Cafferata EG, Gonzalez Guerrico AM, Giordano L, Pivetta OH  Biochim Biophys Acta   2000 00, 1500: 2, 241-8

Abstract: Cystic fibrosis is an autosomal recessive genetic disease, produced by a mutation in the CFTR gene that impairs its function as a chloride channel. In this work, we have examined the effects of interleukin-1beta (IL-1beta) on th e expression of CFTR in human colonic T84 cells. Treatment of T84 cells with IL-1beta (0.25 ng/ml) for 4 h resulted in an increased CFTR expression (mRNA and protein). However, higher doses of IL-1beta (1 ng/ml and over) produced inhibition of CFTR mRNA and protein expression. The protein kinase C (PKC) inhibitors H7 (50 microM) and GF109203X (1 microM) inhibited the stimulatory effect of IL-1beta. Similar effects were seen in the presence of the protein tyrosine kinase (PTK) inhibitors genistein (60 microM) and herbymicin A (2 microM). These results suggest that some PKC isoform(s) and at least a PTK might be involved in the CFTR up-regulation induced by IL-1beta. The repression of CFTR up-regulation by cycloheximide (35.5 microM) suggests the participation of a de novo synthesized protein. Results obtained by using the RNA polymerase II inhibitor DRB (78 microM), suggest that the increased mRNA levels seen after IL-1beta treatment are not due to an increased stability of the message. We conclude that the CFTR mRNA and protein levels are modulated by IL-1beta, this cytokine being the first extracellular protein known to up-regulate CFTR gene expression.

Please Note

NOTICE!!! Please expect a 4-6 week delivery time.
We are sorry but we can offer no international Paypal orders. These must be made by Fax. Any inadvertent international Paypal orders placed will be refunded less $20 transaction fee.

P.O. Box 1357
Sparta, NC 28675
Phone: 336-793-6524
Fax: 336-372-1541

Shipping Charges

Shipping charges have increased by an incredible amount, and so shipping is order dependent. Please contact for more details.