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Further, we also evaluated whether APO could inhibit the activation of other inflammasomes, such as AIM2 and NLRC4. In agreement with the data shown in Figures 1(b)-1(d), the release of IL-1[beta] induced by poly (dA:dT) was significantly (p < 0.001) inhibited by APO (Figure 1(e)).
Khaleghinia et al., "Evaluation of NLRC4, NLRP1, and NLRP3, as components of inflammasomes, in chronic hepatitis B virus-infected patients," Viral Immunology, vol.
Another study showed that both NLRC4 and NLRP3 inflammasomes were important in the induction of secretion IL-1 [beta].
En las investigaciones clinicas con humanos se han descrito cuatro clases de inflamasomas relacionados con procesos inflamatorios; tres de ellos contienen proteinas de la familia NLR (NLRPl, NLRC4 y NLRP3), mientras que el cuarto corresponde a AIM-2 (inflamasoma ausente en melanoma 2) que pertenece a la familia de proteinas PYHIN, que contienen un dominio pirina y un dominio HIN-200 (8,9).
Con respecto a las NLRs, son una familia de 23 proteinas codificadas en el genoma humano, las cuales contienen un dominio de union de nucleotidos y un dominio repetido rico en leucina (que incluye: NALP, NOD, PYPAF y CATERPILLER); hasta ahora, se han identificado 8 miembros de estas 23 proteinas con capacidad para formar los inflamasomas, a saber: la proteina NLRP1, la NLRP3, la NLRP6, la NLRP12, la NLRP2, la NLRC4, la ALR (receptor tipo AIM-2 o ausente en melanoma 2) y el sensor citoplasmatico RIG-1.
Stimulation of NOD1 and NOD2 also induces production of cytokines and chemokines, dependent on MAPK and NF-[kappa]B signaling, whereas activation of NLRs such as NLRC4, NLRP1, NLRP3, and NLRP6 culminates in the formation of inflammasomes.
Similarly, another NLR, NLRC4, forms an inflammasome capable of activating caspase-1, resulting in IL-1[beta] cleavage [19].
Cytosolic flagellin receptor NLRC4 protects mice against mucosal and systemic challenges.
NLRP3, and NLRC4 recognise specific PAMPS and DAMPS to form signaling complexes known as "inflammasomes." Inflammasome assembly may be triggered by diverse stimuli, including uric acid crystals, cholesterol, protein aggregates and, aluminium adjuvants [20-23].
For gut's sake: NLRC4 inflammasomes distinguish friend from foe.
aeruginosa infection through inhibition of NLRC4 and NLRP3 inflammasomes, reduce the frequency of exacerbations, and improve the quality of life for its anti-inflammatory, immunomodulatory, and antiviral properties.[20] However, cautions should be given for the associated increase in microbial resistance, bronchospasm as well as risk of cardiovascular death.[21] Thus, while identifying optimal patient population, its pros and cons should be well balanced.
However, these mechanisms do not work on NLRC4 inflammasomes.