Adenovirus E1A-mediated regulation of class I MHC expression.

Vaessen, R.T.M.J.; Houweling, Ada; Israël, Alain; Kourilsky, P; Eb, A. J. Van Der

doi:10.1002/j.1460-2075.1986.tb04217.x

Cited by 65 publications

(43 citation statements)

References 32 publications

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“…The stable G401 transfectants 21K-C1 and 21K-C8 (21C1 and 21C8, respectively); 21K/E1A-C3 and 21K/E1A-C24 (5/21C3 and 5/21C24, respectively); 5E1B-C2, 5E1B-C3, and 5E1B-C5 (G55C1, G55C3, and G55C5, respectively); 12E1B-C1, 12E1B-C3, and 12E1B-C7 (G54C1, G54C3, and G54C7, respectively); and E4-C3 and E4-C7 (GE4C3 and GE4C7, respectively) have been described previously (28)(29)(30) and were grown on the same medium with addition of G418 (300 g/ml). Primary HER (human embryonic retina), Ad5-transformed HER XC1 and HER XC2, and Ad12-transformed HER RC4 and HER RC6 cell lines have been described previously (33) and were cultured on Eagle's minimal essential medium supplemented with vitamins, nonessential and essential amino acids, glucose, and 10% FBS.…”

Section: Methodsmentioning

confidence: 99%

Distinct Regulation of p53 and p73 Activity by Adenovirus E1A, E1B, and E4orf6 Proteins

Steegenga

Шварц

Riteco

et al. 1999

Molecular and Cellular Biology

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Multiple adenovirus (Ad) early proteins have been shown to inhibit transcription activation by p53 and thereby to alter its normal biological functioning. Since these Ad proteins affect the activity of p53 via different mechanisms, we examined whether this inhibition is target gene specific. In addition, we analyzed whether the same Ad early proteins have a comparable effect on transcription activation by the recently identified p53 homologue p73. Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1 , cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B. The repressive effect of the E1A proteins on p53 activity is less than that seen with the large E1B proteins, but the E1A proteins inhibit the activity of both p53 and p73. We could not detect significant inhibition of p53 functions by E4orf6, but a clear repression of the transcription activation by p73 by this Ad early protein was observed. In addition, we found that stable expression of the Ad5 E1A and that of the E1B protein both caused increased p73 protein expression. The large E1B and the E4orf6 proteins together do not target the p73 protein for rapid degradation after adenoviral infection, as has previously been found for the p53 protein, probably because the large E1B protein does not interact with p73. Our results suggest that the p53 and p73 proteins are both inactivated after Ad infection and transformation but via distinct mechanisms.By regulating the expression of different target genes, p53 can affect important cellular processes like cell cycle progression and apoptosis. Multiple adenovirus early (Ad E) proteins have been shown to inhibit the transcription activation potential of p53 via different mechanisms and thereby to impair its normal biological functioning. The first Ad E protein identified as inhibiting p53 activity was the large E1B protein (38). Yew and colleagues have shown that in the presence of the large E1B protein p53 can still bind to its consensus sequence but that the transcription-repressive regions present in the large E1B protein inhibit the transcription activation potential of p53 (39). In addition, we and others have shown that the E1A proteins also can inhibit transcription activation by p53 (27,30). The E1A proteins can directly interact with the p300 protein, which not only serves as a cofactor for p53 transactivation but also activates its sequence-specific DNA binding by acetylation of the C terminus of p53 (6, 7, 12). The third Ad E protein which has been reported to inhibit transcription activation by p53 is the E4orf6 protein. Dobner and coworkers reported that E4orf6 inhibits the activity of p53 by a direct interaction with the C terminus of p53 which inhibits binding of TAF32 to the transcription activation domain of p53 (2). It is currently unclear why Ads produce such a number of different proteins all causing repression ...

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Section: Methodsmentioning

confidence: 99%

Distinct Regulation of p53 and p73 Activity by Adenovirus E1A, E1B, and E4orf6 Proteins

Steegenga

Шварц

Riteco

et al. 1999

Molecular and Cellular Biology

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“…Adenovirus 12 (Adl2) transformed cells exhibit reduced levels of MHC class I mRNA and surface class I molecules and are oncogenic when injected into syngeneic animals, whereas cells transformed by Ad5 have unaltered or elevated levels of surface class I molecules and their mRNAs and are non-oncogenic [13][14][15]. Recently it has been shown that TAP1/2 and LMP2/7 mRNA and protein levels are also reduced in Adl2-transformed mouse cells [16,17], and in a number of human tumours [18,19].…”

Section: Introductionmentioning

confidence: 99%

The MHC‐encoded TAP1/LMP2 bidirectional promoter is down‐regulated in highly oncogenic adenovirus type 12 transformed cells

Proffitt

Blair

1997

FEBS Letters

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Cells transformed by human adenovirus 12 (Adl2) exhibit extremely low surface levels of MHC class I molecules and contain reduced levels of class I heavy chain mRNAs. We report that levels of MHC-encoded TAP1 and LMP2 mRNAs are also down-regulated in Ad 12-transformed rat cells, and that transcription of rat TAP1 and LMP2 transcripts is directed from a 564 bp intergenic region which is significantly less active in Adl2-transformed cells compared to those transformed with Ad5. Our results suggest that, in common with MHC class I gene expression, TAP1 and LMP2 gene expression is reduced mainly at the level of transcription in Ad 12-transformed cells.

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“…They include tumors induced by DNA viruses (15,23,28), RNA viruses (7,17,22), and chemical carcinogens (5). The observed suppression may have arisen either directly by the expression of specific gene products (1)(2)(3)27) or indirectly through mechanisms involving immunoselection (9,20).…”

mentioning

confidence: 99%

Rejection of B16 melanoma induced by expression of a transfected major histocompatibility complex class I gene.

Tanaka¹,

Gorelik²,

Watanabe³

et al. 1988

Mol. Cell. Biol.

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Transfection of a functional major histocompatibility complex class I gene into certain tumor cells, induced by oncogenic viruses or chemical carcinogens, can effectively abrogate their tumorigenic activity. Since experimentally induced tumors possess strong tumor-specific transplantation antigens, expression of cell surface class I antigens may present the tumor cells to appropriate immune effector cells. Most spontaneously arising tumors do not possess tumor-specific transplantation antigens, and their tumorigenicity may not be affected by the expression of a transfected class I gene. We demonstrate that the poorly immunogenic B16-BL6 melanoma can be rendered nontumorigenic in syngeneic mice by the expression of the class I H-2K antigen but not the class II I-A antigen. Furthermore, the poorly tumorigenic, class I-expressing B16-BL6-transfected cells can effectively immunize syngeneic C57BL/6 mice against the highly tumorigenic, class I-deficient B16-BL6 parental cells. Our success in experimentally manipulating the tumorigenicity of a spontaneously derived neoplasm offers hope for a potential modality for the effective treatment of human cancer.

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Adenovirus E1A-mediated regulation of class I MHC expression.

Cited by 65 publications

References 32 publications

Distinct Regulation of p53 and p73 Activity by Adenovirus E1A, E1B, and E4orf6 Proteins

Distinct Regulation of p53 and p73 Activity by Adenovirus E1A, E1B, and E4orf6 Proteins

The MHC‐encoded TAP1/LMP2 bidirectional promoter is down‐regulated in highly oncogenic adenovirus type 12 transformed cells

Rejection of B16 melanoma induced by expression of a transfected major histocompatibility complex class I gene.

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