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Your search keyword '"Hasnain, Seyed Ehtesham"' showing total 118 results
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118 results on '"Hasnain, Seyed Ehtesham"'

12. MycoVarP: Mycobacterium Variant and Drug Resistance Prediction Pipeline for Whole-Genome Sequence Data Analysis

Author

Swargam, Sandeep, primary, Kumari, Indu, additional, Kumar, Amit, additional, Pradhan, Dibyabhaba, additional, Alam, Anwar, additional, Singh, Harpreet, additional, Jain, Anuja, additional, Devi, Kangjam Rekha, additional, Trivedi, Vishal, additional, Sarma, Jogesh, additional, Hanif, Mahmud, additional, Narain, Kanwar, additional, Ehtesham, Nasreen Zafar, additional, Hasnain, Seyed Ehtesham, additional, and Ahmad, Shandar, additional

Published
2022
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14. Zooming in on common immune evasion mechanisms of pathogens in phagolysosomes: potential broad-spectrum therapeutic targets against infectious diseases.

Author

Selvapandiyan, Angamuthu, Puri, Niti, Kumar, Pankaj, Alam, Anwar, Ehtesham, Nasreen Zafar, Griffin, George, and Hasnain, Seyed Ehtesham

Subjects
DRUG target, COMMUNICABLE diseases, INTRACELLULAR pathogens, REACTIVE oxygen species, PATHOGENIC microorganisms
Abstract

The intracellular viral, bacterial, or parasitic pathogens evade the host immune challenges to propagate and cause fatal diseases. The microbes overpower host immunity at various levels including during entry into host cells, phagosome formation, phagosome maturation, phagosome–lysosome fusion forming phagolysosomes, acidification of phagolysosomes, and at times after escape into the cytosol. Phagolysosome is the final organelle in the phagocyte with sophisticated mechanisms to degrade the pathogens. The immune evasion strategies by the pathogens include the arrest of host cell apoptosis, decrease in reactive oxygen species, the elevation of Th2 anti-inflammatory response, avoidance of autophagy and antigen cross-presentation pathways, and escape from phagolysosomal killing. Since the phagolysosome organelle in relation to infection/cure is seldom discussed in the literature, we summarize here the common host as well as pathogen targets manipulated or utilized by the pathogens established in phagosomes and phagolysosomes, to hijack the host immune system for their benefit. These common molecules or pathways can be broad-spectrum therapeutic targets for drug development for intervention against infectious diseases caused by different intracellular pathogens. [ABSTRACT FROM AUTHOR]

Published
2023
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17. Mycobacterium smegmatis Bacteria Expressing Mycobacterium tuberculosis-Specific Rv1954A Induce Macrophage Activation and Modulate the Immune Response

Author

Arora, Simran Kaur, primary, Naqvi, Nilofer, additional, Alam, Anwar, additional, Ahmad, Javeed, additional, Alsati, Basma Saud, additional, Sheikh, Javaid Ahmad, additional, Kumar, Prabin, additional, Mitra, Dipendra Kumar, additional, Rahman, Syed Asad, additional, Hasnain, Seyed Ehtesham, additional, and Ehtesham, Nasreen Zafar, additional

Published
2020
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24. Molecular Analyses of Over Hundred Sixty Clinical Isolates of SARS-CoV-2: Insights on Likely Origin, Evolution and Spread, and Possible Intervention

Author

Jamal, Salma, primary, Singh, Jasdeep, additional, Sheikh, Javaid Ahmad, additional, Singh, Hina, additional, Khubaib, Mohd, additional, Kohli, Sunil, additional, Dobrindt, Ulrich, additional, Rahman, Syed Asad, additional, Ehtesham, Nasreen Zafar, additional, and Hasnain, Seyed Ehtesham, additional

Published
2020
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27. Amino acid starvation sensing dampens IL-1β production by activating riboclustering and autophagy

Author

Battu, Srikanth, primary, Afroz, Sumbul, additional, Giddaluru, Jeevan, additional, Naz, Saima, additional, Huang, Weishan, additional, Khumukcham, Saratchandra Singh, additional, Khan, Rafiq Ahmad, additional, Bhat, Saleem Yousuf, additional, Qureshi, Insaf Ahmed, additional, Manavathi, Bramanandam, additional, Khan, Aleem Ahmed, additional, August, Avery, additional, Hasnain, Seyed Ehtesham, additional, and Khan, Nooruddin, additional

