1,764 results found
    1. Cancer Biology
    2. Cell Biology

    Bim escapes displacement by BH3-mimetic anti-cancer drugs by double-bolt locking both Bcl-XL and Bcl-2

    Qian Liu et al.
    The pro-apoptotic BH3-protein Bim contains two distinct binding sites for anti-apoptotic proteins that together confer resistance of Bim/Bcl-2 and Bim/Bcl-XL complexes to BH3-mimetic drugs under development for use in humans.
    1. Cell Biology

    IRBIT controls apoptosis by interacting with the Bcl-2 homolog, Bcl2l10, and by promoting ER-mitochondria contact

    Benjamin Bonneau et al.
    IRBIT and the Bcl-2 homolog Bcl2l10 form a complex at the endoplasmic reticulum that controls Ca2+ signaling, however IRBIT turns into an apoptosis facilitator following stress and inhibits anti-apoptotic activity of Bcl2l10.
    1. Structural Biology and Molecular Biophysics

    Patient-specific mutations impair BESTROPHIN1’s essential role in mediating Ca2+-dependent Cl- currents in human RPE

    Yao Li et al.
    A multidisciplinary platform featured by patient-derived RPEs is established to study the disease-causing mechanisms of BEST1 mutations, and demonstrates gene-supplemented rescue of the mutation-caused deficiency in Ca2+-dependent Cl- current in human RPE.
    1. Immunology and Inflammation

    T cell-specific inhibition of multiple apoptotic pathways blocks negative selection and causes autoimmunity

    Megan L Burger et al.
    Using mice expressing a Bcl-2 mutant protein to suppress multiple central tolerance pathways, it is shown that central tolerance is crucial for preventing autoimmunity.
    1. Cell Biology

    Bid maintains mitochondrial cristae structure and function and protects against cardiac disease in an integrative genomics study

    Christi T Salisbury-Ruf et al.
    An integrative approach, combining genetic mouse and large-scale human genetics studies, was used to reveal a novel role for the Bcl-2 protein Bid in maintenance of mitochondrial function that alters susceptibility to myocardial infarction.
    1. Cell Biology

    Disordered clusters of Bak dimers rupture mitochondria during apoptosis

    Rachel T Uren et al.
    Dimers of Bak assemble into clusters without using a distinct protein-protein interface, which may explain the apparent difficulties in obtaining high resolution structures of the pore complex and in targeting dimer-dimer interactions to regulate apoptosis.
    1. Cell Biology
    2. Structural Biology and Molecular Biophysics

    The carboxyl-terminal sequence of bim enables bax activation and killing of unprimed cells

    Xiaoke Chi et al.
    The C-terminal membrane binding domain of Bim is shown to interact with and activate Bim enabling it to kill cells not dependent on anti-apoptotic proteins for survival.
    1. Cancer Biology
    2. Computational and Systems Biology

    Computationally designed high specificity inhibitors delineate the roles of BCL2 family proteins in cancer

    Stephanie Berger et al.
    Six computationally designed and in vitro optimized protein inhibitors serve as molecular probes to reveal BCL2 profiles of different human cancers.
    1. Stem Cells and Regenerative Medicine

    Yap1 safeguards mouse embryonic stem cells from excessive apoptosis during differentiation

    Lucy LeBlanc et al.
    During ES cell differentiation, Yap1 directly regulates apoptosis-related genes like Bcl-2 and Mcl-1 to attenuate apoptosis and promote cell survival to allow for successful cell fate changes.
    1. Developmental Biology

    Autophagic cell death is dependent on lysosomal membrane permeability through Bax and Bak

    Jason Karch et al.
    Molecular pathways controlling autophagic cell death are regulated at the level of the lysosome through the activity of the pro-death Bcl-2 family member Bax/Bak.

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