Linked Life Data

2018515

Source:http://linkedlifedata.com/resource/pubmed/id/2018515

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1991-5-20
pubmed:abstractText
kappa-Bungarotoxin is a high affinity antagonist of neuronal nicotinic acetylcholine receptors of the alpha 3 subtype. Three sequence segments of the alpha 3 subunit that contribute to forming the binding site for kappa-bungarotoxin were previously located using synthetic peptides corresponding to the complete alpha 3 subunit, i.e., alpha 3(1-18), alpha 3(50-71) and alpha 3(180-201). Here we use single residue substituted peptide analogs of the alpha 3(50-71) sequence, in which amino acids are sequentially replaced by Gly, to determine which residues are important for kappa-bungarotoxin binding activity. Although no single substitution obliterated kappa-bungarotoxin binding, several amino acid substitutions lowered the affinity for kappa-bungarotoxin--i.e., two negatively charged residues (Glu51 and Asp62), and several aliphatic and aromatic residues (Leu54, Leu56, and Tyr63). These results indicate that the interface of the alpha 3 subunit with kappa-bungarotoxin involves primarily hydrophobic interactions, and a few negatively charged residues.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
176
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
11-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Amino acid residues forming the interface of a neuronal nicotinic acetylcholine receptor with kappa-bungarotoxin: a study using single residue substituted peptide analogs.
pubmed:affiliation
Department of Biochemistry, College of Biological Sciences, University of Minnesota, St. Paul 55108.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.