S-nitrosylation of NF-kB p65 inhibits TSH-induced Na+/I- symporter expression

NICOLA JUAN P; PEYRET VICTORIA; NAZAR MAGALí; ROMERO JM; LUCERO ARIEL M; MONTESINOS MARIA DEL MAR; BOCCO JOSé LUIS; PELLIZAS CLAUDIA G; MASINI - REPISO ANA M

ENDOCRINE SOC

Año: 2015 vol. 156 p. 4741 - 4741

font size="1" face="Frutiger-Roman">Nitric oxide (NO) is a ubiquitous signaling molecule involved in a wide variety of cellular physiologicalprocesses. In thyroid cells, NO-synthase III-endogenously produced NO reduces TSH-stimulatedthyroid-specific gene expression, suggesting a potential autocrine role ofNOin modulatingthyroid function. Further studies indicate that NO induces thyroid dedifferentiation, because NOdonors repress TSH-stimulated iodide (I) uptake. Here, we investigated the molecular mechanismunderlying the NO-inhibited Na/I