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http://purl.uniprot.org/citations/17501853http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17501853http://www.w3.org/2000/01/rdf-schema#comment"

Background

The 5-HT(1B/1D) receptor agonist sumatriptan is highly effective in the treatment of migraine. However, some patients do not respond to sumatriptan or experience recurrence of the headache after initial relief. In addition, some patients report chest symptoms after the use of sumatriptan.

Objective

To assess whether 2 genetic variants (F124C changing a phenylalanine for a cysteine and polymorphism A/T at nucleotide position -161 in the 5' regulatory region) of the 5-HT(1B) receptor play a major role in the therapeutic response to sumatriptan. The 5-HT(1B) receptor most likely mediates the therapeutic action and coronary side effects of sumatriptan, and both F124C and A-161T have relevant functional consequences on either the affinity of sumatriptan to bind to the 5-HT(1B) receptor or on receptor expression level itself, respectively.

Method

Genomic DNA of a relatively small but very well-characterized set of migraine patients with consistently good response to sumatriptan (n = 14), with no response (n = 12), with recurrence of the headache (n = 12), with chest symptoms (n = 13), and patients without chest symptoms (n = 27) was available for the genetic analyses and screened for the F124C variant and the A-161T polymorphism in the human 5-HT(1B) receptor gene.

Results

F124C was not detected in any of the patients studied. In addition, we did not observe drastic changes in allele frequencies of the A-161T polymorphism that might hint to a causal relation with the therapeutic effect of sumatriptan.

Conclusion

We have not obtained any evidence that variants F124C and A-161T of the 5-HT(1B) receptor are major determinants in the clinical response to sumatriptan."xsd:string
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http://purl.uniprot.org/citations/17501853http://purl.uniprot.org/core/author"Frants R.R."xsd:string
http://purl.uniprot.org/citations/17501853http://purl.uniprot.org/core/author"Mehrotra S."xsd:string
http://purl.uniprot.org/citations/17501853http://purl.uniprot.org/core/author"Ferrari M.D."xsd:string
http://purl.uniprot.org/citations/17501853http://purl.uniprot.org/core/author"van den Maagdenberg A.M."xsd:string
http://purl.uniprot.org/citations/17501853http://purl.uniprot.org/core/author"Vanmolkot K.R."xsd:string
http://purl.uniprot.org/citations/17501853http://purl.uniprot.org/core/author"MaassenVanDenBrink A."xsd:string
http://purl.uniprot.org/citations/17501853http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17501853http://purl.uniprot.org/core/name"Headache"xsd:string
http://purl.uniprot.org/citations/17501853http://purl.uniprot.org/core/pages"711-716"xsd:string
http://purl.uniprot.org/citations/17501853http://purl.uniprot.org/core/title"The phe-124-Cys and A-161T variants of the human 5-HT1B receptor gene are not major determinants of the clinical response to sumatriptan."xsd:string
http://purl.uniprot.org/citations/17501853http://purl.uniprot.org/core/volume"47"xsd:string
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