The Gonadotropin Hormones and Their Receptors∗

Ascoli, Mario; Narayan, Prema

doi:10.1016/b978-1-4557-2758-2.00002-0

Cited by 6 publications

(12 citation statements)

References 362 publications

(442 reference statements)

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“…The available data also show that the extracellular domains of both LHR and FSHR are involved in ligand binding. Based upon available evidence on structure/function studies of LHR and FSHR, Ascoli and Puett (Ascoli and Puett, 2009; Costagliola et al, 2005; Vassart et al, 2004) have summarized three potential models for receptor activation. The first model envisions that a portion of the ligand bound to the extracellular domain interacts with the hinge region or the transmembrane helices leading to receptor activation.…”

Section: Receptor Structure and Mechanism Of Activationmentioning

confidence: 99%

“…Several naturally occurring mutations with reproductive phenotypes have been reported for human LHR and FSHR (reviewed in (Ascoli and Puett, 2009; Segaloff, 2009; Tao and Segaloff, 2009; Themmen, 2005)). As mentioned earlier, the first mutation to be identified for the gonadotropin receptors was the constitutively active mutation of LH receptor in a patient with precocious puberty (Shenker et al, 1993).…”

Section: Mutations Of Lhr and Fshrmentioning

confidence: 99%

“…Asp578His, which is the only somatic mutation identified so far (reviewed in (Segaloff, 2009)), has been shown to be responsible for hyperplasia and leydig cell adenoma (Boot et al, 2011). Activating mutations of LHR occur mainly on exon 11 which codes for the transmembrane domain and the carboxyl terminus region (Ascoli et al, 2002; Ascoli and Puett, 2009; Costagliola et al, 2005; Latronico and Segaloff, 1999; Themmen and Huhtaniemi, 2000). These mutations are localized on the sixth transmembrane domain and the third intracellular loop (Ascoli et al, 2002; Ascoli and Puett, 2009; Costagliola et al, 2005; Latronico and Segaloff, 1999; Themmen and Huhtaniemi, 2000).…”

Section: Mutations Of Lhr and Fshrmentioning

confidence: 99%

“…Activating mutations of LHR occur mainly on exon 11 which codes for the transmembrane domain and the carboxyl terminus region (Ascoli et al, 2002; Ascoli and Puett, 2009; Costagliola et al, 2005; Latronico and Segaloff, 1999; Themmen and Huhtaniemi, 2000). These mutations are localized on the sixth transmembrane domain and the third intracellular loop (Ascoli et al, 2002; Ascoli and Puett, 2009; Costagliola et al, 2005; Latronico and Segaloff, 1999; Themmen and Huhtaniemi, 2000). On the other hand, several of the LHR mutations causing loss of function occur on exon 10 leading to developmental or other disorders of male reproductive function (Gromoll et al, 2000).…”

Section: Mutations Of Lhr and Fshrmentioning

confidence: 99%

“…FSHR and LHR belong to rhodopsin/2 adrenergic receptor-like family A of G protein coupled receptors (GPCR) consisting of a large extracellular domain, seven membrane spanning α helices with intracellular and extracellular loops connecting them and a short intracellular domain. Aberrations in reproductive functions in the female and male have been reported due to naturally occurring mutations in LHR and FSHR (Ascoli and Puett, 2009; Costagliola et al, 2005; Latronico and Segaloff, 1999; Piersma et al, 2007; Segaloff, 2009; Tao and Segaloff, 2009; Themmen, 2005; Themmen and Huhtaniemi, 2000). This review will provide a brief overview of the structure/function relationship of the two receptors and will focus on recent advances in the molecular regulation of LHR expression in the ovary.…”

Section: Introductionmentioning

confidence: 99%

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Structure, function and regulation of gonadotropin receptors – A perspective

Menon

2012

Molecular and Cellular Endocrinology

108

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Luteinizing hormone receptor and follicle stimulating hormone receptor play a crucial role in female and male reproduction. Significant new information has emerged about the structure, mechanism of activation, and regulation of expression of these receptors. Here we provide an overview of the current information on those aspects with an in-depth discussion of the recent developments in the post-transcriptional mechanism of LH receptor expression mediated by a specific LH receptor mRNA binding protein, designated as LRBP. LRBP was identified by electrophoretic gel mobility shift assay using cytosolic fractions from ovaries in the down regulated state. LRBP was purified, its binding site on LH receptor mRNA was identified and characterized. During ligand-induced down regulation, LRBP expression is increased through the cAMP/PKA and ERK signaling pathway, is translocated to translating ribosomes, binds LH receptor mRNA and forms an untranslatable ribonucleoprotein complex. This complex is then routed to the mRNA degradation machinery resulting in diminished levels of both LHR mRNA and cell surface expression of LH receptor. The studies leading to these conclusions are presented.

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Section: Receptor Structure and Mechanism Of Activationmentioning

confidence: 99%

Section: Mutations Of Lhr and Fshrmentioning

confidence: 99%

Section: Mutations Of Lhr and Fshrmentioning

confidence: 99%

Section: Mutations Of Lhr and Fshrmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Structure, function and regulation of gonadotropin receptors – A perspective

Menon

2012

Molecular and Cellular Endocrinology

108

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Steroidogenesis and early response gene expression in MA-10 Leydig tumor cells following heterologous receptor down-regulation and cellular desensitization

Chen

Czerwiec

Puett

2016

Biochemistry and Biophysics Reports

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The Leydig tumor cell line, MA-10, expresses the luteinizing hormone receptor, a G protein-coupled receptor that, when activated with luteinizing hormone or chorionic gonadotropin (CG), stimulates cAMP production and subsequent steroidogenesis, notably progesterone. These cells also respond to epidermal growth factor (EGF) and phorbol esters with increased steroid biosynthesis. In order to probe the intracellular pathways along with heterologous receptor down-regulation and cellular desensitization, cells were preincubated with EGF or phorbol esters and then challenged with CG, EGF, dibutryl-cyclic AMP, and a phorbol ester. Relative receptor numbers, steroid biosynthesis, and expression of the early response genes, JUNB and c-FOS, were measured. It was found that in all cases but one receptor down-regulation and decreased progesterone production were closely coupled under the conditions used; the exception involved preincubation of the cells with EGF followed by addition of CG where the CG-mediated stimulation of steroidogenesis was considerably lower than the level of receptor down-regulation. In a number of instances JUNB and c-FOS expression paralleled the decreases in receptor number and progesterone production, while in some cases these early response genes were affected little if at all by the changes in receptor number. This finding may indicate that even low levels of activated signaling kinases, e.g. protein kinase A, protein kinase C, or receptor tyrosine kinase, may suffice to yield good expression of JUNB and c-FOS, or it may suggest alternative pathways for regulating expression of these two early response genes.

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Estimation of serum visfatin levels of infertile women with polycystic ovary syndrome in Iraqi patients

Kadhim,

Hassan

2024

AIP Conference Proceedings

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The Gonadotropin Hormones and Their Receptors∗

Cited by 6 publications

References 362 publications

Structure, function and regulation of gonadotropin receptors – A perspective

Structure, function and regulation of gonadotropin receptors – A perspective

Steroidogenesis and early response gene expression in MA-10 Leydig tumor cells following heterologous receptor down-regulation and cellular desensitization

Estimation of serum visfatin levels of infertile women with polycystic ovary syndrome in Iraqi patients

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