Orphan nuclear receptor NOR-1 enhances 3',5'-cyclic adenosine 5'-monophosphate-dependent uncoupling protein-1 gene transcription.

Activation of nuclear orphan receptor NURR1 transcription by NF-kappa B and cyclic adenosine 5'-monophosphate response element-binding protein in rheumatoid arthritis synovial tissue.

Modulation of the NURR subfamily of nuclear receptors may be an important mechanism regulating pathways associated with inflammatory joint disease. We examined the signaling mechanisms through which inflammatory mediators, produced by rheumatoid arthritis (RA) synovial tissue, contribute to the regulation of the NURR subfamily. Markedly enhanced expression of NURR1 is observed in synovial tissu...

Activation of Nuclear Orphan Receptor NURR1 Transcription by NF- B and Cyclic Adenosine 5 -Monophosphate Response Element-Binding Protein in Rheumatoid Arthritis Synovial Tissue

Regulation of c-jun gene expression by cAMP in HL-60 myeloid leukemia cells.

Previous studies have demonstrated that expression of the c-jun proto-oncogene is induced by phorbol esters and other agents that activate protein kinase C. The present work has examined the involvement of cAMP-dependent signaling mechanisms in the regulation of c-jun gene expression. Low levels of c-jun transcripts were detectable in untreated HL-60 myeloid leukemia cells. In contrast, treatme...

Regulation of jun-B expression by a cyclic AMP (cAMP)-dependent mechanism in human myeloid cells.

The present studies have examined the regulation of the jun-B early response gene by cyclic AMP (cAMP)-dependent signaling pathways. The 2.0-kb jun-B transcript was at low but detectable levels in uninduced human HL-60 myeloid leukemia cells. In contrast, treatment with 1 mmol/L8-bromo-adenosine 3',5'-cyclic monophosphate (8-Br-cAMP) in the presence of isobutylmethylxanthine, an inhibitor of cA...

Parathyroid hormone enhances bone morphogenetic protein activity by increasing intracellular 3', 5'-cyclic adenosine monophosphate accumulation in osteoblastic MC3T3-E1 cells.

Intermittent subcutaneous injections of parathyroid hormone (PTH) increase bone mass in a variety of animal models and humans. The anabolic actions of PTH on osteogenic cells are mainly mediated through the protein kinase A (PKA) signaling pathway via PTH receptor 1 (PTHR1). We have already reported 3', 5'-cyclic adenosine monophosphate (cAMP)/PKA-mediated enhancement of bone morphogenetic prot...