- Tuberculosis Research and Epidemiology
- Psoriasis: Treatment and Pathogenesis
- Sphingolipid Metabolism and Signaling
- Hepatitis C virus research
- Immune responses and vaccinations
- Autophagy in Disease and Therapy
- Whipple's Disease and Interleukins
- bioluminescence and chemiluminescence research
- Antibiotic Resistance in Bacteria
- Adenosine and Purinergic Signaling
- Calcium signaling and nucleotide metabolism
- Photoreceptor and optogenetics research
- Light effects on plants
International Centre for Genetic Engineering and Biotechnology
2024-2025
International Centre for Genetic Engineering and Biotechnology
2020-2024
Jawaharlal Nehru University
2019
Mycobacterium tuberculosis (Mtb) infection of the lungs, besides producing prolonged cough with mucus, also causes progressive fatigue and cachexia debilitating loss muscle mass. While anti-tuberculosis (TB) drug therapy is directed toward eliminating bacilli, treatment regimen ignores systemic pathogenic derailments that probably dictate TB-associated mortality morbidity. Presently, it not understood whether Mtb spreads to metabolic organs brings about these impairments. Here we show...
Mycobacterium tuberculosis (Mtb) infection of the lungs, besides producing prolonged cough with mucus, also causes progressive fatigue and cachexia debilitating loss muscle mass. While anti-tuberculosis (TB) drug therapy is directed toward eliminating bacilli, treatment regimen ignores systemic pathogenic derailments that probably dictate TB-associated mortality morbidity. Presently, it not understood whether Mtb spreads to metabolic organs brings about these impairments. Here we show...
Abstract Mycobacterium tuberculosis (Mtb) infection of the lungs, besides producing prolonged cough with mucus, also causes progressive fatigue and cachexia debilitating loss muscle mass. While anti-tuberculosis (TB) drug therapy is directed toward eliminating bacilli, treatment regimen ignores systemic pathogenic derailments that probably dictate TB-associated mortality morbidity. Presently, it not understood whether Mtb spreads to metabolic organs brings about these impairments. Here we...
Organisms can respond to varying light conditions using a wide range of sensory photoreceptors. These photoreceptors be standalone proteins or represent module in multidomain proteins, where one more modules sense as an input signal which is converted into output response via structural rearrangements these receptors. The signals are utilized downstream by effector multiprotein clusters modulate their activity, could further affect specific interactions, gene regulation enzymatic catalysis....
The protective correlates of Mycobacterium tuberculosis ( Mtb ) infection-elicited host immune responses are incompletely understood. Here, we report pro-pathogenic crosstalk involving Ly6G + granulocytes (Ly6G Gra), IL-17 and COX2. We show that in the lungs -infected wildtype mice, either BCG-vaccinated or not, most intracellular bacilli Gra-resident four weeks post-infection onwards. In genetically susceptible IFNγ −/− excessive Gra infiltration with severe bacteraemia. Neutralizing...
The protective correlates of Mycobacterium tuberculosis ( Mtb ) infection-elicited host immune responses are incompletely understood. Here, we report pro-pathogenic crosstalk involving Ly6G + granulocytes (Ly6G Gra), IL-17 and COX2. We show that in the lungs -infected wildtype mice, either BCG-vaccinated or not, most intracellular bacilli Gra-resident four weeks post-infection onwards. In genetically susceptible IFNγ −/− excessive Gra infiltration with severe bacteraemia. Neutralizing...
Abstract The protective correlates of Mycobacterium tuberculosis ( Mtb ) infection-elicited host immune responses are incompletely understood. Here, we report pro-pathogenic crosstalk involving Ly6G + granulocytes (Ly6G Gra), IL-17 and COX2. We show that in the lungs -infected wildtype mice, either BCG-vaccinated or not, most intracellular bacilli Gra-resident four weeks post-infection onwards. In genetically susceptible IFNγ −/− excessive Gra infiltration with severe bacteraemia....
Phagosome maturation arrest (PMA) imposed by Mycobacterium tuberculosis ( Mtb ) is a classic tool that helps evade macrophage anti-bacterial responses. The exclusion of RAB7, small GTPase, from -phagosomes underscores PMA. Here we report an unexpected mechanism triggers crosstalk between the mitochondrial quality control (MQC) and phagosome pathways reverses CRISPR-mediated p62/SQSTM1 depletion p62 KD blocks mitophagy flux without impacting quality. In cells, growth survival are diminished,...