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Thread: New apporoach to apoptosis mechanism and cellular reaction

  1. #1 New apporoach to apoptosis mechanism and cellular reaction 
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    Theor Biol Med Model. 2010 Jun 9;7:19.
    Native aggregation as a cause of origin of temporary cellular structures needed for all forms of cellular activity, signaling and transformations.
    Matveev VV.

    Laboratory of Cell Physiology, Institute of Cytology, Russian Academy of Sciences, Tikhoretsky Ave 4, St, Petersburg 194064, Russia.

    Abstract
    According to the hypothesis explored in this paper, native aggregation is genetically controlled (programmed) reversible aggregation that occurs when interacting proteins form new temporary structures through highly specific interactions. It is assumed that Anfinsen's dogma may be extended to protein aggregation: composition and amino acid sequence determine not only the secondary and tertiary structure of single protein, but also the structure of protein aggregates (associates). Cell function is considered as a transition between two states (two states model), the resting state and state of activity (this applies to the cell as a whole and to its individual structures). In the resting state, the key proteins are found in the following inactive forms: natively unfolded and globular. When the cell is activated, secondary structures appear in natively unfolded proteins (including unfolded regions in other proteins), and globular proteins begin to melt and their secondary structures become available for interaction with the secondary structures of other proteins. These temporary secondary structures provide a means for highly specific interactions between proteins. As a result, native aggregation creates temporary structures necessary for cell activity.

    "One of the principal objects of theoretical research in any department of knowledge is to find the point of view from which the subject appears in its greatest simplicity."Josiah Willard Gibbs (1839-1903).

    Full text: http://vladimirmatveev.ru


    Native aggregation in cell physiology
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  3. #2  
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    What is the significance of this paper?

    It is claimed that 'native (programmed) protein aggregation leading to self-assembly of various cell structures is the usual phenomenon of cell life'. However, the genome cannot directly dictate the aggregation of proteins into complexes which are involved in interesting biological events, e.g. cell death. Of course the genome can direct the production of mRNA transcripts encoding proteins of specific conformation. It can also dictate the levels of production of those proteins via cis-acting elements and trans-acting factors. Surely though, it would be folly to suggest that any given protein-protein interaction is directly programmed? The interaction also depends on the proteins being in close enough proximity of one another to interact. Can that be programmed?


    'In terms of the hypothesis of native aggregation, this scheme looks unconvincing.
    Indeed, it is hard to imagine a mechanism (for instance, the mechanism of muscle contraction) or a process in the living cell working on the basis of random collisions. First, if natively unfolded proteins and their targets collide randomly, it means that they are diffusing freely in the cytoplasm or nucleus, i.e., we are dealing with a Brownian mechanism of regulation'

    Whilst it can be appreciated that the cytoplasm of any given cell is of course not just an 'empty bag' and is, in fact, quite a densely packed structure - surely the likelihood of interaction between proteins is still to some extent subject to Brownian motion?

    Tridimity


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  4. #3  
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    On the latter point, if this were not the case, then enzyme kinetics would not be affected by temperature in the way that they have been shown to be.

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  5. #4  
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    My main argument is that it is impossible to imagine a mechanism of regulation on the basis of Brownian motion. You do not have too an example of smart regulation on the basis of random collisions. Thanks.
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