Disease relevance of Dlk1

• We found that Pref-1 was synthesized in normal islets and in RINm5F insulinoma cells and released into the medium in two forms, of which one corresponded to FA1 [1].

High impact information on Dlk1

• This transformation of adipocytes from cells that store triglycerides to fatty acid-oxidizing cells is accompanied by loss of the adipocyte markers, adipocyte fatty acid-binding protein 2, tumor necrosis factor alpha, and leptin, and by the appearance of the preadipocyte marker Pref-1 [2].
• The reduction of the adipocyte markers caused by bezafibrate was accompanied by an increase in the mRNA levels of the preadipocyte marker Pref-1 (1.6-fold induction; P < 0.01) [3].
• Similarly, fatty acid translocase (2.6-fold induction; P = 0.002) and Pref-1 (5.6-fold induction) mRNA levels increased, although differences in the latter were not significant because of huge individual variations [3].
• The expression of preadipocyte factor-1/fetal antigen 1 was decreased during differentiation, and GH treatment prevented this down-regulation of Pref1/FA1 [4].
• The level of Pref-1 message in the adrenal glands of animals having various pituitary-adrenal axis activities, as well as various plasma salt concentrations, correlated with the total number of glomerulosa cells [5].

Biological context of Dlk1

• These findings suggest that the capsular cells, mostly composed of the glomerulosa cells, may have potential for differentiating into other zones' cells, and the down-regulation of Pref-1 expression may be an important step in the adrenal zonal differentiation [5].

Anatomical context of Dlk1

• We recently reported that ZOG, a rat homolog of Pref-1, was specifically expressed in the adrenal zona glomerulosa [6].
• First we studied the biosynthesis and processing of Pref-1 to the soluble form, FA1, in pancreatic islets and insulinoma cells transfected with Pref-1 cDNA [1].
• This element would function as the promoter of the Pref-1 gene in H295R cells, but not in HeLa cells [6].
• Results of the investigation of Pref-1 expression in preadipocyte and in undifferentiated adrenal cortex suggested that down-regulation of Pref-1 gene was closely correlated with the differentiation process [6].
• Between well- and poorly compensated rats, significant differences on expression level were found for Yy1 (liver), Ppargamma (heart), Nfkappab (bone), Pref-1 (spleen), and Lepr (thymus, liver, heart) [7].

Associations of Dlk1 with chemical compounds

• By immunocytochemistry of GH-stimulated islet cells no correlation between high Pref-1 expression and BrdU incorporation was observed and there was an inverse relationship between the levels of insulin and Pref-1 [1].

Other interactions of Dlk1

• These results indicate that Pref-1/FA1 is not mediating the mitogenic effect of GH and PRL [1].
• Mutations of four or five nucleotides in a 7-nucleotides-stretch in the midst of the Egr/GC-box eliminated the binding of Sp1/3, abolished the activation by Egr-factor(s) and diminished the Pref-1 promoter activity [6].

Analytical, diagnostic and therapeutic context of Dlk1

• The experimental treatment resulted in a decrease and increase in Pref-1 expression in ACTH treated and low sodium diet treated rats respectively, in accordance with changes in abundance of glomerulosa cells [8].

References