Linked Life Data

8496800

Source:http://linkedlifedata.com/resource/pubmed/id/8496800

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1993-6-22
pubmed:abstractText
DRK1 is a cloned K+ channel from rat brain with consensus sites for protein kinase-dependent phosphorylation that might be expected to be functionally regulated by phosphorylation. 2,3-Butane-dione-monoxime (BDM) chemically removes phosphate groups from many proteins, and its action on DRK1 channels was examined after expression of DRK1 cRNA in Xenopus oocytes. In two-microelectrode voltage-clamp experiments, the application of BDM to the bath inhibited DRK1 current (ki = 16.6 mM, H = 0.96) rapidly and reversibly, with a time course similar to the time course of solution change within the bath. DRK1 current was inhibited at all potentials; the time course of current activation, deactivation and inactivation were unaffected by BDM. In inside-out patch-clamp experiments, the application of BDM to the cytoplasmic surface similarly inhibited channel activity rapidly and reversibly (ki = 10.7 mM, H = 1.01) in the absence of rephosphorylating substrates. These results are inconsistent with a phosphatase effect, because such an effect should be irreversible in cell-free, ATP-free patches. Instead, the results suggest that BDM can inhibit DRK1 channels directly from inside or outside of the membrane.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
265
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1011-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
2,3-Butanedione monoxime (BDM) inhibition of delayed rectifier DRK1 (Kv2.1) potassium channels expressed in Xenopus oocytes.
pubmed:affiliation
Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.