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Query: UMLS:C0001486 (Adenovirus)
 3,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenovirus (Ad) DNA replication requires nuclear factor I (NFI), a cellular sequence-specific DNA binding protein which binds to the Ad DNA inverted terminal repeat (ITR). The NFI binding consensus sequence, TGGN6-7GCCAA, possibly includes the CCAAT-box which is often observed in regulatory elements of transcription. Adjacent to the NFI binding site on the Ad ITR is the binding site for nuclear factor III (NFIII), another cellular factor that stimulates Ad DNA replication in a cell-free system. Using gel retardation assay, we have examined the tissue specificity of these DNA binding activities in mouse. High NFI activity was detected in nuclear extracts from mouse liver, kidney, and spleen. Competition gel retardation assay with double-stranded oligonucleotides containing herpes simplex virus thymidine kinase (HSV-TK) gene or hsp70 gene CCAAT-box showed no effect on mouse NFI binding to its binding site. In the course of competitive DNA-binding assay, we detected a novel DNA binding protein in mouse kidney nuclear extracts, designated nuclear factor K (NFK). The NFK binding site is included in the NFIII binding site on the Ad ITR. NFK seems to be different from NFIII, in mode of binding to its binding site.
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PMID:Tissue-specific DNA binding of nuclear proteins that bind to the adenovirus inverted terminal repeat. 276 19

Adenovirus contains two nuclear oncogenes, the EIA and EIB genes, which cooperatively can transform cells through mechanisms that are not understood. The transcriptional activities of the E1A gene (transactivation and repression) are well studied. Using transient expression assays, we show here that the 19,000-Da E1B gene product can also activate all the adenovirus early promoters (E1A, E1B, E2e, E3 and E4) and a cellular heat shock gene promoter (hsp70), but not the adenovirus late promoters (IX, IVa2, MLP and E2L). The effect is greatest under conditions where cell growth is inhibited, and appears to operate at the transcriptional level. Possible interactions with enhancer elements are discussed. Although the E1B stimulatory effect does not require the presence of E1A gene products, a synergistic effect is obtained in the presence of E1A 13S product. This activity of the E1B gene is also observed during virus infection and is likely to have important consequences in lytically infected and transformed cells.
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PMID:Transactivation of host and viral genes by the adenovirus E1B 19K tumor antigen. 296 90