Results 191 to 200 of about 3,403,478 (241)
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Transcriptional inhibition by the retinoblastoma protein
Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences, 1993Abstract The retinoblastoma protein, pRB, appears to play a key role in coordinating the regulation of cell cycle position and transcriptional events. pRB undergoes specific cell-cycle-dependent phosphorylation, being underphosphorylated in G1 and heavily phosphorylated in S, G2, and M. The underphosphorylated form is able to interact
Fattaey, A, Helin, K, Harlow, E
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Overexpression and hyperphosphorylation of retinoblastoma protein in the progression of malignant melanoma [PDF]
Mutation, absence or abnormal functioning of retinoblastoma protein are fundamental elements of uncontrolled growth in human cancer. In this study, we analyze the expression of retinoblastoma protein and phosphorylated retinoblastoma protein in ...
Alexander Roesch +2 more
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Transcriptional control by the retinoblastoma protein
Seminars in Cancer Biology, 1995The retinoblastoma gene product is an abundant nuclear protein whose 'pocket domain' mediates numerous protein-protein interactions. A substantial proportion of the RB-interacting proteins are transcription factors suggesting that RB plays a fundamental role in the regulation of transcription.
Tony Kouzarides
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Retinoblastoma protein partners
2001Studies of the retinoblastoma gene (Rb) have shown that its protein product (pRb) acts to restrict cell proliferation, inhibit apoptosis, and promote cell differentiation. The frequent mutation of the Rb gene, and the functional inactivation of pRb in tumor cells, have spurred interest in the mechanism of pRb action.
E J, Morris, N J, Dyson
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The role of retinoblastoma protein in apoptosis
Apoptosis, 1999The retinoblastoma gene and its protein product (Rb) have been studied intensively for their role in development, oncogenesis, cell growth, differentiation and cell cycle regulation. In addition, Rb appears to be a key factor in protecting cells from apoptosis.
G, Fan, C J, Steer
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Functions of the retinoblastoma protein
BioEssays, 1999The retinoblastoma protein (pRB) can both positively and negatively regulate transcription. The former correlates with its ability to promote differentiation and the latter with its ability to regulate entry into S-phase. pRB negatively regulates transcription by forming complexes with members of the E2F transcription factor family.
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Retinoblastoma protein meets chromatin
Trends in Biochemical Sciences, 1999The retinoblastoma (RB) protein exerts its tumour-suppressor function by repressing the transcription of cellular genes required for DNA replication and cell division. Recent investigations into the mechanism of RB repression have revealed that RB can regulate transcription by effecting changes in chromatin structure.
A, Brehm, T, Kouzarides
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Deciphering the retinoblastoma protein phosphorylation code [PDF]
Multisite phosphorylation modulates the function of regulatory proteins with complex signaling properties and outputs. The retinoblastoma tumor suppressor protein (Rb) is inactivated by cyclin-dependent kinase (Cdk) phosphorylation in normal and cancer cell cycles, so understanding the molecular mechanisms and effects of Rb phosphorylation is ...
Seth Rubin
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Retinoblastoma protein in microphthalmic mice
Experimental and Toxicologic Pathology, 2000A microphthalmic strain of mice was used to study immunoresponse of the retinoblastoma protein. Comparing wild-type, heterozygote and homozygote microphthalmic eyes, we found an increasing labelling of phosphorylated retinoblastoma protein (pRb) in the retinal pigment epithelium.
J, Richter +4 more
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Retinoblastoma protein and the cell cycle
Current Opinion in Genetics & Development, 1993Deregulation of the cell cycle may contribute one of the primary mechanisms through which cancer arises. Eukaryotic cell division has been found to be a strictly controlled process, involving response to both positive and negative external signals and assessment of the cell's internal state.
R E, Hollingsworth +2 more
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