Membrane-unstable receptor

Fig. 8. Schematic representation of aberrant mFas, which is expected to attenuate the Fas-mediated signaling. Aberrant mFas is functionally and structurally classified into main three types (a) the membrane-binding decoy receptor, (b) the membrane-binding decorative receptor, and (c) the membrane-unstable or soluble receptor. Although both mFas in models (a) and (b) are normally fixed on the membrane, the mFas in the former can bind Fas ligand, but is defective for trimerization, whereas the mFas in the latter would have no ability to bind Fas ligand in vivo because of conformational alteration. Like model (a), the mFas in model (c) can be reactive for Fas ligand, but it cannot transduce the apoptotic signal into the cytoplasmic death cascade because of incomplete trimerization due to an abnormal TM domain or truncation of the 1C domain. The hatched and jagged markings indicate deduced alterations of amino acid sequence or three-dimensional structure, respectively.

All of the effects of the catecholamines bound to (3 adrenergic receptors and of glucagon, ACTH, and many other hormones appear to be mediated by adenylate cyclase. This integral membrane protein catalyzes the formation of cAMP from ATP (Eq. 11-8, step a). The reaction, whose mechanism is considered in Chapter 12, also produces inorganic pyrophosphate. The released cAMP acts as the second messenger and diffuses rapidly throughout the cell to activate the cAMP-dependent protein kinases and thereby to stimulate phosphorylation of a selected group of proteins (Fig. 11-4). Subsequent relaxation to a low level of cytosolic cAMP is accomplished by hydrolysis of the cAMP by a phosphodiesterase (Eq. 11-8, step fr).166/167 jn thg absence of phosphodiesterase cAMP is extremely stable kinetically. However, it is thermodynamically unstable with respect to hydrolysis. 

TherouxP, KouzS, Roy L, etal. Platdet membrane receptor glycoprotein Ilh/IIIa antagcuiism in unstable... 

Figure 1. Arachidonic acid is cleaved from membrane phospholipids by the action of phospholipase kj The liberated arachidonic acid is then acted upon by prostaglandin G/H synthase to produce the unstable intermediate PGH2. PGH2 is converted to the multiple prostanoids shown by tissue specific isomerases. The resulting prostanoids then activate cell-membrane receptor which couple G proteins leading to the terminal effect designated in each of the boxes (with permission from [8]).

On cleavage of C4 by Cls, C4b acquires two binding sites, a labile site which allows the C4b to attach itself to cell membranes and a stable site which enables cell-bound C4 to react with a C4b receptor on human erythrocytic and lymphocytic cells, producing immune adherence (Cooper, 1969 Bokisch and Sobel, 1974). The labile binding site is thermodynamically unstable and quickly loses its binding ability. Conse-... 

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