tissues
This study aims at modifying the Nuclear Localization Signal (NLS) tag of the apoptosis inducing factor protein (AIF) protein such that it aids in the translocation of the protein to the nucleus by taking precedence over its mitochondrial function
Identification of NLS sites: A Nuclear Localization Signal would be present in all nuclear proteins; such proteins were obtained from the Nuclear Protein Database version.2.1 [19]
Summary
Cancer is the uncontrolled growth of abnormal cells that are invasive and destroy body tissues. It has become one of the most dreaded diseases in the recent times. Treatment for any cancer generally includes a combination of chemotherapy, radiotherapy and surgery. These therapies suffer from a lack of specificity as they may kill normal cells as well, leading to lethal side effects [2]. The protein can localize to the mitochondria (for energy production and subsequent cell growth) as well as the nucleus (inducing caspase independent apoptosis) [3,4,5]. Owing to its weak Nuclear Localization Signal (NLS), the protein does not localize to the nucleus except in response to apoptotic stimuli, preferring to carry out its mitochondrial function [6]
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