Published
2018
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32. Mycobacterium tuberculosisprotein MoxR1 enhances virulence by inhibiting host cell death pathways and disrupting cellular bioenergetics

Author

Quadir, Neha, Shariq, Mohd., Sheikh, Javaid Ahmad, Singh, Jasdeep, Sharma, Neha, Hasnain, Seyed Ehtesham, and Ehtesham, Nasreen Zafar

Abstract

ABSTRACTMycobacterium tuberculosis(M. tb) utilizes the multifunctionality of its protein factors to deceive the host. The unabated global incidence and prevalence of tuberculosis (TB) and the emergence of multidrug-resistant strains warrant the discovery of novel drug targets that can be exploited to manage TB. This study reports the role of M. tbAAA+ family protein MoxR1 in regulating host-pathogen interaction and immune system functions. We report that MoxR1 binds to TLR4 in macrophage cells and further reveal how this signal the release of proinflammatory cytokines. We show that MoxR1 activates the PI3K-AKT-MTOR signalling cascade by inhibiting the autophagy-regulating kinase ULK1 by potentiating its phosphorylation at serine 757, leading to its suppression. Using autophagy-activating and repressing agents such as rapamycin and bafilomycin A1 suggested that MoxR1 inhibits autophagy flux by inhibiting autophagy initiation. MoxR1 also inhibits apoptosis by suppressing the expression of MAPK JNK1/2 and cFOS, which play critical roles in apoptosis induction. Intriguingly, MoxR1 also induced robust disruption of cellular bioenergetics by metabolic reprogramming to rewire the citric acid cycle intermediates, as evidenced by the lower levels of citric acid and electron transport chain enzymes (ETC) to dampen host defence. These results point to a multifunctional role of M. tbMoxR1 in dampening host defences by inhibiting autophagy, apoptosis, and inducing metabolic reprogramming. These mechanistic insights can be utilized to devise strategies to combat TB and better understand survival tactics by intracellular pathogens.

Published
2023
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33. Interaction of Mycobacterium tuberculosisVirulence Factor RipA with Chaperone MoxR1 Is Required for Transport through the TAT Secretion System

Author

Bhuwan, Manish, Arora, Naresh, Sharma, Ashish, Khubaib, Mohd, Pandey, Saurabh, Chaudhuri, Tapan Kumar, Hasnain, Seyed Ehtesham, and Ehtesham, Nasreen Zafar

Abstract

ABSTRACTMycobacterium tuberculosisis a leading cause of death worldwide. The M. tuberculosisTAT (twin-arginine translocation) protein secretion system is present at the cytoplasmic membrane of mycobacteria and is known to transport folded proteins. The TAT secretion system is reported to be essential for many important bacterial processes that include cell wall biosynthesis. The M. tuberculosissecretion and invasion protein RipA has endopeptidase activity and interacts with one of the resuscitation antigens (RpfB) that are expressed during pathogen reactivation. MoxR1, a member of the ATPase family that is associated with various cellular activities, was predicted to interact with RipA based on in silicoanalyses. A bimolecular fluorescence complementation (BiFC) assay confirmed the interaction of these two proteins in HEK293T cells. The overexpression of RipA in Mycobacterium smegmatisand copurification with MoxR1 further validated their interaction in vivo. Recombinant MoxR1 protein, expressed in Escherichia coli, displays ATP-enhanced chaperone activity. Secretion of recombinant RipA (rRipA) protein into the E. coliculture filtrate was not observed in the absence of RipA-MoxR interaction. Inhibition of this export system in M. tuberculosis, including the key players, will prevent localization of peptidoglycan hydrolase and result in sensitivity to existing β-lactam antibiotics, opening up new candidates for drug repurposing.IMPORTANCEThe virulence mechanism of mycobacteria is very complex. Broadly, the virulence factors can be classified as secretion factors, cell surface components, enzymes involved in cellular metabolism, and transcriptional regulators. The mycobacteria have evolved several mechanisms to secrete its proteins. Here, we have identified one of the virulence proteins of Mycobacterium tuberculosis, RipA, possessing peptidoglycan hydrolase activities secreted by the TAT secretion pathway. We also identified MoxR1 as a protein-protein interaction partner of RipA and demonstrated chaperone activity of this protein. We show that MoxR1-mediated folding is critical for the secretion of RipA within the TAT system. Inhibition of this export system in M. tuberculosiswill prevent localization of peptidoglycan hydrolase and result in sensitivity to existing β-lactam antibiotics, opening up new candidates for drug repurposing.

Published
2016
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