Expression of Factor

Different mutations in the disease-causing locus may cause more or less severe expression. For example, mis-sense mutations in the factor VIII gene tend to produce less severe hemophQia than do nonsense mutations, which result in a truncated protein product and little, if any, expression of factor VIII. The presence of different mutations, or alleles, in the same locus is termed allelic heterc eneity. 

Fig. 9.5 Molecular cloning and expression of Factor C in the baculo viral system and expression in insect cells produced an rFC with remarkable sensitivity of 0.001 EU/mL endotoxin. (B BamHl, E EcoRI, X Xhol, H Hindlll, P PstI, N Ncol)...

Kay MA, Manno CS, Ragni MV et al. (2000) Evidence for gene transfer and expression of factor IX in haemophilia... 

Kay MA, Manno CS, Ragni MV et al. (2000) Evidence for gene transfer and expression of factor IX in haemophilia B patients with an AAV vector. Nature Genetics 24 257-261 Kung J, Hagstrom J, Cass D et al. (1998) Human FIX corrects bleeding diathesis of mice with hemophilia B. Blood 91 784-790... 

In vitro and animal studies clearly point to a central role of several distinct but interconnected redox-sensitive pathways in the pathogenesis of inflammation [47]. It has been hypothesized that oxidative stress occurs as a result of the depletion of the cellular content of reduced glutathione. A sublethal oxidative stress can activate redox-sensitive kinase cascades and transcription factors, NF-kB and AP-1, with resulting increases in the expression of factors associated with an inflammatory response and cellular proliferation. Evidence has been collected suggesting that oxidative stress and the ensuing modification of the cellular redox status may be associated with the induction of cell death either via stimulation of apoptosis and/or necrosis. It is well known that cell death is a common feature of the inflammatory process [48]. 

S-100 protein, CD56, or CD57. GCT also shares with neurofibroma (but not neurilemmoma) the expression of factor Xnia, and it is also potentially reactive for protein gene product 9.5, calretinin, and inhibin (Fig. 

Altman DA, Nickoloff BJ, Fivenson DP. Differential expression of factor Xllla and CD34 in cutaneous mesenchymal tumors. J Cutan Pathol. 1993 20 154-158. 

Offspring null for both Cdxl and RARy exhibit a significant increase in the penetrance of certain vertebral transformations relative to either single mutant. This clearly demonstrates that RARy must regulate the expression of factors involved in vertebral patterning in addition to Cdxl. Further evidence to this effect is provided by the finding that Cdxl null mutants remain sensitive to certain of the effects of exogenous RA on the vertebral axis (Allan et al., 2001). 

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