Three regions of the pRB pocket domain affect its inactivation by human papillomavirus E7 proteins

Journal of Virology

Volumn 76, Issue 12, 2002, Pages 6224-6234

  Dick, Frederick A ^a   Dyson, Nicholas J ^a  

^a MASSACHUSETTS GENERAL HOSPITAL CANCER CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

GENE PRODUCT; PROTEIN PRB; UNCLASSIFIED DRUG; VIRUS PROTEIN;

AMINO ACID COMPOSITION; ANIMAL CELL; ARTICLE; BINDING SITE; CELL CYCLE G1 PHASE; CONTROLLED STUDY; EMBRYO; GENE DISRUPTION; GENE INACTIVATION; GENETIC CONSERVATION; HUMAN; HUMAN CELL; MITOSIS INHIBITION; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN DOMAIN; PROTEIN MOTIF; PROTEIN PROTEIN INTERACTION; PROTEIN STABILITY; VIRUS TRANSFORMATION; WART VIRUS;

AMINO ACID MOTIFS; AMINO ACID SEQUENCE; G1 PHASE; GENE EXPRESSION REGULATION; HELA CELLS; HUMANS; MOLECULAR SEQUENCE DATA; MUTAGENESIS, SITE-DIRECTED; MUTATION; ONCOGENE PROTEINS, VIRAL; PAPILLOMAVIRIDAE; RETINOBLASTOMA PROTEIN;

EID: 0036100267     PISSN: 0022538X     EISSN: None     Source Type: Journal    
DOI: 10.1128/JVI.76.12.6224-6234.2002     Document Type: Article

References (50)

1. Differential regulation of the pocket domains of the retinoblastoma family proteins by the HPV16 E7 oncoprotein
2. E7 protein of human papilloma virus-16 induces degradation of retinoblastoma protein through the ubiquitin-proteasome pathway
3. Cumulative effect of phosphorylation of pRB on regulation of E2F activity
4. Acetylation control of the retinoblastoma tumour-suppressor protein
5. Role of LXCXE motif-dependent interactions in the activity of the retinoblastoma protein
6. Adenovirus E1A, simian virus 40 tumor antigen, and the human papillomavirus E7 protein share the capacity to disrupt the interaction between transcription factor E2F and the retinoblastoma gene product
7. Establishment of irreversible growth arrest in myogenic differentiation requires the RB LXCXE-binding function
8. Role of the LXCXE binding site in Rb function
9. SV40 large tumor antigen forms a specific complex with the product of the retinoblastoma susceptibility gene
10. Abrogation of growth arrest signals by human papillomavirus type 16 E7 is mediated by sequences required for transformation
11. Mutagenesis of the pRB pocket domain reveals that cell cycle arrest functions are separable from binding to viral oncoproteins
12. The regulation of E2F by pRB-family proteins
13. Homologous sequences in adenovirus E1A and human papillomavirus E7 proteins mediate interaction with the same set of cellular proteins
14. The human papilloma virus-16 E7 oncoprotein is able to bind to the retinoblastoma gene product
15. An N-terminal transformation-governing sequence of SV40 large T antigen contributes to the binding of both p110Rb and a second cellular protein, p120
16. Prediction of similar transforming regions in simian virus 40 large T, adenovirus E1A, and myc oncoproteins
17. Degradation of the retinoblastoma tumor suppressor by the human papillo- mavirus type 16 oncoprotein is important for functional inactivation and is separable from proteasomal degradation of E7
18. Repression of human papillomavirus oncogenes in HeLa cervical carcinoma cells causes the orderly reactivation of dormant tumor suppressor pathways
19. Transactivation-competent papillomavirus E2 protein is specifically required for efficient repression of human papillomavirus oncogene expression and for acute growth inhibition of cervical carcinoma cell lines
20. 1
21. Association of adenovirus early region 1A proteins with cellular polypeptides
22. Efficiency of binding the retinoblastoma protein correlates with the transforming capacity of the E7 oncoproteins of the human papillomaviruses
23. Destabilization of the retinoblastoma tumor suppressor by human papillomavirus type 16 E7 is not sufficient to overcome cell cycle arrest in human keratinocytes
24. Protein domains governing interactions between E2F, the retinoblastoma gene product, and human papillomavirus type 16 E7 protein
25. pRB and p107/p130 are required for the regulated expression of different sets of E2F responsive genes
26. Inhibition of cervical carcinoma cell line proliferation by the introduction of a bovine papillomavirus regulatory gene
27. Destabilization of the RB tumor suppressor protein and stabilization of p53 contribute to HPV type 16 E7-induced apoptosis
28. Identification of HPV-16 E7 peptides that are potent antagonists of E7 binding to the retinoblastoma suppressor protein
29. Structural basis for the inactivation of retinoblastoma tumor suppressor by SV40 large T antigen
30. Dual mechanisms for the inhibition of E2F binding to RB by cyclin-dependent kinase-mediated RB phosphorylation
31. Structure of the retino-blastoma tumour-suppressor pocket domain bound to a peptide from HPV E7
32. Cyclin E-induced S phase without activation of the pRb/E2F pathway
33. The carboxyl-terminal zinc-binding domain of the human papillomavirus E7 protein can be functionally replaced by the homologous sequences of the E6 protein
34. Control of pRB phosphorylation
35. The retinoblastoma gene family: Cousins with overlapping interests
36. Complex formation of human papillomavirus E7 proteins with the retinoblastoma tumor suppressor gene product
37. Bovine papillomavirus E2 protein activates a complex growth-inhibitory program in p53 negative HT-3 cervical carcinoma cells that includes repression of cyclin A and cdc25A phosphatase genes and accumulation of hypophosphorylated retinoblastoma protein
38. Binding of the human E2F transcription factor to the retinoblastoma protein but not to cyclin A is abolished in HPV-16-immortalized cells
39. Identification of a novel retinoblastoma gene product binding site on human papillomavirus type 16 E7 protein
40. Structure-function analysis of the human papillomavirus type 16 E7 onco-protein
41. The human papillomavirus type 16 E7 gene encodes transactivation and transformation functions similar to those of adenovirus E1A
42. Cancer cell cycles
43. The release of growth arrest by microinjection of adenovirus E1A DNA
44. Distinct roles for cyclin-dependent kinases in cell cycle control
45. Both Rb and E7 are regulated by the ubiquitin proteasome pathway in HPV-containing cervical tumor cells
46. The retinoblastoma protein and cell cycle control
47. Two regions of the adenovirus early region 1A proteins are required for transformation
48. Cellular targets for transformation by the adenovirus E1A proteins
49. The human papillomavirus E7 oncoprotein and the cellular transcription factor E2F bind to separate sites on the retinoblastoma tumor suppresoor protein
50. Immortalization of human cells and their malignant conversion by high risk papillomavirus genotypes