Journal of Molecular Endocrinology (J MOL ENDOCRINOL)

Publisher: Society for Endocrinology, BioScientifica

Journal description

Journal of Molecular Endocrinology focuses specifically on endocrinology research at the cellular and molecular level, thus complementing Journal of Endocrinology.

Current impact factor: 3.08

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 3.081
2013 Impact Factor 3.621
2012 Impact Factor 3.577
2011 Impact Factor 3.485
2010 Impact Factor 3.628
2009 Impact Factor 3.221
2008 Impact Factor 3.225
2007 Impact Factor 2.801
2006 Impact Factor 2.988
2005 Impact Factor 2.474
2004 Impact Factor 3.855
2003 Impact Factor 3.701
2002 Impact Factor 4.359
2001 Impact Factor 3.649
2000 Impact Factor 2.654
1999 Impact Factor 2.331
1998 Impact Factor 1.88
1997 Impact Factor 1.856
1996 Impact Factor 2.381
1995 Impact Factor 2.727
1994 Impact Factor 2.232
1993 Impact Factor 1.946
1992 Impact Factor 2.156

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.44
Cited half-life 8.20
Immediacy index 0.73
Eigenfactor 0.01
Article influence 1.10
Website Journal of Molecular Endocrinology website
Other titles Journal of molecular endocrinology (Online), JME
ISSN 0952-5041
OCLC 44451537
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

BioScientifica

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • In any repository
    • Publisher's version/PDF cannot be used
    • Set statement to accompany deposit (see policy)
    • Publisher last contacted on 18/04/2013
  • Classification
    white

