Endoplasmic reticulum defined

Another pathway is the L-glycerol 3-phosphate shuttle (Figure 11). Cytosolic dihydroxyacetone phosphate is reduced by NADFl to s.n-glycerol 3-phosphate, catalyzed by s,n-glycerol 3-phosphate dehydrogenase, and this is then oxidized by s,n-glycerol 3-phosphate ubiquinone oxidoreductase to dihydroxyacetone phosphate, which is a flavoprotein on the outer surface of the inner membrane. By this route electrons enter the respiratory chain.from cytosolic NADH at the level of complex III. Less well defined is the possibility that cytosolic NADH is oxidized by cytochrome bs reductase in the outer mitochondrial membrane and that electrons are transferred via cytochrome b5 in the endoplasmic reticulum to the respiratory chain at the level of cytochrome c (Fischer et al., 1985). 

Of particular interest from the physiological point of view is the fact that the Km value for glucose, as defined by this kinetic treatment [see Eq. (5b)] [which equals Ki for glucose in Eqs. (8a) and (9a) since k., = k, and fc i = fc8], contains a water concentration term in the numerator. Conceivably, in the environment of the enzyme within the phospholipid-rich membrane of the endoplasmic reticulum, water concentrations may be much less than 55.5 M, and the Km value for glucose under such conditions would be appreciably lower (10). 

In addition to their plasma membrane eukaryotic cells also contain internal membranes that define a variety of organelles (fig. 17.2). Each of these organelles is specialized for particular functions The nucleus synthesizes nucleic acids, mitochondria oxidize carbohydrates and lipids and make ATP, chloroplasts carry out photosynthesis, the endoplasmic reticulum and the Golgi apparatus synthesize and secrete proteins, and lysosomes digest proteins. Additional membranes divide mitochondria and chloroplasts into even finer, more specialized subcompartments. Like the plasma membrane, organellar membranes act as barriers to the leakage of proteins, metabolites, and ions they contain transport systems for import and export of materials, and they are the sites of enzymatic activities as diverse as cholesterol biosynthesis and oxidative phosphorylation. 

SOCs, also known as ICRAC (calcium-release activated channels), have been observed in a wide range of cell types (Parekh and Penner, 1997). The defining property is that depletion of intracellular calcium stores results in increased calcium influx at the plasma membrane. The actual SOC that carries this calcium influx may vary between cells, and cloning studies have identified transient receptor potential channel (TRPC) (Parekh and Penner, 1997, Vandebrouck et al., 2002b) and CRACM1 (Peinelt et al., 2006) as candidate genes. Also, the exact mechanism by which SOCs are activated by store depletion has only been partly elucidated, with a role suggested for a calcium sensor on the endoplasmic reticulum (see Peinelt et al., 2006) and for IP3 (Kiselyov et al., 1998). 

Cell swelling first manifests as dilation of the endoplasmic reticulum (ER). Detachment of ribosomes from the rough ER and dissociation of polysomes into monosomes occurs next because of diminished ATP generation, causing reduced protein synthesis. If hypoxia persists, further membrane dysfunction, manifested by more severe increase in permeability, occurs. Cell surface blebs and loss of microvilli in cells so endowed are ultrastructural correlates of more severe membrane damage (Figure 16.4A,B). The point of irreversibility has not yet been reached if oxygen is restored. Indeed, it is very difficult to define precisely when the cell is irreversibly injured. 

The acquisition of a lipid bilayer from the infected host cell is the defining feature of enveloped viruses. However, the origin and composition of the bilayer can differ from virus to virus. Viruses are known to acquire a membrane, or bud, from various cellular compartments that include the nucleus, the endoplasmic reticulum (ER), the Golgi, and the plasma membrane. As the Upid contents of those membranes differ, so do the contents of the viral membranes. In some, if not all, cases the composition of the lipid bUayer is an important aspect of the viral assembly pathway. 

Another area that requires additional understanding is the role of cytoplasmic organelles in the fate of platinum drugs. Platinum has been shown to be localized within the Golgi apparatus, endoplasmic reticulum, mitochondria, and lysosomes, the cytosol, and the nucleus. However, only the consequences of nuclear localization have been defined satisfactorily (19-21). 

An extensive array of internal membranes in eukaryotes creates compartments within a cell for distinct biochemical functions. For instance, a double membrane surrounds the nucleus, the location of most of the cell s genetic material, and the mitochondria, the location of most ATP synthesis. A single membrane defines the other internal compartments, such as the endoplasmic reticulum. Some compartments can exchange material by the process of membrane budding and fusion. As with all membranes, the proteins associated with these membranes determine the specific biochemical function. Specific amino acid sequences in the proteins direct these molecules to the appropriate compartment. 

Calcification in eucaryotic organisms is frequently related to the Golgi apparatus (see review by Barley, 1974 and Degens, 1976). The Golgi and/or dictyosomes are defined areas of the cytoplasm and endoplasmic reticulum... 

HMG-CoA reductase is an integral protein of the endoplasmic reticulum and the primary site of regulation of synthesis of cholesterol and nonsterol isoprenoid derivatives. Its activity has a well-defined diurnal rhythm in rats and mice, coinciding with that of the enzyme s synthesis and of the mRNA concentration. Activity is highest at about the middle of the dark period and lowest at about the middle of the light period. Its mechanism may be related to food consumption. Rats are nocturnal animals and consume food in the dark the increased bile production and excretion depletes liver cholesterol and may stimulate the increased synthesis of HMG-CoA reductase as a compensatory mechanism. 

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