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In biochemistry, denaturation is a process in which proteins or nucleic acids lose folded structure present in their native state due to various factors, including application of some external stress or compound, such as a strong acid or base, a concentrated inorganic salt, an organic solvent (e.g., alcohol or chloroform), agitation and radiation, or heat. [3]
In one study, rad9 mutant and normal cells in the exponential phase of growth were exposed to UV-irradiation and synchronized in specific phases of the cell cycle. After being incubated to permit DNA repair, the extent of pyrimidine dimerization (which is indicative of DNA damage) was assessed using sensitive primer extension techniques.
Furthermore, one can assess whether the folding proceeds according to a two-state unfolding as described above. This can be done with differential scanning calorimetry by comparing the calorimetric enthalpy of denaturation i.e. the area under the peak, A peak {\displaystyle A_{\text{peak}}} to the van 't Hoff enthalpy described as follows:
Overview of signal transduction pathways involved in apoptosis. Cell death is the event of a biological cell ceasing to carry out its functions. This may be the result of the natural process of old cells dying and being replaced by new ones, as in programmed cell death, or may result from factors such as diseases, localized injury, or the death of the organism of which the cells are part.
Denaturation (biochemistry), a structural change in macromolecules caused by extreme conditions; Denaturation (fissile materials), transforming fissile materials so that they cannot be used in nuclear weapons; Denaturation (food), intentional adulteration of food or drink rendering it unfit for consumption while remaining suitable for other uses
An important downstream target of ATM and ATR is p53, as it is required for inducing apoptosis following DNA damage. [60] The cyclin-dependent kinase inhibitor p21 is induced by both p53-dependent and p53-independent mechanisms and can arrest the cell cycle at the G1/S and G2/M checkpoints by deactivating cyclin/cyclin-dependent kinase ...
At the molecular level, hyperactive apoptosis can be caused by defects in signaling pathways that regulate the Bcl-2 family proteins. Increased expression of apoptotic proteins such as BIM, or their decreased proteolysis, leads to cell death and can cause a number of pathologies, depending on the cells where excessive activity of BIM occurs.
Proteases prevent this cycle from occurring by altering the rate of one of the pathways, or by cleaving a key enzyme, they can stop one of the pathways. Proteases are also nonspecific when binding to substrate , allowing for great amounts of diversity inside the cells and other proteins, as they can be cleaved much easier in an energy efficient ...