CoChat
Sign Up
Cited by 729Cancer-related Molecular PathwaysVirus-based gene therapy researchViral-associated cancers and disorders

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Cellular targets for transformation by the adenovirus E1A proteins

Whyte, Peter, Williamson, Nicola M., Harlow, Ed·1989·Cell
DOI 10.1016/0092-8674(89)90984-7
Open this paper in CoChat — free account

Abstract

Three cellular proteins, including species of 300,000 daltons and 107,000 daltons as well as p105-RB, the product of the retinoblastoma susceptibility gene, stably interact with the adenovirus E1A proteins. To help determine the functional basis of these interactions, the regions of E1A that participate in these interactions were mapped using a series of deletion mutants. The 300,000 dalton and the 107,000 dalton proteins interacted with sequences within amino acids 1 to 76 and 121 to 127, respectively. Interaction with the third cellular protein, p105-RB, required the presence of sequences from two noncontiguous regions of the E1A polypeptide chain, amino acids 30 to 60 and 121 to 127. The regions of E1A that are required for these interactions coincided precisely with the regions of E1A that are required for its transforming function. These results suggest that the interactions with these cellular proteins are fundamental to the transforming activity of E1A.

Overview

Integrity signals

Registry

Crossref · 10.1016/0092-8674(89)90984-7

Cites

3 of 3 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Show all 3 references

