Publications by authors named "Rajeshree Pujari"
Article Synopsis
- Persistent activation of NF-κB by the Tax protein from HTLV-1 is crucial for the development of adult T-cell leukemia (ATL) and associated neurological disorders.
- Tax interacts with various cellular components, notably CADM1, to activate the IKK complex and inhibit the negative regulator A20, which impacts NF-κB signaling.
- The study highlights the importance of CADM1 as a scaffold that supports the formation of a complex necessary for Tax to maximize NF-κB activation in infected cells.
Article Synopsis
- - The nuclear factor kappa B (NF-κB) is essential for immune regulation, influencing both innate and adaptive immunity, lymphocyte survival, and lymphoid organ development, with activation converging on the IKK complex.
- - The IKK complex has two key catalytic subunits, IKKα and IKKβ, along with a regulatory subunit (NEMO/IKKγ), with distinct roles in activating both canonical and non-canonical NF-κB pathways, although the activation mechanisms of IKKα remain less understood.
- - Uncontrolled NF-κB activation can lead to autoimmune diseases and cancers, with regulatory proteins like IκBα and A20 helping to terminate this signaling, while
In response to stimulation with proinflammatory cytokines, the deubiquitinase A20 inducibly interacts with the regulatory molecules TAX1BP1, Itch and RNF11 to form the A20 ubiquitin-editing complex. However, the molecular signal that coordinates the assembly of this complex has remained elusive. Here we demonstrate that TAX1BP1 was inducibly phosphorylated on Ser593 and Ser624 in response to proinflammatory stimuli.
View Article and Find Full Text PDFPhosphatidic acid (PA), generated downstream of monomeric Rho GTPases via phospholipase D (PLD) and additionally by diacylglycerol kinases (DGK), both stimulates phospholipase C-beta(1) (PLC-beta(1)) and potentiates stimulation of PLC-beta(1) activity by Galpha(q) in vitro. PA is a potential candidate for integrating signaling by monomeric and heterotrimeric G proteins to regulate signal output by G protein coupled receptors (GPCR), and we have sought to understand the mechanisms involved. We previously identified the region spanning residues 944-957, lying within the PLC-beta(1) C-terminus alphaA helix and flexible loop of the Galpha(q) binding domain, as required for stimulation of lipase activity by PA in vitro.
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