Gain of function of mutant p53: the mutant p53/NF-Y protein complex reveals an aberrant transcriptional mechanism of cell cycle regulation (Q24301892)

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Marcella Mottolese

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author name string

Silvia Di Agostino

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Sabrina Strano

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Velia Emiliozzi

3

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Valentina Zerbini

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Giovanni Blandino

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Giulia Piaggio

CBP and p300: HATs for different occasions

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language of work or name

English

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publication date

September 2006

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published in

Cancer Cell

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volume

10

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issue

3

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page(s)

191-202

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cites work

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p53, the cellular gatekeeper for growth and division

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Cell-cycle regulation of the DNA topoisomerase IIalpha promoter is mediated by proximal CCAAT boxes: possible involvement of acetylation

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Regulation of the p300 HAT domain via a novel activation loop.

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Mutant p53 protein expression interferes with p53-independent apoptotic pathways

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Mutant p53 gain of function: differential effects of different p53 mutants on resistance of cultured cells to chemotherapy

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Down-regulation of cyclin B1 gene transcription in terminally differentiated skeletal muscle cells is associated with loss of functional CCAAT-binding NF-Y complex

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The cyclin B2 promoter depends on NF-Y, a trimer whose CCAAT-binding activity is cell-cycle regulated

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The p53 pathway: positive and negative feedback loops

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Repression of the MSP/MST-1 gene contributes to the antiapoptotic gain of function of mutant p53

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Human TAFII31 protein is a transcriptional coactivator of the p53 protein

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Cell cycle regulation of the cyclin A gene promoter is mediated by a variant E2F site

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An oncogenic form of p53 confers a dominant, gain-of-function phenotype that disrupts spindle checkpoint control

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E2F-mediated growth regulation requires transcription factor cooperation

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p53 negatively regulates cdc2 transcription via the CCAAT-binding NF-Y transcription factor

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Transcriptional activation of the MDR1 gene by UV irradiation. Role of NF-Y and Sp1.

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Physical and Functional Interaction between p53 Mutants and Different Isoforms of p73

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NF-Y mediates the transcriptional inhibition of the cyclin B1, cyclin B2, and cdc25C promoters upon induced G2 arrest

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Physical interaction with human tumor-derived p53 mutants inhibits p63 activities.

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Abrogation of the S phase DNA damage checkpoint results in S phase progression or premature mitosis depending on the concentration of 7-hydroxystaurosporine and the kinetics of Cdc25C activation.

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Identification of direct p73 target genes combining DNA microarray and chromatin immunoprecipitation analyses.

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Dynamic recruitment of NF-Y and histone acetyltransferases on cell-cycle promoters.

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Requirement for down-regulation of the CCAAT-binding activity of the NF-Y transcription factor during skeletal muscle differentiation.

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Transcriptional repression by p53 involves molecular interactions distinct from those with the TATA box binding protein

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A survey of 178 NF-Y binding CCAAT boxes

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A gain of function p53 mutant promotes both genomic instability and cell survival in a novel p53-null mammary epithelial cell model

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Cyclin A expression is under negative transcriptional control during the cell cycle

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A subset of tumor-derived mutant forms of p53 down-regulate p63 and p73 through a direct interaction with the p53 core domain

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