Research works printed but not linked: 47

  1. Benedict, 1987, Recessive human cancer susceptibility genes (Retinoblastoma and Wilm's loci), Adv. Virol. Oncol., 7, 19
  2. Berk, 1986, Adenovirus promoters and E1A transactivation, Annu. Rev. Genet., 20, 45, 10.1146/annurev.ge.20.120186.000401 · DOI
  3. Berk, 1978, Structure of the adenovirus 2 early mRNAs, Cell, 14, 695, 10.1016/0092-8674(78)90252-0 · DOI
  4. Bonner, 1974, A film detection method for tritium-labelled proteins and nucleic acids in polyacrylamide gels, Eur. J. Biochem., 46, 83, 10.1111/j.1432-1033.1974.tb03599.x · DOI
  5. Borrelli, 1984, Adenovirus 2 E1A products repress enhancer-induced stimulation of transcription, Nature, 312, 608, 10.1038/312608a0 · DOI
  6. Braithwaite, 1983, Adenovirus-induced alteration of the cell growth cycle: a requirement for expression of E1A but not of E1B, J. Virol., 45, 192, 10.1128/JVI.45.1.192-199.1983 · DOI
  7. Carlock, 1981, Transformation-defective mutant of adenovirus type 5 containing a single altered E1A mRNA species, J. Virol., 40, 657, 10.1128/JVI.40.3.657-664.1981 · DOI
  8. DeCaprio, 1988, SV40 large T antigen forms a specific complex with the product of the retinoblastoma susceptibility gene, Cell, 54, 275, 10.1016/0092-8674(88)90559-4 · DOI · Paper page
  9. Eliyahu, 1984, Participation of p53 cellular tumour antigen in transformation of normal embryonic cells, Nature, 312, 646, 10.1038/312646a0 · DOI
  10. Gallimore, 1974, Viral DNA transformed cells. II. A study of the sequences of adenovirus 2 DNA in nine lines of transformed rat cells using specific fragments of the viral genome, J. Mol. Biol., 89, 49, 10.1016/0022-2836(74)90162-4 · DOI
  11. Graham, 1974, Size and location of the transforming region in human adenovirus type 5 DNA, Nature, 251, 687, 10.1038/251687a0 · DOI
  12. Hansen, 1985, Osteosarcoma and retinoblastoma: a shared chromosomal mechanism revealing recessive predisposition, Proc. Natl. Acad. Sci. USA, 82, 6216, 10.1073/pnas.82.18.6216 · DOI
  13. Harbour, 1988, Abnormalities in structure and expression of the human retinoblastoma gene in SCLC, Science, 241, 353, 10.1126/science.2838909 · DOI
  14. Harlow, 1981, Monoclonal antibodies specific for simian virus 40 tumor antigens, J. Virol., 39, 861, 10.1128/JVI.39.3.861-869.1981 · DOI
  15. Harlow, 1985, Monoclonal antibodies specific for adenovirus early region 1A proteins: extensive heterogeneity in earlregion 1A products, J. Virol., 55, 533, 10.1128/JVI.55.3.533-546.1985 · DOI
  16. Harlow, 1986, Association of adenovirus early-region 1A proteins with cellular polypeptides, Mol. Cell. Biol., 6, 1579, 10.1128/MCB.6.5.1579 · DOI
  17. Hen, 1985, Repression of the immunoglobulin heavy chain enhancer by the adenovirus-2 E1A products, Science, 230, 1391, 10.1126/science.2999984 · DOI
  18. Houweling, 1980, Partial transformation of primary rat cells by the leftmost 4.5% fragment of adenovirus 5 DNA, Virology, 105, 537, 10.1016/0042-6822(80)90054-9 · DOI
  19. Jenkins, 1984, Cellular immortalization by a cDNA clone encoding the transformation-associated phosphoprotein p53, Nature, 312, 651, 10.1038/312651a0 · DOI
  20. Kaczmarek, 1986, Induction of cellular DNA synthesis by purified adenovirus E1A proteins, Virology, 152, 1, 10.1016/0042-6822(86)90366-1 · DOI
  21. Kalderon, 1984, In vitro mutagenesis of a putative DNA binding domain of SV40 large-T, Virology, 139, 109, 10.1016/0042-6822(84)90334-9 · DOI
  22. Kimchi, 1988, Absence of TGF-β receptors and growth inhibitory responses in retinoblastoma cells, Science, 240, 196, 10.1126/science.2895499 · DOI
  23. Kimmelman, 1985, E1A regions of the human adenoviruses and the highly oncogenic simian adenovirus 7 are closely related, J. Virol., 53, 399, 10.1128/JVI.53.2.399-409.1985 · DOI
  24. Lee, 1988, Inactivation of the retinoblastoma susceptibility gene in human breast cancers, Science, 241, 218, 10.1126/science.3388033 · DOI
  25. Lee, 1984, Expression and amplification of the N-myc gene in primary retinoblastoma, Nature, 309, 458, 10.1038/309458a0 · DOI
  26. Lillie, 1986, An adenovirus E1a protein region required for transformation and transcriptional repression, Cell, 46, 1043, 10.1016/0092-8674(86)90704-X · DOI
  27. Lillie, 1987, Functional domains of adenovirus type 5 E1A proteins, Cell, 50, 1091, 10.1016/0092-8674(87)90175-9 · DOI
  28. Montell, 1982, Resolving the functions of overlapping viral genes by site-specific mutagenesis at an mRNA splice site, Nature, 295, 380, 10.1038/295380a0 · DOI
  29. Moran, 1988, Interactions between cell growth-regulating domains in the products of the adenovirus E1A oncogene, Mol. Cell. Biol., 8, 1756, 10.1128/MCB.8.4.1756 · DOI
  30. Moran, 1987, Multiple functional domains in the adenovirus E1A gene, Cell, 48, 177, 10.1016/0092-8674(87)90418-1 · DOI
  31. Moran, 1986, Identification of separate domains in the adenovirus E1A gene for immortalization activity and the activation of virus early genes, Mol. Cell. Biol., 6, 3470, 10.1128/MCB.6.10.3470 · DOI
  32. Parada, 1984, Cooperation between gene encoding p53 tumour antigen and ras in cellular transformation, Nature, 312, 649, 10.1038/312649a0 · DOI
  33. Perricaudet, 1979, Structure of two spliced mRNAs from the transforming region of human subgroup C adenoviruses, Nature, 218, 694, 10.1038/281694a0 · DOI
  34. Phelps, 1988, The human papillovirus type 16 E7 gene encodes transactivation and transformation functions similar to those of adenovirus E1A, Cell, 53, 539, 10.1016/0092-8674(88)90570-3 · DOI
  35. Quinlan, 1988, Growth factor induction by the adenovirus type 5 E1A 12S protein is required for immortalization of primary epithelial cells, Mol. Cell. Biol., 8, 3191, 10.1128/MCB.8.8.3191 · DOI
  36. Schneider, 1987, Mutational analysis of the adenovirus E1A gene: the role of transcriptional regulation in transformation, EMBO J., 6, 2053, 10.1002/j.1460-2075.1987.tb02470.x · DOI
  37. Schwab, 1985, Human N-myc gene contributes to nepplastic transformation of mammalian cell in culture, Nature, 316, 160, 10.1038/316160a0 · DOI
  38. Squire, 1986, Tumour induction by the retinoblastoma mutation is independent of N-myc expression, Nature, 322, 555, 10.1038/322555a0 · DOI
  39. Stabel, 1985, The release of growth arrest by microinjection of adenovirus E1A DNA, EMBO J., 4, 2329, 10.1002/j.1460-2075.1985.tb03934.x · DOI
  40. Subramanian, 1988, An N-terminal region of adenovirus E1A essential for cell transformation and induction of an epithelial growth factor, Oncogene, 2, 105
  41. van den Elsen, 1983, Expression of region E1B of human adenovirus in the absence of region E1A is not sufficient for complete transformation, Virology, 128, 377, 10.1016/0042-6822(83)90264-7 · DOI
  42. Velcich, 1985, Adenovirus E1A proteins repress transcription from the SV40 early promoter, Cell, 40, 705, 10.1016/0092-8674(85)90219-3 · DOI
  43. Velcich, 1988, Adenovirus E1A ras cooperation activity is separate from its positive and negative transcription regulatory functions, Mol. Cell. Biol., 8, 2177, 10.1128/MCB.8.5.2177 · DOI
  44. Whyte, 1988, Association between an oncogene and an anti-oncogene: the adenovirus E1A proteins bind to the retinoblastoma gene product, Nature, 334, 124, 10.1038/334124a0 · DOI · Paper page
  45. Whyte, 1988, Two regions of the adenovirus early region 1A proteins are required for transformation, J. Virol., 62, 257, 10.1128/JVI.62.1.257-265.1988 · DOI
  46. Yee, 1985, Detection of cellular proteins associated with human adenovirus type 5 early region 1A polypeptides, Virology, 147, 142, 10.1016/0042-6822(85)90234-X · DOI
  47. Zerler, 1986, Adenovirus E1A coding sequences that enable ras and pmt oncogenes to transform cultured primary cells, Mol. Cell. Biol., 6, 887, 10.1128/MCB.6.3.887 · DOI

