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Molecule Parameter List for AA

The statistics table lists the distribution of a molecule acting either as a substrate, product, enzyme or as a molecule within the network.
The text color of a molecule is highlighted by color.
Statistics
AA participated asMoleculeSum total ofEnzymeSubstrate of an enzymeProduct of an enzymeSubstrate in ReactionProduct in Reaction
No. of occurrences1000540

Accession and Pathway Details
Accession NameAccession No.Accession TypePathway Link
  • MAPK-bistability
    -fig1c
  • 35Network
    Shared_Object_MAPK-bistability-fig1c Sos PKC 
    MAPK PLA2 Ras 
    PDGFR 
    Model for figure 1c in Bhalla US et al. Science (2002) 297(5583):1018-23.
    The demo for this figure is available here. This synaptic signaling model is without the MKP-1 feedback, so it is bistable and remains so over long periods.

    AA acting as a Molecule in  
    MAPK-bistability-fig1c Network
    NameAccession NamePathway NameInitial Conc.
    (uM)
    Volume
    (fL)
    Buffered
    AA
  • MAPK-bistability
    -fig1c

    Accession No. : 35
  • Shared_Object_
    MAPK-bistability
    -fig1c

    Pathway No. : 179
  • 6.121000No
    Arachidonic Acid. This messenger diffuses through membranes as well as cytosolically, has been suggested as a possible retrograde messenger at synapses.

    AA acting as a Product of an Enzyme in  
    MAPK-bistability-fig1c Network
     Enzyme Molecule /
    Enzyme Activity
    Accession NamePathway NameKm (uM)kcat (s^-1)RatioEnzyme TypeReagents
    1PLA2-Ca*  /
    kenz
  • MAPK-bistability
    -fig1c

    Accession No. : 35
  • PLA2
    Pathway No. : 183
    205.44explicit E-S complexSubstrate
    APC

    Product
    AA
        Based on Leslie and Channon 1990 BBA 1045:261, in relation to the other PLA2 inputs (not including MAPK). Ca alone is rather a weak input.
    2PIP2-PLA2*  /
    kenz
  • MAPK-bistability
    -fig1c

    Accession No. : 35
  • PLA2
    Pathway No. : 183
    2011.044explicit E-S complexSubstrate
    APC

    Product
    AA
        Based on Leslie and Channon 1990 BBA 1045:261.
    3PIP2-Ca-PLA2*  /
    kenz
  • MAPK-bistability
    -fig1c

    Accession No. : 35
  • PLA2
    Pathway No. : 183
    20364explicit E-S complexSubstrate
    APC

    Product
    AA
        Based on AA generation by different stimuli according to Leslie and Channon 1990 BBA 1045:261
    4DAG-Ca-PLA2*  /
    kenz
  • MAPK-bistability
    -fig1c

    Accession No. : 35
  • PLA2
    Pathway No. : 183
    20604explicit E-S complexSubstrate
    APC

    Product
    AA
        Based on Leslie and Channon 1990 BBA 1045:261.
    5PLA2*-Ca  /
    kenz
  • MAPK-bistability
    -fig1c

    Accession No. : 35
  • PLA2
    Pathway No. : 183
    201204explicit E-S complexSubstrate
    APC

    Product
    AA
        This form should be 3 to 6 times as fast as the Ca-only form, from Lin et al 1993 Cell 269-278 Nemenoff et al 1993 JBC 268:1960 Several forms contribute to the Ca-stimulated form, so this rate has to be a factor larger than their total contribution. I assign Vmax as the scale factor here because there is lots of APC substrate, so all the PLA2 complex enzymes are limited primarily by Vmax.

    AA acting as a Substrate in a reaction in  
    MAPK-bistability-fig1c Network
    Kd is calculated only for second order reactions, like nA+nB <->nC or nA<->nC+nD, where n is number and A,B,C,D are molecules, where as for first order reactions Keq is calculated. Kd for higher order reaction are not consider.
     NameAccession NamePathway NameKfKbKdtauReagents
    1
  • PKC-act-by-Ca-AA
  • MAPK-bistability
    -fig1c

    Accession No. : 35
  • PKC
    Pathway No. : 181
    0.0012
    (uM^-1 s^-1)
    0.1
    (s^-1)
    Kd(bf) = 83.3333(uM)-Substrate
    AA
    PKC-Ca

    Product
    PKC-Ca-AA*
      Ca-dependent AA activation of PKC. Note that this step combines the AA activation and also the membrane translocation. From Schaechter and Benowitz 1993 J Neurosci 13(10):4361
    2PKC-act-by-AA
  • MAPK-bistability
    -fig1c

    Accession No. : 35
  • PKC
    Pathway No. : 181
    0.0001
    (uM^-1 s^-1)
    0.1
    (s^-1)
    Kd(bf) = 833.3333(uM)-Substrate
    AA
    PKC-cytosolic

    Product
    PKC-AA*
      AA stimulates PKC activity even at rather low Ca. Schaechter and Benowitz 1993 J Neurosci 13(10):4361 Note that this one reaction combines the initial interaction and also membrane translocation.
    3PKC-n-DAG-AA
  • MAPK-bistability
    -fig1c

    Accession No. : 35
  • PKC
    Pathway No. : 181
    0.018
    (uM^-1 s^-1)
    2
    (s^-1)
    Kd(bf) = 111.1111(uM)-Substrate
    AA
    PKC-DAG

    Product
    PKC-DAG-AA
      This is one of the more interesting steps. Mechanistically it does not seem necessary at first glance. Turns out that one needs this step to quantitatively match the curves in Schaechter and Benowitz 1993 J Neurosci 13(10):4361 and Shinomura et al 1991 PNAS 88:5149-5153. There is a synergy between DAG and AA activation even at low Ca levels, which is most simply represented by this reaction. Tau is assumed to be fast. Kd comes from matching the experimental curves.
    4Degrade-AA
  • MAPK-bistability
    -fig1c

    Accession No. : 35
  • PLA2
    Pathway No. : 183
    0.4
    (s^-1)
    0
    (s^-1)
    --Substrate
    AA

    Product
    APC
      Degradation pathway for AA. APC is a convenient buffered pool to dump it back into, though the actual metabolism is probably far more complex. For the purposes of the full model we use a rate of degradation of 0.4/sec to give a dynamic range of AA comparable to what is seen experimentally. Wijkander and Sundler 1991 Eur J Biochem 202:873 Leslie and Channon 1990 BBA 1045:261



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