The proteins studied are known as "inflammasomes." ❋ Suzanne O'Malley (2012)
AIM2 belongs to a class of proteins called inflammasomes, which are multi-protein complexes that play major roles as guardians against both viral and bacterial infections. ❋ Unknown (2009)
The research team found that a deficiency in components of two particular types of inflammasomes in mice caused changes in the intestinal tract's microbial community and that the changes were associated with increased bacteria that determined the severity of obesity and NAFLD in the mice. ❋ Suzanne O'Malley (2012)
Areas of interest include inflammatory cytokine signaling, regulation of Th-17, Th-1, and TReg cells, regulation of transcription factors and inflammatory biomolecules, inflammasomes, and translational medicine ❋ Unknown (2010)
Figure 7: M2 triggers inflammasomes through perturbation of ionic homeostasis of the Golgi. ❋ Takeshi Ichinohe (2010)
Particular components of inflammasomes -- protein complexes needed for generating immune responses to pathogens and cellular damage-lessen the severity of colitis and colitis-associated colon cancer in mice, according to a study published online this week in the Journal of Experimental Medicine. ❋ Unknown (2010)
However, the precise regulation of inflammasomes at the level of ASC is still not completely understood. ❋ Nicole Bryan (2010)
Additional work is needed to determine how specific inflammasome components protect against colitis in mice, and whether inflammasomes play similar roles in humans. ❋ Unknown (2010)
Alternative splicing and potentially other editing mechanisms generate ASC isoforms with distinct abilities to function as inflammasome adaptor, which is potentially utilized to regulate inflammasomes during the inflammatory host response. ❋ Nicole Bryan (2010)
M2 channel activity was required for the activation of inflammasomes by influenza and was sufficient to activate inflammasomes in primed macrophages and dendritic cells. ❋ Takeshi Ichinohe (2010)
M2-induced activation of inflammasomes required its localization to the Golgi apparatus and was dependent on the pH gradient. ❋ Takeshi Ichinohe (2010)
We hypothesized that inflammasomes could mediate the activation of caspase-1 due to the shortage of GGPP. ❋ Alessandra Pontillo (2010)
Our results show a mechanism by which influenza virus infection activates inflammasomes and identify the sensing of disturbances in intracellular ionic concentrations as a previously unknown pathogen-recognition pathway. ❋ Takeshi Ichinohe (2010)
The apoptotic speck-like protein containing a caspase recruitment domain (ASC) is the essential adaptor protein for caspase 1 mediated interleukin (IL) - 1beta and IL-18 processing in inflammasomes. ❋ Nicole Bryan (2010)
Figure 8: M2 channel-induced activation of inflammasomes requires an acidified Golgi compartment. ❋ Takeshi Ichinohe (2010)
The inflammasomes mobilize, precipitating a chain of chemical events that cause inflammation. ❋ Unknown (2009)
