Cystic fibrosis transmembrane regulator (CFTR), the gene product that is mutated in cystic fibrosis (CF) patients, has a well-recognized function as a cyclic adenosine 3',5'-monophosphate (cAMP)-regulated chloride channel, but this property does not account for the abnormally high basal rate and cAMP sensitivity of sodium ion absorption in CF airway epithelia. Expression of complementary DNAs for rat epithelial Na+ channel (rENaC) alone in Madin Darby canine kidney (MDCK) epithelial cells generated large amiloride-sensitive sodium currents that were stimulated by cAMP, whereas coexpression of human CFTR with rENaC generated smaller basal sodium currents that were inhibited by cAMP. Parallel studies that measured regulation of sodium permeability in fibroblasts showed similar results. In CF airway epithelia, the absence of this second function of CFTR as a cAMP-dependent regulator likely accounts for abnormal sodium transport.

Equine infectious anemia virus (EIAV) is a lentivirus in the genes into cultured human cells. In addition, stable helper retrovirus family of viruses. Replication-defective EIAV veccell lines were created by modifying human 293 cells to tors have been constructed that encode bacterial puromyexpress EIAV proteins. Unlike retroviral vectors based on cin-N-acetyl transferase and E. coli ␤-galactosidase. These murine leukemia virus, EIAV lentiviral vectors transduce vectors could be prepared with titers greater than 10 5 infecnondividing (aphidicolin-arrested) cells. These properties tious units/ml and were able to act as vehicles to carry make EIAV vectors promising gene transfer vehicles.

One of the most challenging issues of anti-inflammatory lines. In conditionally immortalized human endometrial gene therapy is the complexity of inflammatory pathways.stromal cells, overexpression of IB␣ prevented both Transcription factor NF-B plays a pivotal role in activation interleukin-1 (IL-1)-inducible degradation of endogenous of multiple inflammatory molecules, and therefore rep-IB␣ protein and activation of NF-B. Accordingly, inducresents the logical target for intervention. We evaluated the tion of cytokines interleukin-8 (IL-8) and Gro␥ was markfeasibility of suppressing the inflammatory responses in difedly suppressed. In monocytic THP-1 cells, both lipopolyferent cell lines through specific inhibition of NF-B by gene saccharide (

No abstract