Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2 Pt 2
pubmed:dateCreated
1994-4-26
pubmed:abstractText
Treatment with trypsin of the cytoplasmic surface of excised inside-out membrane patches from guinea pig ventricular myocytes altered multiple regulatory properties of ATP-sensitive K+ (KATP) channels including their sensitivity to intracellular ATP (ATPi), intracellular ADP (ADPi), glibenclamide, and cromakalim. The single-channel conductance, reversal potential, and inward rectification (in the presence of intracellular Mg2+) were unaltered after trypsin treatment. KATP channels also remained sensitive to intracellular Ca(2+)-induced rundown after trypsin treatment (n = 6). The effects of trypsin were not prevented by including either 15 mM ATPi (n = 7), 1 mM ADPi (n = 4), or 10 microM glibenclamide (n = 4) during exposure to trypsin, suggesting that occupancy of these binding sites did not prevent access of trypsin to the proteolytic sites responsible for its effects. Treatment of excised membrane patches with 1 mM phenylglyoxal (n = 4) or 5 mM glyoxal (n = 4), which cleave polypeptides at arginine residues, did not increase the dissociation constant for suppression of KATP channels by ATPi. Because trypsin cleaves peptides at both arginine and lysine residues, these results suggest that modification of the regulatory properties of KATP channels by trypsin may result from proteolytic digestion of lysine residues located in cytosolic regions of the channel protein.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
266
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H613-22
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Effects of trypsin on cardiac ATP-sensitive K+ channels.
pubmed:affiliation
Department of Anesthesiology, MacDonald Research Laboratories 3-579, University of California, Los Angeles, School of Medicine 90024.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't