PubMed · 10096872
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H G Döbereiner. 1999. Quantifying membrane asymmetry.. https://doi.org/10.1016/s0006-3495(99)77333-9
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The downhill folding observed experimentally for a small protein BBL is studied using off-lattice Gō-like model. Our simulations show that the downhill folding has low cooperativity and is barrierless, which is consistent with the experimental findings. As an example of comparison in detail, the two-state folding behavior of proteins, for example, protein CI2, is also simulated. By observing the formation of contacts between the residues for these two proteins, it is found that the physical origin of the downhill folding is due to the deficiency of nonlocal contacts which determine the folding cooperatively. From a statistics on contacts of the native structures of 17 well-studied proteins and the calculation of their cooperativity factors kappa2 based on folding simulations, a strong correlation between the number of nonlocal contacts per residue NN and the factors kappa2 is obtained. Protein BBL with a value of NN = 0.73 has the lowest cooperativity factor kappa2 = 0.34 among all 17 proteins. A crossover around NNc approximately 0.9 could be defined to separate the two-state folders and the downhill folder roughly. A protein would behave downhill folding when its NN = NNc. For proteins with their NN values are about (or slightly larger than) NNc, the folding behaves with low cooperativity and the barriers are small, showing a weak two-state behavior or a downhill-like behavior. Furthermore, simulations on mutants of a two-state folder show that a mutant becomes a downhill folder when its NN is reduced to a value smaller than NNc. These could enable us to identify the downhill folding or the cooperative two-state folding behavior solely from the native structures of proteins.
Cells face a constant struggle against unwanted instructions that arrive in the form of viruses and transposons. At the core of this battle are two issues: how can cellular machinery recognize certain informational molecules as 'unwanted' and how can the cell use this recognition to effectively silence malicious genetic activity. While defenses against some specific parasites may be triggered by individual nucleic acid or protein sequences, such sequence-specific mechanisms have the limitation of allowing the parasite to evade following relatively minor evolutionary change. A more general set of defense mechanisms is based on recognition of structural features that are intrinsic aspects of one or more parasitic lifestyle. Recognition of extended regions of double-stranded RNA (dsRNA) provides cells with one such defensive modality. Essentially absent during 'normal' gene expression, long stretches of dsRNA within a cell serve as a dramatic warning that a segment of information may be replicating as RNA. In addition to exemplifying many of the mechanistic issues in genome defense, the cellular response to dsRNA provides several examples of the logic by which organisms attempt to focus their limited immunity resources on the most immediate and dangerous targets.
The extracellular matrix of articular cartilage modulates the mechanical signals sensed by the chondrocytes. In the present study, a finite element model (FEM) of the chondrocyte and its microenvironment was reconstructed using the information from fourier transform infrared imaging spectroscopy. This environment consisted of pericellular, territorial (mainly proteoglycans), and inter-territorial (mainly collagen) matrices. The chondrocyte, pericellular, and territorial matrix were assumed to be mechanically isotropic and poroelastic, whereas the inter-territorial matrix, due to its high collagen content, was assumed to be transversely isotropic and poroelastic. Under instantaneous strain-controlled compression, the FEM indicated that the fluid pressure within the chondrocyte increased nonlinearly as a function of the in-plane Young's modulus of the collagen network. Under instantaneous force-controlled compression, the chondrocyte experienced the highest fluid pressure when the in-plane Young's modulus of the collagen network was approximately 4 MPa. Based on the present results, the mechanical characteristics of the collagen network of articular cartilage can modify fluid flow and stresses in chondrocytes. Therefore, the integrity of the collagen network may be an important determinant in cell stimulation and in the control of the matrix maintenance.