The endoplasmic reticulum (ER) has been considered as the key site of protein biosynthesis and maturation in the eukaryotic cell. In recent years, the sequence at the N-terminal region of translated protein has shown a particular emphasis as a signal responsible for site-specific translocation mediated by post-translational modification. Once the native conformation is not achieved, the degradation pathway is activated, and therefore the restoration of the homeostasis of ER function in UPR pathway is initiated.
View Article and Find Full Text PDFPurpose Of Review: Neuropathic pain (NP) has been ubiquitously characterized by lesion and its linked somatosensory system either the central nervous system (CNS) or peripheral nervous system (PNS) This PNS episode is the most prevalent site of NP origin and is found to be associated with afferent nerve fibers carrying pain signals from injured/trauma site to the CNS including the brain. Several kinds of pharmacotherapeutic drugs shuch as analgesics, anti-convulsants, and anti-depressants are being employed for the its possible interventions. The NP has been a great interest to follow different pathophysiological mechanisms which are often considered to correlate with the metabolic pathways and its mediated disease.
View Article and Find Full Text PDFThe aim of this study is to biodegrade the reactive azo dyes- Reactive black 5 (B-GDN), Reactive red 120 (RP) and Reactive blue 19 (RNB) using bacteria Acinetobacter baumannii JC359. Optimization of the process variables such as pH, temperature, dye concentration, incubation time, inoculum volume and dynamic incubating conditions for dye decolorization were performed using One Factor At a Time (OFAT) approach. Box- Behnken Design (BBD) of Response Surface Methodology (RSM) was further used to optimize the process variables.
View Article and Find Full Text PDFMitochondria are the crucial regulators for the major source of ATP for different cellular events. Due to damage episodes, mitochondria have been established for a plethora ofalarming signals of stress that lead to cellular deterioration, thereby causing programmed cell death. Defects in mitochondria play a key role in arbitrating pathophysiological machinery with recent evince delineating a constructive role in mitophagy mediated mitochondrial injury.
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