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Titolo:
Dysregulation of cyclin E gene expression in human cytomegalovirus-infected cells requires viral early gene expression and is associated with changesin the Rb-related protein p130
Autore:
Mcelroy, AK; Dwarakanath, RS; Spector, DH;
Indirizzi:
Univ Calif San Diego, Dept Biol, La Jolla, CA 92093 USA Univ Calif San Diego La Jolla CA USA 92093 t Biol, La Jolla, CA 92093 USA Univ Calif San Diego, Ctr Mol Genet, La Jolla, CA 92093 USA Univ Calif SanDiego La Jolla CA USA 92093 Genet, La Jolla, CA 92093 USA
Titolo Testata:
JOURNAL OF VIROLOGY
fascicolo: 9, volume: 74, anno: 2000,
pagine: 4192 - 4206
SICI:
0022-538X(200005)74:9<4192:DOCEGE>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN-IMMUNODEFICIENCY-VIRUS; E2F TRANSCRIPTION FACTOR; B-MYB TRANSCRIPTION; RETINOBLASTOMA PROTEIN; SUBCELLULAR-LOCALIZATION; DIFFERENTIAL REGULATION; FAMILY PROTEINS; BINDING-SITES; DNA ELEMENTS; S-PHASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
63
Recensione:
Indirizzi per estratti:
Indirizzo: Spector, DH Univ Calif San Diego, Dept Biol, 9500 Gilman Dr,Mailcode 0366,La Jolla, CA 92093 USA Univ Calif San Diego 9500 Gilman Dr,Mailcode 0366 La Jolla CA USA 92093
Citazione:
A.K. Mcelroy et al., "Dysregulation of cyclin E gene expression in human cytomegalovirus-infected cells requires viral early gene expression and is associated with changesin the Rb-related protein p130", J VIROLOGY, 74(9), 2000, pp. 4192-4206

Abstract

We have previously shown that many cell cycle regulatory gene products aremarkedly affected by infection of primary fibroblasts with human cytomegalovirus (HCMV) (F. M. Jault, J. M. Jault, F. Ruchti, E. A. Fortunate, C. Clark, J. Corbeil, D. D. Richman, and D. II. Spector, J. Virol. 69:6697-6704, 1995). One of these proteins, cyclin E, is a key determinant of cell cycle progression during G(1), and its mRNA levels are significantly increased inHCMV-infected fibroblasts (B. S. Salvant, E, A. Fortunate, and D. II. Spector, J. Virol. 72:3729-3741, 1998). To determine the molecular basis of this effect, we have examined the events that occur at the endogenous cyclin Epromoter during the course of infection. In vivo dimethyl sulfate footprinting of the cyclin E promoter revealed several regions of protection and hypersensitivity that were unique to infected cells. In accord with this observation, we find that the virus-induced cyclin E transcripts initiate downstream of the start site identified in mock-infected cells, in regions wherethese newly appearing protected and hypersensitive sites occur. Viral geneexpression is required for this induction. However, the viral immediate-early proteins IE1-72 and IE2-86, either alone or in combination, cannot induce expression of the endogenous cyclin E. The virus must progress past the immediate-early phase and express an early gene product(s) for activation of cyclin E expression. Moreover, IE1-72 does not appear to be required, as infection of cells with an HCMV mutant containing a deletion in the IE1-72 gene leads to full upregulation of cyclin E expression. Using electrophoretic mobility shift assays with infected cell extracts and a region of the cyclin E promoter that includes two previously defined E2F sites as the probe, we detected the appearance of an infection specific banding pattern. One of the infection-specific bands contained the proteins E2F-4, DP-1, and p130, which were maintained in the infected cells as uniquely phosphorylated species. These results suggest that an altered E2F-4-DP-1-p130 complex alongwith viral early gene expression may play a role in the transcriptional regulation of cyclin E mRNA during HCMV infection.

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Documento generato il 18/09/20 alle ore 14:49:37