Increased adipogenesis in cultured embryonic chondrocytes and in adult bone marrow of dominant negative Erg transgenic mice.

In monolayer culture, primary articular chondrocytes have an intrinsic tendency to lose their phenotype during expansion. The molecular events underlying this chondrocyte dedifferentiation are still largely unknown. Several transcription factors are important for chondrocyte differentiation.

Abnormal expression of the ERG transcription factor in prostate cancer cells activates osteopontin.

Osteopontin (OPN) is an extracellular matrix glycophosphoprotein that plays a key role in the metastasis of a wide variety of cancers. The high level of OPN expression in prostate cells is associated with malignancy and reduced survival of the patient. Recent studies on prostate cancer (PCa) tissue have revealed recurrent genomic rearrangements involving the fusion of the 5' untranslated region of a prostate-specific androgen-responsive gene with a gene coding for transcription factors from the ETS family.

Identification of four alternatively spliced transcripts of the Ucma/GRP gene, encoding a new Gla-containing protein.

The Ucma protein (Upper zone of growth plate and cartilage matrix associated protein) has recently been described as a novel secretory protein mainly expressed in cartilage and also as a novel vitamin-K-dependent protein named GRP (Gla-rich protein). This protein has the highest Gla content of any protein known to date. In this article, we identify four alternatively spliced variants of Ucma/GRP gene transcripts in mouse chondrocytes.

Mutual repression of transcriptional activation between the ETS-related factor ERG and estrogen receptor.

Transcription factors are known to interact with each other to modulate their transcriptional activity. In this study, we found that the transcriptional activity of human Erg (one of the Ets family-transcription factors) was repressed by several nuclear receptors, including human estrogen receptor ERalpha, nonsteroid receptors and orphan receptors. Conversely, Erg inhibited ERalpha-dependent transcription.