N‐terminally extended somatostatin: The primary structure of somatostatin‐28

Pradayrol, Lucien; Jörnvall, Hans; Mutt, Viktor; Ribet, A

doi:10.1016/0014-5793(80)81310-x

Cited by 509 publications

(184 citation statements)

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“…SS1 has subsequently been demonstrated to exist in two forms, SS-14, composed of 14 amino acids (Brazeau et al 1973), and SS-28, its N-terminally extended form, composed of 28 residues, first characterized in porcine gut (Esch et al 1980, Pradayrol et al 1980. Both peptides are generated from the same precursor molecule (called prepro-SS1 or PSS1) through post-translational processing at two cleavage sites, a dibasic Arg-Lys site and a monobasic Arg site respectively (Patel & Galanopoulou 1995).…”

Section: Ss1mentioning

confidence: 99%

MOLECULAR EVOLUTION OF GPCRS: Somatostatin/urotensin II receptors

Tostivint¹,

Daza²,

Bergqvist³

et al. 2014

Journal of Molecular Endocrinology

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Somatostatin (SS) and urotensin II (UII) are members of two families of structurally related neuropeptides present in all vertebrates. They exert a large array of biological activities that are mediated by two families of G-protein-coupled receptors called SSTR and UTS2R respectively. It is proposed that the two families of peptides as well as those of their receptors probably derive from a single ancestral ligand-receptor pair. This pair had already been duplicated before the emergence of vertebrates to generate one SS peptide with two receptors and one UII peptide with one receptor. Thereafter, each family expanded in the three whole-genome duplications (1R, 2R, and 3R) that occurred during the evolution of vertebrates, whereupon some local duplications and gene losses occurred. Following the 2R event, the vertebrate ancestor is deduced to have possessed three SS (SS1, SS2, and SS5) and six SSTR (SSTR1-6) genes, on the one hand, and four UII (UII, URP, URP1, and URP2) and five UTS2R (UTS2R1-5) genes, on the other hand. In the teleost lineage, all these have been preserved with the exception of SSTR4. Moreover, several additional genes have been gained through the 3R event, such as SS4 and a second copy of the UII, SSTR2, SSTR3, and SSTR5 genes, and through local duplications, such as SS3. In mammals, all the genes of the SSTR family have been preserved, with the exception of SSTR6. In contrast, for the other families, extensive gene losses occurred, as only the SS1, SS2, UII, and URP genes and one UTS2R gene are still present.

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Section: Ss1mentioning

confidence: 99%

MOLECULAR EVOLUTION OF GPCRS: Somatostatin/urotensin II receptors

Tostivint¹,

Daza²,

Bergqvist³

et al. 2014

Journal of Molecular Endocrinology

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“…SS1 is synthesized as part of a larger precursor molecule, named prepro-SS1 (PSS1), which is also able to generate, notably in mammals, an N-terminally-extended form of 28 residues, called somatostatin-28 (SS-28; Fig. 1; Esch et al 1980;Pradayrol et al, 1980). The two peptides SS1 and SS-28 are synthesized in variable amounts by distinct PSS1-producing cells as a result of differential precursor processing.…”

Section: Somatostatinmentioning

confidence: 99%

New insight into the molecular evolution of the somatostatin family

Tostivint

Lihrmann

Vaudry

2008

Molecular and Cellular Endocrinology

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Please cite this article as: Tostivint, H., Lihrmann, I., Vaudry, H., New insight into the molecular evolution of the somatostatin family, Molecular and Cellular Endocrinology (2007), doi:10.1016/j.mce.2008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 2 AbstractThe present review describes the molecular evolution of the somatostatin family and its relationships with that of the urotensin II family. Most of the somatostatin sequences collected from different vertebrate species can be grouped as the products of at least four loci. The somatostatin 1 (SS1) gene is present in all vertebrate classes from agnathans to mammals. The SS1 gene has given rise to the somatostatin 2 (SS2) gene by a segment/chromosome duplication that is probably the result of a tetraploidization event according to the 2R hypothesis. The somatostatin-related peptide cortistatin, first identified in rodents and human, is the counterpart of SS2 in placental mammals. In fish, the existence of two additional somatostatin genes has been reported. The first gene, which encodes a peptide usually named somatostatin II (SSII), exists in almost all teleost species investigated so far and is thought to have arisen through local duplication of the SS1 gene. The second gene, which has been characterized in only a few teleost species, encodes a peptide also named SSII that exhibits a totally atypical structure. The origin of this gene is currently unknown. Nevertheless, because the two latter genes are clearly paralogous genes, we propose to rename them SS3 and SS4, respectively, in order to clarify the current confusing nomenclature. The urotensin II family consists of two genes, namely the urotensin II (UII) gene and the UII-related peptide (URP) gene. Both UII and URP exhibit limited structural identity to somatostatin so that UII was originally described as a "somatostatin-like peptide". Recent comparative genomics studies have revealed that the SS1 and URP genes, on the one hand, and the SS2 and UII genes, on the other hand, are closely linked on the same chromosomes, thus confirming that the SS1/SS2 and the UII/URP genes belong to the same superfamily. According to these data, it appears that an ancestral somatostatin/urotensin II gene gave rise by local duplication to a somatostatin ancestor and a urotensin II ancestor, whereupon this pair was duplicated (presumably by a segment/chromosome duplication) to give rise to the SS1-UII pair and the SS2-URP pair.

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“…There are two major circulating SST-isoforms, which consist of 14 and 28 amino acids, respectively, which are processed from a common precursor protein in a cell-and tissue-specific pattern (Brazeau et al, 1973;Burgus et al, 1973;Pradayrol et al, 1980). In the adult, the primary secretory product of pancreatic D-cells is SST-14 (Noe 1981;Patel et al, 1981), which contributes to less than 5% of circulating SST (Taborsky, Jr. and Ensinck 1984).…”

mentioning

confidence: 99%