Purification, amino acid composition and N-terminus of the hypothalamic luteinizing hormone releasing factor (LRF) of ovine origin

Amoss, Max S.; Burgus, Roger; Blackwell, Richard E.; Vale, W.; Fellows, Robert E.; Guillemin, Roger

doi:10.1016/s0006-291x(71)80179-1

Cited by 374 publications

(121 citation statements)

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“…As GnRH ligands, we used GnRH-I and II and Cetrorelix (synthetic type I GnRH receptor antagonist) (Reissmann et al ., 2000). Humans GnRHs consist of GnRH-I and II (Matsuo et al ., 1971;Amoss et al ., 1971;Miyamoto et al ., 1984). The results revealed that the stimulatory and inhibitory effects exhibited distinct patterns (Fig.…”

Section: Effects Of Gnrh On Colony-formation 1-stimulatory and Inhibimentioning

confidence: 99%

“…GnRH was originally identified as a hypothalamic decapeptide which promotes gonadotropin secretion from pituitary gonadotropes and was named gonadotropin-releasing hormone (Matsuo et al ., 1971;Amoss et al ., 1971). Thereafter, multiple GnRH isoforms and multiple types of GnRH receptors were reported in a wide range of organisms in addition to vertebrates and broad distribution of them in extrapituitary tissues and organs has been demonstrated (Klausen et al ., 2002;Millar, 2003;Ikemoto et al ., 2003Ikemoto et al ., , 2004.…”

Section: Introductionmentioning

confidence: 99%

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Human Type II GnRH Receptor Mediates Effects of GnRH on Cell Proliferation

et al. 2004

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Section: Effects Of Gnrh On Colony-formation 1-stimulatory and Inhibimentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Human Type II GnRH Receptor Mediates Effects of GnRH on Cell Proliferation

et al. 2004

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“…Subsequent studies led to the hypothesis that the pituitary is controlled by a hypothalamic factor (3)(4)(5)(6). It was not until 1971, however, that the amino acid sequence of GnRH was determined after extraction from the hypothalami of thousands of pigs and sheep by the groups of Schally and Guillemin (7,8).…”

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confidence: 99%

GNRH1 mutations in patients with idiopathic hypogonadotropic hypogonadism

Chan

Guillebon

Lang‐Muritano

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

177

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Idiopathic hypogonadotropic hypogonadism (IHH) is a condition characterized by failure to undergo puberty in the setting of low sex steroids and low gonadotropins. IHH is due to abnormal secretion or action of the master reproductive hormone gonadotropin-releasing hormone (GnRH). Several genes have been found to be mutated in patients with IHH, yet to date no mutations have been identified in the most obvious candidate gene, GNRH1 itself, which encodes the preprohormone that is ultimately processed to produce GnRH. We screened DNA from 310 patients with normosmic IHH (nIHH) and 192 healthy control subjects for sequence changes in GNRH1. In 1 patient with severe congenital nIHH (with micropenis, bilateral cryptorchidism, and absent puberty), a homozygous frameshift mutation that is predicted to disrupt the 3 C-terminal amino acids of the GnRH decapeptide and to produce a premature stop codon was identified. Heterozygous variants not seen in controls were identified in 4 patients with nIHH: 1 nonsynonymous missense mutation in the eighth amino acid of the GnRH decapeptide, 1 nonsense mutation that causes premature termination within the GnRH-associated peptide (GAP), which lies C-terminal to the GnRH decapeptide within the GnRH precursor, and 2 sequence variants that cause nonsynonymous amino-acid substitutions in the signal peptide and in GnRH-associated peptide. Our results establish mutations in GNRH1 as a genetic cause of nIHH.GnRH ͉ luteinizing hormone-releasing hormone ͉ LHRH

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“…Harris' "humoral" substance (gonadotropin releasing hormone, GnRH) and its mode of release After many years of herculean effort, a struggle between two rival laboratories and many setbacks 1 , the isolation of the humoral substance of hypothalamic origin that is secreted into the hypophysial portal circulation to regulate the synthesis and secretion of the gonadotopins, luteinizing hormone (LH) and follicle stimulating hormone (FSH), was independently achieved from bovine and ovine brain by the groups of Schally and Guilleman, respectively; ironically this work was published in 1971, the year of Harris' death (Amoss, et al 1971;Matsuo, et al 1971). It was a decapeptide that was initially termed luteinizing hormone releasing hormone (LHRH) or luteinizing hormone releasing factor (LRF), but the molecule is now generally referred to as GnRH1 2 .…”

Section: Author Manuscriptmentioning

confidence: 99%

Hypothalamo-pituitary-gonadal Axis

2009

Encyclopedia of Neuroscience

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IntroductionIn the fourth chapter of Geoffrey Harris' widely acclaimed 1955 monograph (Harris 1955), which now 60 years later provides the corner stone of this special issue of the journal, he succinctly and systematically presented his views, and the evidence upon which they were based, on the neural mechanisms controlling the pituitary-gonadal axis. That gonadal function was under control by the central nervous system was well established at the time of Harris' monograph, as was the recognition of the gonad-stimulating properties of pituitary gonadotropin, the relative insignificance of gonadal nerves to gonadal function and the concept of neurosecretion. The problem for Harris and his fellow neuroendocrinologists was how did the hypothalamus regulate the secretion of the anterior pituitary hormones, specifically gonadotropin in the context of this review, and what was the role of the hypopophysial portal system in this regard. After elegantly interpreting and summarizing the extant data, Harris proposed that of the hypotheses that were being debated at the time "the most likely seems to be that nerve fibres from the hypothalmus liberate some humoral substance(s) into the capillaries of the primary plexus in the median eminence and that this substance is carried by the portal vessels to excite or inhibit the cells of the pars distalis." It is to be recalled, that this idea had been proposed by Harris and Green and Harris on several occasions prior to publication of the monograph (see Harris, 1955). It is also worth noting that the evidence upon which Harris' hypothesis was based had been obtained primarily from studies of the female, most likely because ovulation was a discrete and readily detected event and, at the time, the only reliable surrogate marker of acute hypothalamic activation.The main purpose of the present chapter is to describe the essential refinements and additional complexities that have been added to the fundamental model Harris put forward in 1955 for the neuroendocrine control of gonadal function (Figure 1). The major additions Postal address: Magee-Womens Research Institute, 204 Craft Avenue; Room B311, Pittsburgh, PA 15213 USA, planttm@mwri.magee.edu. Declaration of interest: I declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of my interpretation of the research reported in this review. HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author Manuscriptto the neuroendocrinologist's armamentarium that have facilitated the development of the ideas of Harris are, according to an historical timeline, the introduction of radioimmunoassay to measure concentrations of pituitary and gonadal hormones in the peripheral circulation and GnRH in portal blood, the development of immunohistochemical techniques to localize neuropeptides and neurotransmitters in the hypothalamus, the application of techniques in molecular endocrinology to the study of gene expression in the hypothalamus and pituitary, the introduction of transgeni...

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Purification, amino acid composition and N-terminus of the hypothalamic luteinizing hormone releasing factor (LRF) of ovine origin

Cited by 374 publications

References 5 publications

Human Type II GnRH Receptor Mediates Effects of GnRH on Cell Proliferation

Human Type II GnRH Receptor Mediates Effects of GnRH on Cell Proliferation

GNRH1 mutations in patients with idiopathic hypogonadotropic hypogonadism

Hypothalamo-pituitary-gonadal Axis

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