Zobrazeno 1 - 10
of 27
pro vyhledávání: '"Manoj Veleeparambil"'
Autor:
Sukanya Chakravarty, Gayatri Subramanian, Sonam Popli, Manoj Veleeparambil, Shumin Fan, Ritu Chakravarti, Saurabh Chattopadhyay
Publikováno v:
mBio, Vol 14, Iss 5 (2023)
ABSTRACT Many viruses activate cellular autophagy in infected cells to facilitate their replication. Recently, we identified an interferon (IFN)-stimulated gene (ISG) Tudor domain containing 7 (TDRD7), which inhibits viral replication by blocking aut
Externí odkaz:
https://doaj.org/article/d4bec7584bed4ff0b03ef12fe76a638e
Autor:
Chenyao Wang, Nikhil Sharma, Manoj Veleeparambil, Patricia M. Kessler, Belinda Willard, Ganes C. Sen
Publikováno v:
mBio, Vol 12, Iss 6 (2021)
ABSTRACT The nature and the intensity of innate immune response to virus infection determine the course of pathogenesis in the host. Among the many pathogen-associated molecular pattern recognition receptors, STING, an endoplasmic reticulum (ER)-asso
Externí odkaz:
https://doaj.org/article/42def7bec8994298a479d134c00e4bc6
Autor:
Gayatri Subramanian, Teodora Kuzmanovic, Ying Zhang, Cara Beate Peter, Manoj Veleeparambil, Ritu Chakravarti, Ganes C Sen, Saurabh Chattopadhyay
Publikováno v:
PLoS Pathogens, Vol 14, Iss 1, p e1006877 (2018)
The interferon (IFN) system represents the first line of defense against a wide range of viruses. Virus infection rapidly triggers the transcriptional induction of IFN-β and IFN Stimulated Genes (ISGs), whose protein products act as viral restrictio
Externí odkaz:
https://doaj.org/article/ebaa662cbebb4bc98f8a1757fc9a5790
Autor:
Saurabh Chattopadhyay, Volker Fensterl, Ying Zhang, Manoj Veleeparambil, Jaime L. Wetzel, Ganes C. Sen
Publikováno v:
mBio, Vol 4, Iss 2 (2013)
ABSTRACT Interferon (IFN) is required for protecting mice from viral pathogenesis; reciprocally, it mediates the deleterious septic shock response to bacterial infection. The critical transcription factor for IFN induction, in both cases, is IRF-3, w
Externí odkaz:
https://doaj.org/article/c01906a0d1de483f9a7d3798980120bf
Autor:
Tejasvi Dudiki, Manoj Veleeparambil, Irina Zhevlakova, Sudipta Biswas, Eric A. Klein, Peter Ford, Eugene A. Podrez, Tatiana V. Byzova
Publikováno v:
Circulation Research. 132:1447-1461
Background: Thrombosis is one of the main complications in cancer patients often leading to mortality. However, the mechanisms underlying platelet hyperactivation are poorly understood. Methods: Murine and human platelets were isolated and treated wi
Autor:
Svyatoslav Tkachenko, Tatiana V. Byzova, Eugene A. Podrez, Detao Gao, Michael G. McCoy, Daniel W. Nascimento, Rakhylia Murtazina, Manoj Veleeparambil
Publikováno v:
Sci Signal
Toll-like receptor 2 (TLR2) is implicated in various pathologies, mainly in terms of its function within innate immune cells. However, TLR2 is also present in endothelial cells. Here, we explored the physiological and pathophysiological roles of endo
Autor:
Ganes C. Sen, Saurabh Chattopadhyay, Patricia M Kessler, Xin Wang, Belinda Willard, Manoj Veleeparambil, Chenyao Wang
Publikováno v:
EMBO J
STING (STimulator of INterferon Genes) mediates protective cellular response to microbial infection and tissue damage, but its aberrant activation can lead to autoinflammatory diseases. Upon ligand stimulation, the endoplasmic reticulum (ER) protein
Autor:
Ganes C. Sen, Ritu Chakravarti, Saurabh Chattopadhyay, Manoj Veleeparambil, Ying Zhang, Teodora Kuzmanovic, Gayatri Subramanian, Cara Peter
Publikováno v:
PLoS Pathogens
PLoS Pathogens, Vol 14, Iss 1, p e1006877 (2018)
PLoS Pathogens, Vol 14, Iss 1, p e1006877 (2018)
The interferon (IFN) system represents the first line of defense against a wide range of viruses. Virus infection rapidly triggers the transcriptional induction of IFN-β and IFN Stimulated Genes (ISGs), whose protein products act as viral restrictio
Autor:
Manoj Veleeparambil, Samar Abdulkhalek, Saurabh Chattopadhyay, Darshana Poddar, Volker Fensterl, Sudip K Bandyopadhyay, Ganes C. Sen
Publikováno v:
EMBO reports. 16:1535-1547
Mammalian Toll-like receptors (TLR) recognize microbial products and elicit transient immune responses that protect the infected host from disease. TLR4--which signals from both plasma and endosomal membranes--is activated by bacterial lipopolysaccha
Autor:
Darshana Poddar, Patricia M Kessler, Samar Abdulkhalek, Ganes C. Sen, Michifumi Yamashita, Saurabh Chattopadhyay, Manoj Veleeparambil
Publikováno v:
Journal of immunology (Baltimore, Md. : 1950). 200(8)
Mammalian TLRs recognize microbial infection or cell death–associated danger signals and trigger the appropriate cellular response. These responses determine the strength and the outcome of the host–microbe interaction. TLRs are transmembrane pro