High impact information on Cebpd

• A high level of CCAAT-enhancer binding protein-delta expression is a major determinant for markedly elevated differential gene expression of the platelet-derived growth factor-alpha receptor in vascular smooth muscle cells of genetically hypertensive rats [1].
• Some genes, for example GLUT-1, MT-1, CELF, MKP-1, and t-PA did not show any hypoxic regulation in either astrocytes or neurons, suggesting that other cells are responsible for the up-regulation of these genes in the hypoxic brain [2].
• Cell-free transcription analyses indicate that CELF is a constitutive transcriptional activator without apparent phosphorylation by protein kinase A. These results demonstrate that multiple factors are responsible for transcriptional control of the substance P precursor gene through the CRE region [3].
• The sequence analysis indicates that the novel protein, designated CELF, has a significant homology to C/EBP gene family proteins in the carboxyl-terminal part containing the basic region and the leucine zipper motif [3].
• Activation domains of CCAAT enhancer binding protein delta: regions required for native activity and prostaglandin E2-dependent transactivation of insulin-like growth factor I gene expression in rat osteoblasts [4].

Biological context of Cebpd

• Molecular structure and function of rat CCAAT-enhancer binding protein-delta gene promoter [5].

Associations of Cebpd with chemical compounds

• One of them (C3) belongs to the proteins of the CELF (CUG-BP-ETR-3-like factors) family and thus bears three RNA recognition motif domains [6].

References