Alterations to DNA methylation and expression of CXCL14 are associated with suboptimal birth outcomes.

CXCL14 is a chemokine that has previously been implicated in insulin resistance in mice. In humans, the role of CXCL14 in metabolic processes is not well established, and we sought to determine whether CXCL14 is a risk susceptibility gene important in fetal programming of metabolic disease. For this purpose, we investigated whether CXCL14 is differentially regulated in human umbilical cords of infants with varying birth weights.

Galactose induction of the GAL1 gene requires conditional degradation of the Mig2 repressor.

Skp1 an essential component of the SCF (Skp1/cullin/F-box) E3 ubiquitin ligases, which target proteins for degradation by the 26S proteasome. We generated a skp1dM mutant strain that is defective for galactose induction of the GAL1 gene and we have found that galactose-induced protein degradation of the repressor Mig2 is defective in this strain. Mig2 degradation was also abolished in cells lacking the protein kinase Snf1 and the F-box protein Das1, suggesting that Snf1 triggers galactose-induced protein degradation of Mig2 by SCFDas1.

Role of p63/p73 in epithelial remodeling and their response to steroid treatment in nasal polyposis.

Background: Nasal polyposis (NP) is recognized as aberrant epithelial remodeling, but the molecular mechanism underlying this process is poorly understood. Two important p53 homologues (p63 and p73) play a key role in orchestrating the epithelial development.

Objective: We intended to study whether p63 and p73 are involved in the epithelial remodeling seen in patients with NP and their response to oral glucocorticosteroid (GC) treatment.

Gal11p dosage-compensates transcriptional activator deletions via Taf14p.

Transcriptional activators work by recruiting transcription factors that are required for the process of transcription to their target genes. We have used the Split-Ubiquitin system to identify eight transcription factors that interacted with both the transcriptional activators Gal4p and Gcn4p in living cells. The over-expression of one of the activator-interacting proteins, Gal11p, partially suppressed GAL4 and GCN4 deletions.