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    Saheed Abdulkarim
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    This document outlines the mitochondrial control of apoptosis, or programmed cell death. It shows that death stimuli like FasL or survival factor withdrawal can trigger apoptosis through the Fas/CD95 receptor or withdrawal of survival factors. This activates caspases and pro-apoptotic and pro-survival Bcl-2 family proteins located in the mitochondria, regulating the release of cytochrome c and other factors from the mitochondria to activate downstream caspases and cell death. The pathway diagram also shows various kinases, phosphatases and other regulators that control the mitochondrial and caspase apoptotic pathways in response to death stimuli or survival signals.

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    This document outlines the mitochondrial control of apoptosis, or programmed cell death. It shows that death stimuli like FasL or survival factor withdrawal can trigger apoptosis through the Fas/CD95 receptor or withdrawal of survival factors. This activates caspases and pro-apoptotic and pro-survival Bcl-2 family proteins located in the mitochondria, regulating the release of cytochrome c and other factors from the mitochondria to activate downstream caspases and cell death. The pathway diagram also shows various kinases, phosphatases and other regulators that control the mitochondrial and caspase apoptotic pathways in response to death stimuli or survival signals.

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    © All Rights Reserved
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    3 views1 page

    APO2

    Uploaded by

    Saheed Abdulkarim
    This document outlines the mitochondrial control of apoptosis, or programmed cell death. It shows that death stimuli like FasL or survival factor withdrawal can trigger apoptosis through the Fas/CD95 receptor or withdrawal of survival factors. This activates caspases and pro-apoptotic and pro-survival Bcl-2 family proteins located in the mitochondria, regulating the release of cytochrome c and other factors from the mitochondria to activate downstream caspases and cell death. The pathway diagram also shows various kinases, phosphatases and other regulators that control the mitochondrial and caspase apoptotic pathways in response to death stimuli or survival signals.

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    of 1

    CELL SIGNALING TECHNOLOGY www.cellsignal.

    com

    Mitochondrial Control of Apoptosis


    Death Stimuli:
    FasL
    Survival Factor Withdrawal
    Survival Factors:
    Growth Factors, Cytokines, etc.
    Fas/
    CD95

    FADD Bim
    LC8
    Casp-8,-10

    Microtubules
    DLC2
    PI3K HECTH9 JNK
    Bmf
    Erk1/2
    BID Mcl-1
    JNK
    Hrk
    PKC Bcl-xL Bim DP5
    Bcl-2 ARD1
    tBID
    Bmf NatA
    PKA p90RSK Akt p70 S6K Bak Hrk Bax
    DP5 Acetyl-CoA
    Bax
    Bcl-2
    tBID
    CaMKII
    Calcineurin Bax
    Bad Bax Bak
    14-3-3 Bak Casp-2
    Bcl-2
    RAIDD
    Bad Noxa
    PIDD
    14-3-3 [NAD]
    Bcl-xL Bcl-2
    Bad Puma
    Apaf-1
    Mcl-1

    Cytosolic SirT2
    Cyto c
    Sequestration Casp-9
    p53
    Arts HECTH9
    HSP60 HtrA2

    Smac/ Endo G
    XIAP Diablo ATM/
    AIF ATR ING2
    Casp-3 ub

    Bcl-2 Family
    DNA Damage
    Pro-Apoptotic Apoptosis Genotoxic Stress
    Pro-Survival

    Pathway Diagram Keys


    Kinase Enzyme G-protein Direct Inhibitory Tentative Inhibitory Translocation
    Modification Modification Transcriptional
    Phosphatase pro-apoptotic Acetylase
    Multistep Stimulatory Separation of Subunits Stimulatory Modification
    Transcription Factor pro-survival Deacetylase Modification or Cleavage Products Transcriptional
    Multistep Inhibitory Joining of Subunits Inhibitory Modification
    Caspase GAP/GEF Ribosomal subunit Modification
    Receptor Direct Stimulatory Tentative Stimulatory
    GTPase
    Modification Modification

    © 2003 – 2014 Cell Signaling Technology, Inc.

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