Publications by authors named "J J Aloor"

Prohibitins (PHB1 and PHB2) are ubiquitously expressed proteins which play critical roles in multiple biological processes, and together form the ring-like PHB complex found in phospholipid-rich cellular compartments including lipid rafts. Recent studies have implicated PHB1 as a mediator of fatty acid transport as well as a membrane scaffold mediating B lymphocyte and mast cell signal transduction. However, the specific role of PHBs in the macrophage have not been characterized, including their role in fatty acid uptake and lipid raft-mediated inflammatory signaling.

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Lung disease causes significant morbidity and mortality, and is exacerbated by environmental injury, for example through lipopolysaccharide (LPS) or ozone (O). Toll-like receptors (TLRs) orchestrate immune responses to injury by recognizing pathogen- or danger-associated molecular patterns. TLR4, the prototypic receptor for LPS, also mediates inflammation after O, triggered by endogenous hyaluronan.

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Article Synopsis
  • TLR2 is a receptor that triggers inflammation in response to microbial signals, and its interactions with proteins can be influenced by statins, which are commonly used to lower cholesterol.
  • Researchers investigated how statins affect TLR2's interacting proteins using a specific laboratory technique called coimmunoprecipitation.
  • The study identified a protein called ACTR1A, linked to the dynactin complex, as an important interactor of TLR2, suggesting that statins can change the way TLR2 signals immune responses.
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Toll-like receptors (TLRs) are pathogen-recognition receptors that trigger the innate immune response. Recent reports have identified accessory proteins that provide essential support to TLR function through ligand delivery and receptor trafficking. Herein, we introduce leucine-rich repeats (LRRs) and calponin homology containing 4 (Lrch4) as a novel TLR accessory protein.

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Background: Arsenic exposure via drinking water impacts millions of people worldwide. Although arsenic has been associated epidemiologically with increased lung infections, the identity of the lung cell types targeted by peroral arsenic and the associated immune mechanisms remain poorly defined.

Objectives: We aimed to determine the impact of peroral arsenic on pulmonary antibacterial host defense.

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