Publications by authors named "Akhil Raj Pushparajan"

Mycobacterium tuberculosis is exposed to diverse stresses inside the host during dormancy. Meanwhile, many metabolic and transcriptional regulatory changes occur, resulting in physiological modifications that help M. tuberculosis to adapt to these stresses.

View Article and Find Full Text PDF

The main obstacle in eradicating tuberculosis is the ability of Mycobacterium tuberculosis to remain dormant in the host, and then to get reactivated even years later under immunocompromised conditions. Transcriptional regulation in intracellular pathogens plays an important role in their adapting to the challenging environment inside the host cells. Previously, we demonstrated that Rv1019, a putative transcriptional regulator of M.

View Article and Find Full Text PDF
Article Synopsis
  • Intracellular pathogens, like those causing tuberculosis, downregulate host gene expression to survive in macrophages, a crucial strategy for their pathogenesis.
  • In infected macrophages, levels of HDAC1 increase and it becomes phosphorylated, which leads to the recruitment of ZBTB25 and Sin3a to silence gene expression.
  • Targeting components of the HDAC1/Sin3a complex, particularly ZBTB25, may provide a new approach for host-directed therapy against tuberculosis amid increasing drug resistance.
View Article and Find Full Text PDF

Rv1019, a member of an uncharacterized tetracycline resistance regulator family of transcriptional regulators of Mycobacterium tuberculosis H37Rv, was found to be differentially expressed during dormancy and reactivation in vitro. In this study, we show that this protein binds to its own promoter and acts as a negative regulator of its own expression. It forms dimers in vitro which is essential for the DNA binding activity.

View Article and Find Full Text PDF

Tuberculosis, caused by Mycobacterium tuberculosis, still remains a major global health problem. The main obstacle in eradicating this disease is the ability of this pathogen to remain dormant in macrophages, and then reactivate later under immuno-compromised conditions. The physiology of hypoxic nonreplicating M.

View Article and Find Full Text PDF