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Titolo:
THE MELANOCORTIN-1, MELANOCORTIN-3, MELANOCORTIN-4 OR MELANOCORTIN-5 RECEPTORS DO NOT HAVE A BINDING EPITOPE FOR ACTH BEYOND THE SEQUENCE OF ALPHA-MSH
Autore:
SCHIOTH HB; MUCENIECE R; LARSSON M; WIKBERG JES;
Indirizzi:
UNIV UPPSALA,DEPT PHARMACEUT PHARMACOL,CTR BIOMED,BOX 591 S-75124 UPPSALA SWEDEN INST ORGAN SYNTH,PHARMACOL LAB RIGA LATVIA
Titolo Testata:
Journal of Endocrinology
fascicolo: 1, volume: 155, anno: 1997,
pagine: 73 - 78
SICI:
0022-0795(1997)155:1<73:TMMMOM>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
MOLECULAR-CLONING; RADIOLIGAND BINDING; PERIPHERAL-TISSUES; FACTOR RELEASE; EXPRESSION; LOCALIZATION; PEPTIDES; HYPOTHALAMUS; SUBTYPES; SYSTEM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
28
Recensione:
Indirizzi per estratti:
Citazione:
H.B. Schioth et al., "THE MELANOCORTIN-1, MELANOCORTIN-3, MELANOCORTIN-4 OR MELANOCORTIN-5 RECEPTORS DO NOT HAVE A BINDING EPITOPE FOR ACTH BEYOND THE SEQUENCE OF ALPHA-MSH", Journal of Endocrinology, 155(1), 1997, pp. 73-78

Abstract

ACTH(1-39), and several shorter N- and/or C-terminally truncated fragments of ACTH, with and without N-terminal acetylation and/or C-terminal amidation, were tested for binding on a single eukaryotic cell linetransiently and independently expressing the melanocortin MC1, MC3, MC4 and MC5 receptors. The results show that none of these MC receptorshas specific binding epitopes for the ACTH peptides beyond the amino acid sequence of a-MSH, when tested for their ability to compete with I-125-labelled [Nle(4),D-Phe(7)]alpha-MSH and ACTH. The MC3 receptor favours the natural desacetylated N-terminal end of the ACTH peptides, and it has generally more than 10-fold higher affinity for the ACTH peptides than the MC4 receptor. Considering earlier anatomical localisation data, together with the present data, we suggest that the MC3 receptor is the most likely candidate of the MC receptors to mediate the short-loop negative feedback release of corticotrophin-releasing factor(CRF) caused by ACTH/MSH peptides.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 10:25:24