Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of the E1A protein of adenovirus-5 on the differentiation program of F9 teratocarcinoma cells were examined by the stable introduction of plasmids that expressed wild-type or mutated forms of E1A. Constitutive expression of plasmids for most of the mutant E1As induced loss of expression of the cell-surface antigen SSEA-1 and the enhanced expression of genes specific for the differentiated phenotype of F9 cells, such as genes for laminin B1, tissue-type plasminogen activator (tPA) and type IV collagen, as well as the altered cell morphology that is associated with the differentiated state. However, such changes were not observed in the case of genes for mutant proteins from which a conserved region (CR1) of E1A had been deleted. Furthermore, no significant induction of expression of the c-jun gene or transactivation of the c-jun-CAT reporter gene were observed when the sequence that encodes CR1 of E1A had been deleted. A palindromic sequence element (DRE) of the c-jun promoter was essential for the E1A-mediated up-regulation of the c-jun gene. These results imply that CR1 is required for activation of the c-jun gene and that it is implicated in the growth arrest, expression of parietal endoderm-specific functions and the orderly differentiation of F9 cells.
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PMID:Induction by adenovirus-5 E1A of the differentiation phenotype of F9 teratocarcinoma cells involves a conserved region (CR1) of E1A. 774 80

Transforming growth factor-betas (TGF-betas) 2 and 3 are expressed in murine embryonic astrocytes in vivo, but their cellular functions are not known. Primary cultures of rat neonatal astroglial cells express mRNA transcripts for TGF-betas 1, 2, and 3, as well as basic fibroblast growth factor (bFGF) and secrete TGF-beta1 and TGF-beta2 protein. TGF-beta3 protein levels cannot be determined at present. While bFGF is mitogenic for these cells, addition of TGF-betas 1, 2, or 3 alone has little effect. However, the effects of bFGF are modulated by TGF-betas in an isoform-specific fashion. Thus, TGF-beta3 and to a lesser extent TGF-beta2, but not TGF-beta1, can reduce the mitogenic effect of bFGF, but TGF-beta1 selectively leads to a change in cell morphology accompanied by colony formation. Basic FGF and TGF-betas alone, but not combinations of bFGF and TGF-betas, increase plasminogen activator (PA) activity of proliferating cultures, while on confluent cultures TGF-betas and bFGF show additive increases in PA activity. While bFGF and TGF-betas alone have little effect on expression of fibronectin, collagen I, or laminin B1 mRNA by these cells, the combination of TGF-betas and bFGF increases expression of collagen I mRNA. The expression of TGF-beta3, but not TGF-beta1 or TGF-beta2, mRNA is increased almost 10-fold by treatment with any TGF-beta isoform. These data show that TGF-betas alone have little effect on astrocyte growth and gene expression, but can alter effects of bFGF in an isoform-dependent manner. Changes in astrocyte proliferation and morphology, as well as expression of collagen and PA, induced by bFGF and TGF-beta1 are discussed in relation to astroglial scarring.
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PMID:Effects of TGF-betas and bFGF on Astroglial Cell Growth and Gene Expression in Vitro. 1991 47