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Human Knowledge: Foundations and Limits

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Future Directions. Notwithstanding the attractiveness of the induced-proximity model, there remain a number of open questions. For example, although the data support the hypothesis, the molecular mechanisms of the event(s) have not been explained, and there are a number of issues that need to be addressed in the near future. These issues are as follows. (i) Must the processed caspase-8 be released from the DISC to diffuse toward its downstream substrates? (ii) Does activation require dimerization, a consensus for the catalytic form of caspases 1 and 3 at least? (iii) Does processing occur in cis (intramolecular) or in trans (intermolecular)? (iv) Must the zymogens be specifically aligned within the recruitment complex, and how many zymogen molecules constitute an activation locus? (v) Is the minimal operative DISC as simple as the one depicted in , or are other proteins required ()? These questions cut to the heart of uncertainties surrounding the fundamental activation mechanism of all the caspases, and each is (in principle) answerable by generating specific mutants and by using the artificial death-switch technique. Perhaps it is already possible to settle the issue of cis versus trans processing; in our hands, it is rarely possible to observe activation of caspase zymogens in the nanomolar range, but on artificial concentration toward the micromolar range, one observes processing and activation. This observation would imply a second-order reaction, which is most easily understood in terms of trans processing. Indeed, this proposal makes sense, because it is much easier to regulate zymogen activation in trans than in cis. The answers to these questions will require the molecular structure of at least one caspase zymogen (preferably caspase-8). Their resolution will certainly lead to a better understanding of the molecular mechanism of the DISC, with the attendant possibilities of interfering therapeutically to either initiate or prevent the commitment step in death-receptor-mediated apoptosis.

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Densitometric scanning of SDS-polyacrylamide gels was used to measure myosin heavy chain concentration in left ventricular specimens obtained from cat heart 3 to 12 months after healing of small experimental myocardial infarctions. The study was designed to test the hypothesis that myosin concentration varies as a function of anatomic proximity to the infarct scar. Myosin heavy chain concentration was elevated in non-scarred areas adjacent to a healed infarct and normal in areas remote from the scar. The scar itself had reduced concentrations, reflecting the loss of muscle mass in this area. The increased myosin heavy chain concentration in regions adjacent to the scar may be an attempt to regulate or compensate for the decrease in mechanical function of the scarred area.

Caspase activation: The induced-proximity model

11/12/2013 · This paper proposes a proximity-concentration tradeoff in product ..

N2 - Densitometric scanning of SDS-polyacrylamide gels was used to measure myosin heavy chain concentration in left ventricular specimens obtained from cat heart 3 to 12 months after healing of small experimental myocardial infarctions. The study was designed to test the hypothesis that myosin concentration varies as a function of anatomic proximity to the infarct scar. Myosin heavy chain concentration was elevated in non-scarred areas adjacent to a healed infarct and normal in areas remote from the scar. The scar itself had reduced concentrations, reflecting the loss of muscle mass in this area. The increased myosin heavy chain concentration in regions adjacent to the scar may be an attempt to regulate or compensate for the decrease in mechanical function of the scarred area.

AB - Densitometric scanning of SDS-polyacrylamide gels was used to measure myosin heavy chain concentration in left ventricular specimens obtained from cat heart 3 to 12 months after healing of small experimental myocardial infarctions. The study was designed to test the hypothesis that myosin concentration varies as a function of anatomic proximity to the infarct scar. Myosin heavy chain concentration was elevated in non-scarred areas adjacent to a healed infarct and normal in areas remote from the scar. The scar itself had reduced concentrations, reflecting the loss of muscle mass in this area. The increased myosin heavy chain concentration in regions adjacent to the scar may be an attempt to regulate or compensate for the decrease in mechanical function of the scarred area.

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Proximity stigma: testing the hypothesis.

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