D-locus

Frydman,M.,Bonne-Tamir,B.,Farrer,L. A. etal.Assignment of the gene for Wilson disease to chromosome 13 Linkage to the esterase d locus. Proc. Natl Acad. Sci. USA 82 1819-1821,1985. 

The metabolic defect in Wilson s disease is located in the liver on chromosome 13 close to the esterase-D locus (ATP 7B). (325,346,359) Apparently, this is a genetically determined disturbance of hepatobiliary copper discharge due to a defect in lysosomal copper-transporting ATPase, which is localized in the trans-Golgi network. As a result, apoceruloplasmin cannot be loaded with copper, and is therefore degraded. The reduced secretion of ceruloplasmin explains the low... 

The el5 marker was identified in the sera of all 35 cottontails tested and in 20 of 26 hares. The dll, dl2, and el4 markers could not be detected in any of these sera (116). Mandy and Rodkey suggest that the gene was present in the common ancestor of modern lagomorphs and that and the d locus genes arose subsequently in Oryctolagus as a result of mutations. 

Two AT-II receptors, AT and AT2 are known and show wide distribution (27). The AT receptor has been cloned and predominates ia regions iavolved ia the regulation of blood pressure and water and sodium retention, eg, the aorta, Hver, adrenal cortex, and ia the CNS ia the paraventricular nucleus, area postrema, and nucleus of the soHtary tract. AT2 receptors are found primarily ia the adrenal medulla, utems, and ia the brain ia the locus coeruleus and the medial geniculate nucleus. AT receptors are GCPRs inhibiting adenylate cyclase activity and stimulating phosphoHpases C, A2, and D. AT2 receptors use phosphotyrosiae phosphatase as a transduction system. 

It is the a2A/D-adrenoceptor that predominates in the locus coeruleus and this subtype seems to be responsible for reducing neuronal excitability and transmitter release. Strangely, immunocytochemical studies suggest that most a2c-receptors are intracellular. The explanation for this finding and its functional implications are as yet unknown but it could reflect differences in intracellular trafficking of different receptor subtypes. 

Chabot, B., Stephenson, D. A., Chapman, V. M., Besmer, P., and Bernstein, A. (1988). The proto-oncogene c-kit encoding a transmembrane tyrosine kinase receptor maps to the mouse W locus. Nature 335 88-89. 

Geissler, E. N., Ryan, M. A., and Housman, D. E. (1988). The dominant-white spotting (W) locus of the mouse encodes the c-kit proto-oncogene. Cell 55 185-192. 

Orr-Urtreger, A., Avivi, A., Zimmer, Y Givol, D Yarde, Y., and Lonai, P. (1990). Developmental expression of c-kit, a proto-oncogene encoded by the W locus. Development 109 911-923. 

Li, S., Crenshaw, E. B., Rawson, E. J., Simmons, D. M., Swanson, L. W and Rosenfeld, M. G. (1990). Dwarf locus mutants lacking three pituitary cell types result from mutations in the POU-domain gene pit-1. Nature 347 528-533. 

Robbins, L. S., Nadeau, J. H., Johnson, K. R., Kelly, M. A., Roselli-Rehfuss, L., Baack, E Mountjoy, K. G and Cone, R. D. (1993). Pigmentation phenotypes of variant extension locus alleles result from point mutations that alter MSH receptor function. Cell 72 827-834. 

Note that with this very specific case by choosing x = 1, the open-loop zero introduced by the PI controller cancels one of the open-loop poles of the process function at -1. If we do a root locus plot later, we d see how the root loci change to that of a purely second order system. With respect to this example, the value is not important as long as x > 1/2. 

Do the root locus plots in Example 10-l(d). Confirm the stability analysis in Example 10-... 

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