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    1. Chromosomes and Gene Expression

    SETD2 is required for DNA double-strand break repair and activation of the p53-mediated checkpoint

    Sílvia Carvalho et al.
    The involvement of SETD2 in an important DNA repair pathway could explain the high frequency of SETD2 mutations in several cancers and may provide an alternative mechanism to evade the p53-mediated checkpoint.
    1. Cell Biology

    The transcription factors TFE3 and TFEB amplify p53 dependent transcriptional programs in response to DNA damage

    Eutteum Jeong et al.
    Disruption of TFEB and TFE3 results in diminished p53 signaling capacity and altered cell cycle regulation under genotoxic stress conditions.
    1. Cancer Biology
    2. Cell Biology

    Laminin signals initiate the reciprocal loop that informs breast-specific gene expression and homeostasis by activating NO, p53 and microRNAs

    Saori Furuta et al.
    Endogenous laminins are necessary to build a functional acinus via generating NO, activating p53, HOXD10 and other positive players, but tumor cells neither make laminin nor generate NO, unless they are reverted to an organized structure.
    1. Chromosomes and Gene Expression

    p53 orchestrates DNA replication restart homeostasis by suppressing mutagenic RAD52 and POLθ pathways

    Sunetra Roy et al.
    p53 suppresses genome instability by direct role at stalled replication forks for pathway regulation that explains transcription-independent p53 tumor-suppressor functions.
    1. Cancer Biology
    2. Cell Biology

    TP53 exon-6 truncating mutations produce separation of function isoforms with pro-tumorigenic functions

    Nitin H Shirole et al.
    Genetic and molecular analysis of TP53 exon-6 truncating mutations reveal that these mutations, contrary to current belief, promote tumorigenesis and point towards strategies for treating cancers driven by these prevalent mutations.
    1. Structural Biology and Molecular Biophysics
    2. Cell Biology

    Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level

    Daniel Coutandin et al.
    p63 uses an intricate network of domain-domain interactions to control its function in long-term quality maintenance of resting oocytes.
    1. Cancer Biology

    Loss of p53 suppresses replication-stress-induced DNA breakage in G1/S checkpoint deficient cells

    Bente Benedict et al.
    During tumorigenesis loss of p53 not only abrogates cell cycle arrest and apoptosis, but also suppresses the induction of replication-stress-induced DNA double-stranded breaks.
    1. Cancer Biology

    FXR1 regulates transcription and is required for growth of human cancer cells with TP53/FXR2 homozygous deletion

    Yichao Fan et al.
    Functional and mechanistic analyses of cancer cells containing homozygous deletion of TP53 and FXR2 reveal that inhibition of FXR1 blocks cell proliferation in a collateral lethality manner, opening an avenue to develop therapies targeting such cancers.
    1. Human Biology and Medicine

    A distinct p53 target gene set predicts for response to the selective p53–HDM2 inhibitor NVP-CGM097

    Sébastien Jeay et al.
    The discovery and preclinical validation of a novel gene signature predictive for response to HDM2-targeting drug NVP-CGM097 could significantly improve the clinical response rate to all p53-HDM2 inhibitors.
    1. Cell Biology
    2. Developmental Biology

    Ribosomal protein S27-like is a physiological regulator of p53 that suppresses genomic instability and tumorigenesis

    Xiufang Xiong et al.
    The ribosomal protein, Rps27l, plays an oncogenic role by promoting p53 degradation via stabilizing the Mdm2-Mdm4 complex, but a tumor suppressor role by preventing the aneuploidy and loss of p53 heterozygosity.