Functional analysis at the Cys706 residue of the retinoblastoma protein.

Kratzke, Robert A.; Otterson, Gregory A.; Lin, Alison; Shimizu, Eiji; Alexandrova, N.; Zajac-Kaye, Maria; Horowitz, Jordan M.; Kaye, Frederic J.

doi:10.1016/s0021-9258(18)35707-7

Cited by 25 publications

(2 citation statements)

References 44 publications

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“…Proteins were identified using the fragment masses searching in a publicly available database (http://129.85. 19.192/pro-found_bin/WebProFound.exe).…”

Section: Methodsmentioning

confidence: 99%

“…Hereby, an intact pocket domain of pRB was identified to be required for interaction with Alien. Interestingly, the pRBmutant with an amino acid exchange in the pocket domain of pRB, pRB706, that lacks silencing function 19 also lacks interaction with Alien (Figure 4C). Thus, Alien is also in a complex with pRB and is complexed with factors known to interact with pRB.…”

Section: Alien Represses the Transcriptional Activity Of E2f-1mentioning

confidence: 99%

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Various Members of the E2F Transcription Factor Family Interact in vivo with the Corepressor Alien

et al. 2007

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Proteins perform their activities in cells by the cooperation within protein complexes. For this reason, it is important to investigate protein-protein interactions to receive insights in physiological processes. A multitude of proteins are involved in the regulation of the cell cycle. Specific key factors participating here are members of the E2F transcription factors. Using an in vivo protein-protein complex detection assay, which comprises mass spectrometric and immunological techniques, we detected a number of known as well as new protein-protein interactions. We describe here for the first time protein complexes containing the corepressor Alien and members of the E2F transcription factor family. Furthermore, we assessed the functional relevance and show a repression of the transcriptional activity of E2F by Alien. Additionally, we detected new interactions that link endogenously expressed Alien with the tumor suppressor retinoblastoma protein (pRB) and with proteins involved in cell cycle regulation.

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“…Proteins were identified using the fragment masses searching in a publicly available database (http://129.85. 19.192/pro-found_bin/WebProFound.exe).…”

Section: Methodsmentioning

confidence: 99%

Section: Alien Represses the Transcriptional Activity Of E2f-1mentioning

confidence: 99%

Various Members of the E2F Transcription Factor Family Interact in vivo with the Corepressor Alien

et al. 2007

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Mutations in the retinoblastoma gene and their expression in somatic and tumor cells of patients with hereditary retinoblastoma

et al. 1994

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Two intragenic deletions (exon 18-19 and exon 24) and two point mutations (one missense mutation in exon 21 and one mutation at splice-donor site for exon 13) were detected in the retinoblastoma gene in somatic and tumor cells of patients with hereditary retinoblastoma. Three mutations were located in a domain essential for binding to oncoproteins encoded by DNA tumor viruses (Hu et al., 1990; Huang et al., 1990). One mutation (deletion of exon 24) was outside this domain but it is in the region essential for binding to transcriptional factor E2F, and for suppression of malignant phenotypes (Qian et al., 1992; Qin et al., 1992). A minisatellite-like sequence and short repeated sequences were located at the breakpoint of the deletion of exon 24, suggesting that two deletions on both sides of the minisatellite-like sequence may be generated by a "DNA slippage and misalignment" mechanism. Upon amplification of cDNA by the polymerase chain reaction, no transcript of gene with frameshift mutation (deletion of exon 24) was detected in skin fibroblasts, while transcripts of genes with missense mutations were detected. The results, in combination with previous reports (Dunn et al., 1989; Hashimoto et al., 1991), suggest the instability of transcripts with a premature stop codon or the suppressed expression of alleles with a premature stop codon in the retinoblastoma gene in somatic cells of hereditary patients.

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Sv40‐induced immortalization and ras‐transformation of human bronchial epithelial cells

Reddel

Silva

Duncan

et al. 1995

Intl Journal of Cancer

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Non-tumorigenic SV40-immortalized human cells may be transformed to tumorigenicity by activated oncogenes, but the molecular genetics of this process are still poorly understood. We describe here 4SV40-transformed bronchial epithelial (BE) cell lines that became immortalized after a period of crisis, and then transfection of 6 BE lines or sub-lines with an activated c-Ha-ras (EJ-ras) oncogene. pSV2neo-transfected cells did not form any tumors in athymic nude mice. Even though each of the EJ-ras-transfected lines was shown to be expressing the mutant ras gene, only one cell line, BEAS-2B, and 2 of its sub-lines were tumorigenic after transfection. We conclude that immortalization is not sufficient for BE cells to be transformed by the EJ-ras oncogene. Thus there are at least 2 unknown genetic events in this in vitro model of carcinogenesis: escape from crisis (immortalization), and development of ability to cooperate with activated ras in tumorigenic transformation. We found no evidence that either immortalization or ability to complement ras is related to abnormalities of the SV40 T antigens, of p110RB or of p53.

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Functional analysis at the Cys706 residue of the retinoblastoma protein.

Cited by 25 publications

References 44 publications

Various Members of the E2F Transcription Factor Family Interact in vivo with the Corepressor Alien

Various Members of the E2F Transcription Factor Family Interact in vivo with the Corepressor Alien

Mutations in the retinoblastoma gene and their expression in somatic and tumor cells of patients with hereditary retinoblastoma

Sv40‐induced immortalization and ras‐transformation of human bronchial epithelial cells

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