Activating transcription factor 2 targets c-Fos, but not c-Jun, in growth plate chondrocytes.

Activating transcription factor 2 (ATF-2), c-Fos, and c-Jun belong to the bZIP family of transcription factors. Promoters of c-Fos, c-Jun, cyclin D1, and cyclin A are targets of ATF-2 in primary mouse chondrocytes. An ATF-2 expression vector was co-transfected with either c-Fos or c-Jun promoters in mutant ATF-2 chondrocytes in order to show by luciferase assay that ATF-2 increased promoter activity of c-Fos, but not c-Jun.

Dynamics of lamin-A processing following precursor accumulation.

Lamin A (LaA) is a component of the nuclear lamina, an intermediate filament meshwork that underlies the inner nuclear membrane (INM) of the nuclear envelope (NE). Newly synthesized prelamin A (PreA) undergoes extensive processing involving C-terminal farnesylation followed by proteolysis yielding non-farnesylated mature lamin A. Different inhibitors of these processing events are currently used therapeutically.

Activating transcription factor-2 affects skeletal growth by modulating pRb gene expression.

Endochondral ossification is the process of skeletal bone growth via the formation of a cartilage template that subsequently undergoes mineralization to form trabecular bone. Genetic mutations affecting the proliferation or differentiation of chondrocytes result in skeletal abnormalities. Activating transcription factor-2 (ATF-2) modulates expression of cell cycle regulatory genes in chondrocytes, and mutation of ATF-2 results in a dwarfed phenotype.

Activating transcription factor 2 controls Bcl-2 promoter activity in growth plate chondrocytes.

Activating transcription factor 2 (ATF-2) is expressed ubiquitously in mammals. Mice deficient in ATF-2 (ATF-2 m/m) are slightly smaller than their normal littermates at birth. Approximately 50% of mice born mutant in both alleles die within the first month.

The cyclin D1 and cyclin A genes are targets of activated PTH/PTHrP receptors in Jansen's metaphyseal chondrodysplasia.

Jansen's metaphyseal chondrodysplasia (JMC) is an autosomal dominant disorder characterized by short-limbed dwarfism, delayed ossification, and hypercalcemia. Activating mutations in the PTH/PTHrP receptor have been identified as the molecular cause of this disorder. Although these mutations have been shown to increase cAMP accumulation, little is known about possible target genes of the downstream signaling pathways that may contribute to the pathogenesis of the disease.