Cited by

Sorted by citations

See all 729

Metadata

Authors
Whyte, P., Williamson, N. M., & Harlow, E.
Affiliations
Cold Spring Harbor Laboratory (US)
Venue
Cell
Publisher
Elsevier BV
Published
1989-01
Volume
56
Issue
1
Pages
67-75
ISSN
0092-8674 (ISSN-L)
DOI
10.1016/0092-8674(89)90984-7
OpenAlex
W1967404701
Cited by
729
References
3
Citations by year
2025: 3 · 2024: 6 · 2023: 4 · 2022: 8 · 2021: 3 · 2020: 5 · 2019: 2 · 2018: 1 · 2017: 7 · 2016: 3 · 2015: 9 · 2014: 6 · 2013: 6 · 2012: 8
FWCI
34.59
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
  • Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
Funders
National Cancer Institute (CA13106)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Virus-based gene therapy research
  • Health Sciences › Medicine › Oncology › Viral-associated cancers and disorders
Keywords
adenovirus E1A, viral oncogenesis, cell transformation, protein-protein interaction, retinoblastoma gene, transforming activity, viral oncoproteins
MeSH terms
Cell Transformation, Viral, DNA Mutational Analysis, HeLa Cells, Humans, Molecular Weight, Nuclear Proteins, Oncogene Proteins, Viral, Precipitin Tests, Protein Binding, Retinoblastoma, Structure-Activity Relationship, Adenovirus Early Proteins, In Vitro Techniques

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review