Key molecular players

Key Molecular Players Change Charge in Both Photosynthesis and Respiration... 

Key Molecular Players Perform Mechanical Work in Model Proteins... 

Chemical neurotransmission can be described more completely as a team of molecular players. The neurotransmitter may be the captain of the team, but it is only one key player. Other molecular players on the synaptic transmission team include the specific ions (Fig. 2—8), that interact with the ion channels (e.g., Fig. 2—6), various enzymes (Fig 2—9), transport carriers (Fig. 2—10), active transport pumps (Fig. 2—11), second messengers (Fig. 2—12), receptors (Fig. 2—13), transcription factors (Fig. 2—14), genes (Fig. 2—15), and gene products (Fig. 2—16). 

What can magnetism do better than other methods I have stressed that the PM cations (Table 1) are also the ones that can have several different valence states, thereby giving them prominent roles in biogeochemical reactions. Mineral magnetism, therefore, is a mineralogy focussed on the key reactive players in the environmental cycling of nutrients and toxic substances, most of which are nanoparticles or molecular clusters or PM active center metabolites. 

As seen above, the two primary molecular players of photosynthesis and respiration are nicotinamide and ATP. Both of these key molecules effect change in the charge of a protein machine during its function. In particular. 

Pyridoxal phosphate is a required coenzyme for many enzyme-catalyzed reactions. Most of these reactions are associated with the metabolism of amino acids, including the decarboxylation reactions involved in the synthesis of the neurotransmitters dopamine and serotonin. In addition, pyridoxal phosphate is required for a key step in the synthesis of porphyrins, including the heme group that is an essential player in the transport of molecular oxygen by hemoglobin. Finally, pyridoxal phosphate-dependent reactions link amino acid metabolism to the citric acid cycle (chapter 16). 

Potential direct nephrotoxicity and the underlying molecular mechanisms were analyzed by in vitro studies in renal proximal tubular cells exposed to IFNa. IFNa was shown to induce apoptosis in LLC-PKl renal proximal tubular like epithelium [216]. Caspase-8, a key player in death receptor signaling and caspase-9 that is involved in mitochondrial apoptosis were shown to be activated in addition to caspase-3. Furthermore, IFNa induced a breakdown of the inner mitochondrial membrane potential, further implying mitochondrial signahng in IFNa-induced apoptosis. The deafh receptor pathway and the mitochondrial pathway appear to both be necessary for efficient executor caspase activation by IFNa. The apoptotic signaling pathways activated by IFNa in proximal tubular cells, thus, resemble the pathways induced by IFNa in melanoma and bladder carcinoma cells [217, 218]. In addition to caspase activation, nuclear condensation, DNA fragmentation and a delayed LDH release were observed. DNA fragmentation and LDH release were partially prevented by caspase inhibition. Thus, caspase-inde-pendent death is also possible - albeit delayed and at a reduced extent [216]. 

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