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B-Myb overcomes a p107-mediated cell proliferation block by interacting with an N-terminal domain of p107
- Source :
- Oncogene. 21(52)
- Publication Year :
- 2002
-
Abstract
- B-Myb is a cell-cycle regulated transcription factor which is implicated in cell proliferation and has an essential role in early embryonic development. In this study we examined the functions of B-Myb required to overcome G1 arrest in Saos-2 cells induced by the retinoblastoma-related p107 protein. Our results demonstrated that this activity was independent of B-Myb transactivation function, but correlated with its capacity to form an in vivo complex with p107. A large proportion of B-Myb formed complexes with p107 in cotransfected cells, however, B-Myb bound weakly to the related p130 protein and not at all to pRb. In contrast to the E2F transcription factors, which bind the p107 C-terminal pocket domain, B-Myb recognizes an N-terminal p107 region which overlaps the larger cyclin-binding domain. B-Myb and cyclin A2 formed mutually exclusive complexes with p107, and B-Myb enhanced the activity of co-transfected cyclin E kinase activity, implying that B-Myb affects the cell cycle by preventing sequestration of active cyclin/cdk2 complexes. This study defines a novel function of B-Myb and further suggests that the p107 N-terminus provides an interaction domain for transcription factors involved in cell cycle control.
- Subjects :
- Transcriptional Activation
Cancer Research
animal structures
Cyclin A
Molecular Sequence Data
Cell Cycle Proteins
Retinoblastoma-Like Protein p107
Cyclin-dependent kinase
Cyclin E
Genetics
Tumor Cells, Cultured
Humans
Amino Acid Sequence
Molecular Biology
Transcription factor
Binding Sites
biology
fungi
Cyclin-dependent kinase 2
G1 Phase
Nuclear Proteins
Cell cycle
Precipitin Tests
Cell biology
DNA-Binding Proteins
embryonic structures
Cyclin-dependent kinase complex
biology.protein
Trans-Activators
biological phenomena, cell phenomena, and immunity
E2F Transcription Factors
Cyclin A2
Cell Division
Protein Binding
Subjects
Details
- ISSN :
- 09509232
- Volume :
- 21
- Issue :
- 52
- Database :
- OpenAIRE
- Journal :
- Oncogene
- Accession number :
- edsair.doi.dedup.....e3e9ede206eaca19baca2b6c47b9a5a0