Publications by authors named "P Kirthika"
Article Synopsis
- Two Typhimurium strains, JOL 912 and JOL 1800, were engineered from the wild-type strain by deleting specific genes, which weakened their ability to survive inside host cells and gave them distinct immune responses.
- The study examined how these strains reacted to different stress factors like temperature and acidity, finding that cold stress slightly increased their invasion abilities, while their entry mechanisms stayed consistent across cell types.
- JOL 912 triggered a strong immune response, activating important immune factors, whereas JOL 1800 had a minimal response, and the gene deletions affected cell cycle progression and apoptosis in infected cells.
The fusion of haemagglutinin-neuraminidase (HN) protein of peste des petits ruminant (PPR) virus with signaling lymphocyte activation molecules (SLAM) host cell receptor consequences the virus entry and multiplication inside the host cell. The use of synthetic SLAM homologous peptides (i.e.
View Article and Find Full Text PDFThe non-structural protein (NSs) and nucleoprotein (NP) of the severe fever with thrombocytopenia syndrome virus (SFTSV) encoded by the S segment are crucial for viral pathogenesis. They reside in viroplasm-like structures (VLS), but their interaction and their significance in viral propagation remain unclear. Here, we investigated the significance of the association between NSs and NP during viral infection through in-silico and in-vitro analyses.
View Article and Find Full Text PDFProteases are the group of enzymes that carry out proteolysis in all forms of life and play an essential role in cell survival. By acting on specific functional proteins, proteases affect the transcriptional and post-translational pathways in a cell. Lon, FtsH, HslVU and the Clp family are among the ATP-dependent proteases responsible for intracellular proteolysis in bacteria.
View Article and Find Full Text PDFMetastatic prostate cancer (PCa) inevitably acquires resistance to standard therapy preceding lethality. Here, we unveil a chromosomal instability (CIN) tolerance mechanism as a therapeutic vulnerability of therapy-refractory lethal PCa. Through genomic and transcriptomic analysis of patient datasets, we find that castration and chemotherapy-resistant tumors display the highest CIN and mitotic kinase levels.
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