Cystic fibrosis gene expression is not correlated with rectifying Cl sup minus channels

Journal Article · Sat Jun 15 04:00:00 EDT 1991 · Proceedings of the National Academy of Sciences of the United States of America; (United States)

DOI:https://doi.org/10.1073/pnas.88.12.5277· OSTI ID:6101184

Ward, C L; Krouse, M E; Kopito, R R; Wine, J J ^[1]; Gruenert, D C ^[2]

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1. Stanford Univ., CA (United States)
2. Univ. of California, San Francisco (United States)

Cystic fibrosis (CF) involves a profound reduction of Cl{sup {minus}} permeability in several exocrine tissues. A distinctive, outwardly rectifying, depolarization-induced Cl{sup {minus}} channel (ORDIC channel) has been proposed to account for the Cl{sup {minus}} conductance that is defective in CF. The recently identified CF gene is predicted to code for a 1480-amino acid integral membrane protein termed the CF transmembrane conductance regulator (CFTR). The CFTR shares sequence similarity with a superfamily of ATP-binding membrane transport proteins such as P-glycoprotein and STE6, but it also has features consistent with an ion channel function. It has been proposed that the CFTR might be an ORDIC channel. To determine if CFTR and ORDIC channel expression are correlated, the authors surveyed various cell lines for natural variation in CFTR and ORDIC channel expression. In four human epithelial cell lines (T84, CaCo2, PANC-1, and 9HTEo-/S) that encompass the full observed range of CFTR mRNA levels and ORDIC channel density the authors found no correlation.

• OSTI ID: 6101184
• Journal Information: Proceedings of the National Academy of Sciences of the United States of America; (United States), Journal Name: Proceedings of the National Academy of Sciences of the United States of America; (United States) Vol. 88:12; ISSN 0027-8424; ISSN PNASA
• Country of Publication: United States
• Language: English

Related Subjects

550200* -- Biochemistry
59 BASIC BIOLOGICAL SCIENCES
ANIMAL TISSUES
ANIMALS
BODY
CHLORIDES
CHLORINE COMPOUNDS
DISEASES
DNA POLYMERASES
ENZYMES
EPITHELIUM
ETIOLOGY
FIBROSIS
GENE REGULATION
HALIDES
HALOGEN COMPOUNDS
HEREDITARY DISEASES
MAMMALS
MAN
MEMBRANE TRANSPORT
MESSENGER-RNA
NUCLEIC ACIDS
NUCLEOTIDYLTRANSFERASES
ORGANIC COMPOUNDS
PATHOLOGICAL CHANGES
PERMEABILITY
PHOSPHORUS-GROUP TRANSFERASES
POLYMERASES
PRIMATES
PROTEINS
RNA
TISSUES
TRANSFERASES
VERTEBRATES