Disease relevance of Nr1h2

• We investigated the effects of chronic relapsing experimental allergic encephalomyelitis (first attack and first recovery) on uric acid (UR) concentrations in Lewis rat spinal cord [1].

High impact information on Nr1h2

• UR may play an important role in normal growth and differentiation by modulating gene activation in retinoic acid and thyroid hormone signaling pathways [2].
• Rat UR/human retinoid X receptor alpha (hRXR alpha) heterodimers bound preferentially to double-stranded oligonucleotide direct repeats having the consensus half-site sequence AGGTCA and 4-nt spacing (DR-4) [2].
• Coexpression of UR in COS-1 cells inhibited the stimulation of chloramphenicol acetyltransferase (CAT) reporter gene expression by hRXR alpha and human retinoic acid receptor alpha in the presence of all-trans-retinoic acid when DR-4 (but not DR-5) was present upstream of the promoter of a CAT reporter gene (DR-4-CAT) [2].
• However, in the absence of 9-cis-retinoic acid, UR in combination with hRXR alpha stimulation DR-4-CAT expression [2].
• Heterodimeric interaction between retinoid X receptor alpha and orphan nuclear receptor OR1 reveals dimerization-induced activation as a novel mechanism of nuclear receptor activation [3].

Anatomical context of Nr1h2

• Perchloric extracts of 9 regions between spinal cord segments C3 and Co1 were injected into a reversed-phase high-performance liquid chromatographic system, and UR was quantified electrochemically [1].
• In all regions UR, which was lower than 0.5 micrograms/g wet tissue in rats injected with adjuvant (controls), increased to a variable extent during the attack (5-12 micrograms/g, maximum in T11-L2) and returned during recovery to a residual level of 1-2 micrograms/g. These findings can be partly attributed to blood-brain barrier damage [1].

References