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BOK Is a Non-canonical BCL-2 Family Effector of Apoptosis Regulated by ER-Associated Degradation

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An interconnected hierarchical model of cell death regulation by the BCL-2 family

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Bax Exists in a Dynamic Equilibrium between the Cytosol and Mitochondria to Control Apoptotic Priming

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Structural Model of Active Bax at the Membrane

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VDAC2 enables BAX to mediate apoptosis and limit tumor development

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Lysosomal membrane permeabilization and cathepsin release is a Bax/Bak-dependent, amplifying event of apoptosis in fibroblasts and monocytes

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Bax dimerizes via a symmetric BH3:groove interface during apoptosis

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Differential retrotranslocation of mitochondrial Bax and Bak

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Genetic Control of Programmed Cell Death During Animal Development

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Bak Core and Latch Domains Separate during Activation, and Freed Core Domains Form Symmetric Homodimers

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Bax targets mitochondria by distinct mechanisms before or during apoptotic cell death: a requirement for VDAC2 or Bak for efficient Bax apoptotic function

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Intracellular localization of the BCL-2 family member BOK and functional implications

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A conserved intronic response element mediates direct p53-dependent transcriptional activation of both the human and murine bax genes

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BCL-2 family member BOK promotes apoptosis in response to endoplasmic reticulum stress

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The role of apoptosis in megakaryocytes and platelets

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Mechanisms and consequences of entosis

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BCL-2 family member BOK is widely expressed but its loss has only minimal impact in mice

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Inhibition of Bak Activation by VDAC2 Is Dependent on the Bak Transmembrane Anchor

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The Proapoptotic Factors Bax and Bak Regulate T Cell Proliferation through Control of Endoplasmic Reticulum Ca2+ Homeostasis

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The proapoptotic activities of Bax and Bak limit the size of the neural stem cell pool

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Identification of novel direct transcriptional targets of glucocorticoid receptor

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Hyperoxia-induced Apoptosis Does Not Require Mitochondrial Reactive Oxygen Species and Is Regulated by Bcl-2 Proteins

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SARS-CoV-2 membrane protein causes the mitochondrial apoptosis and pulmonary edema via targeting BOK

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Role of Atg5-dependent cell death in the embryonic development of Bax/Bak double-knockout mice

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Non-apoptotic cell death in animal development

Kutscher, L. M., & Shaham, S. (2017) · Cell Death & Differentiation · doi:10.1038/cdd.2017.20 · Cited by 67 · see citing works

Consequences of the combined loss of BOK and BAK or BOK and BAX

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Rethinking the regulation of cellular metabolism

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Bok is a genuine multi-BH-domain protein that triggers apoptosis in the absence of Bax and Bak

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Maintenance of the relative proportion of oligodendrocytes to axons even in the absence of BAX and BAK

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Estrogen-dependent proteolytic cleavage of semaphorin 4D and plexin-B1 enhances semaphorin 4D-induced apoptosis during postnatal vaginal remodeling in pubescent mice

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Differential mechanisms involved in RG-7388 and Nutlin-3 induced cell death in SJSA-1 osteosarcoma cells

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ИСПОЛЬЗОВAНИЕ ПОТЕНЦИAЛA СОЦИAЛЬНЫХ ПAРТНЕРОВ В ПОДГОТОВКЕ БУДУЩИХ ПЕДAГОГОВ

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Identification of specific genes and pathways involved in NSAIDs-induced apoptosis of human colon cancer cells

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Relationships between induction of apoptosis by CDDP in Scaber cell and apoptosis-related proteins

Wang, Y. (2003) · Zhongguo yaolixue tongbao

Apoptosis of human pancreatic cancer cells induced by Triptolide

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