Publications in this journal

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    ABSTRACT: Steroid hormone receptors (SRs) are heavily post-translationally modified by the reversible addition of a variety of molecular moieties, including phosphorylation, acetylation, methylation, sumoylation, and ubiquitination. These rapid and dynamic modifications may be combinatorial and interact (i.e. may be sequential, complement or oppose each other), creating a vast array of uniquely modified receptor sub-species that allow for diverse receptor behaviors that enable highly sensitive and context-dependent hormone action. For example, in response to hormone or growth factor membrane-initiated signaling events, post-translational modifications (PTMs) to SRs alter protein-protein interactions that govern the complex process of promoter or gene-set selection coupled to transcriptional repression or activation. Unique phosphorylation events allow SRs to associate or disassociate with specific co-factors that may include pioneer factors and other tethering partners that specify the resulting transcriptome and ultimately change cell fate. The impact of PTMs on SR action is particularly profound in the context of breast tumorigenesis, where frequent alterations in growth factor-initiated signaling pathways occur early and act as drivers of breast cancer progression towards endocrine resistance. Herein, with primary focus on breast cancer relevance, we review the mechanisms by which PTMs, including reversible phosphorylation events, regulate the closely related SRs, glucocorticoid receptor (GR) and progesterone receptor (PR), allowing for precise biological responses to ever-changing hormonal stimuli.
    Preview · Article · Feb 2016 · Journal of Molecular Endocrinology
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    ABSTRACT: The pituitary adrenocorticotropic hormone (ACTH) plays a pivotal role in homeostasis and stress response and is thus the major component of the hypothalamo-pituitary-adrenal (HPA) axis. After a brief summary of ACTH production from proopiomelanocortin (POMC) and on the ACTH receptor properties, the first part of the review covers the roles of ACTH in steroidogenesis and steroid secretion. We highlight the mechanisms explaining the differential acute versus chronic effects of ACTH on aldosterone and glucocorticoid secretion. The second part summarizes the effects of ACTH on adrenal growth, addressing its role as either a mitogenic or a differentiating factor. We then review the mechanisms involved in steroid secretion, from the classical cAMP second messenger system to various signaling cascades. We also consider how the interaction between the extracellular matrix and the cytoskeleton may trigger activation of signaling platforms potentially stimulating or repressing the steroidogenic potency of ACTH. Finally, we consider the extra-adrenal actions of ACTH, in particular its role in differentiation in a variety of cell types, in addition to its known lypolytic effects on adipocytes. In each section, we endeavor to correlate basic mechanisms of ACTH function with the pathological consequences of ACTH signaling deficiency and of overproduction of ACTH.
    Preview · Article · Jan 2016 · Journal of Molecular Endocrinology
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    ABSTRACT: The evolution of the melanocortin receptors is linked to the evolution of ACTH, the MSHs, and their common precursor POMC. The origin of the melanocortin receptors and POMC appears to be grounded in the early radiation of the ancestral protochordates. During the genome duplications that have occurred during the evolution of the chordates, the organization plan for POMC was established, and features that have been retained include, the high conservation of the amino acid sequences of α-MSH and ACTH, and the presence of the HFRW melanocortin receptor activation motif in all of the melanocortin peptides (i.e., ACTH, α-MSH, β-MSH, γ-MSH & δ-MSH). For the melanocortin receptors, the chordate genome duplications resulted in the proliferation of paralagous receptor genes, and a divergence in ligand selectivity. While, most gnathostome melanocortin receptors can be activated by either ACTH or the MSHs, teleost and tetrapod MC2R orthologs can only be activated by ACTH. The appearance of the accessory protein, MRAP1, paralleled the emergence of teleost and tetrapods MC2R ligand selectivity, and the dependence of these orthologs on MRAP1 for trafficking to the plasma membrane. The accessory protein, MRAP2, does not affect MC2R ligand selectivity, but does influence the functionality of MC4R orthologs. In this regard, the roles that these accessory proteins may play in the physiology of the five melanocortin receptors (i.e., MC1R, MC2R, MC3R, MC4R & MC5R) are discussed.
    Preview · Article · Jan 2016 · Journal of Molecular Endocrinology
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    ABSTRACT: The Sidt2 global knockout mouse Sidt2-/- has impaired insulin secretion. The aim of this study was to assess the role of Sidt2 protein in glucose-induced insulin secretion in primary cultured mouse β-cells. The major metabolic and electrophysiological steps of glucose-induced insulin secretion of primary cultured β-cells from Sidt2-/- mice were investigated. The β-cells from Sidt2-/- mice had normal NAD(P)H responses, KATP and KV currents. However, they exhibited a lower [Ca2+]i peak height when stimulated with 20 mM glucose compared with those from WT mice. Furthermore, it took a longer time for the [Ca2+]i of β-cell from Sidt2-/- mice to reach the peak. Ryanodine or 2-Aminoethoxydiphenyl borate (2-APB) pretreatment did not change [Ca2+]i response pattern to glucose in Sidt2-/- cells. Extraordinarily, pretreatment with bafilomycin A1(Baf-A1) led to a comparable [Ca2+]i increase pattern between these two groups, suggesting that calcium traffic from the intracellular acidic compartment is defective in Sidt2-/- β-cells. Bath-mediated application of 50 nM Nicotinic acid adenine dinucleotide phosphate (NAADP) normalized the [Ca2+]i response of Sidt2-/- β-cells. Finally, glucose-induced CD38 expression increased to a comparable level between Sidt2-/- and WT islets, suggesting that Sidt2-/- islets generated NAADP normally. We conclude that Sidt2 is involved in NAADP-mediated insulin secretory granule calcium release and thus regulates insulin secretion.
    No preview · Article · Jan 2016 · Journal of Molecular Endocrinology
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    ABSTRACT: A critical role for peptide C-terminal amidation was apparent when the first bioactive peptides were identified. The conversion of POMC into ACTH and then into αMSH, an amidated peptide, provided a model system for identifying the amidating enzyme. Peptidylglycine α-amidating monooxygenase (PAM), the only enzyme that catalyzes this modification, is essential; mice lacking PAM survive only until mid-gestation. Purification and cloning led to the discovery that the amidation of peptidylglycine substrates proceeds in two steps: peptidylglycine α-hydroxylating monooxygenase (PHM) catalyzes the copper and ascorbate-dependent α-hydroxylation of the peptidylglycine substrate; peptidyl-α-hydroxyglycine α-amidating lyase (PAL) cleaves the N-C bond, producing amidated product plus glyoxylate. Both enzymes are contained in the luminal domain of PAM, a type 1 integral membrane protein. The structures of both catalytic cores have been determined, revealing how they interact with metals, molecular oxygen and substrate to catalyze both reactions. Although not essential for activity, the intrinsically disordered cytosolic domain is essential for PAM trafficking. A phylogenetic survey led to identification of bifunctional membrane PAM in Chlamydomonas, a unicellular eukaryote. Accumulating evidence points to a role for PAM in copper homeostasis and in retrograde signaling from the lumen of the secretory pathway to the nucleus. The discovery of PAM in cilia, cellular antennae that sense and respond to environmental stimuli, suggests that much remains to be learned about this ancient protein.
    Preview · Article · Dec 2015 · Journal of Molecular Endocrinology
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    ABSTRACT: Leptin (Lep) is an anorexigenic hormone and regulates appetite-related neuropeptides in mammals. A number of neuropeptides have also been linked to appetite regulation of teleost fish, but Lep signaling activation and effects on appetite-regulating neurons are poorly elucidated in early vertebrates. This study uses cellular, tissue and organismal approaches to elucidate the acute, central Lep action in rainbow trout. The results demonstrate that Lep activates phosphorylation of protein kinase B (Akt) and signal transducer and activator of transcription 3 in rainbow trout hypothalamus-derived cells, and that the phosphatidylinositol 3-kinase (Pi3k) inhibitor LY294002 can suppress the Lep-induced Akt phosphorylation. Intracerebroventricular (ICV) Lep administration strongly suppresses food intake at the doses of 0.05 and 0.5 µg Lep fish(-1). At low dose, Lep stimulates hypothalamic transcription of anorexigenic cocaine- and amphetamine-regulated transcript (Cart) and orexigenic neuropeptide Y. At high dose Lep stimulates hypothalamic transcription of anorexigenic proopiomelanocortin (Pomc) A1, A2 and B, while co-injection with LY294002 reverses this upregulation. The data suggest that the anorexigenic action of Lep in rainbow trout is mediated through stimulation of the anorexigenic neuropeptides Pomc and Cart. Furthermore, ICV Lep treatment increases phosphor-Akt immunoreactive cells in nucleus lateralis tuberis, periventricular zone along infundibulum, and lateral recess surrounded by nucleus anterior tuberis, while LY294002 inhibits this effect. Lep receptor-immunoreactive cells are also predominant in these regions. These results demonstrate that Lep activates the Pi3k-Akt pathway in the lateral tuberal hypothalamus of rainbow trout for acute appetite regulation, indicating conservation of anorexigenic Lep action in the mediobasal hypothalamus.
    No preview · Article · Dec 2015 · Journal of Molecular Endocrinology
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    ABSTRACT: TMEFF2 is a transmembrane protein with unknown function, containing an altered epidermal growth factor (EGF)-like motif, two follistatin-like domains, and a cytosolic tail with a putative G-protein-activating motif. TMEFF2 is predominantly expressed in brain and prostate and has been implicated in cell signaling, neuronal cell survival, and tumor suppression. We found that expression of TMEFF2 in pituitary corticotrope cells inhibits the effects of corticotropin-releasing hormone (CRH) on the production of intracellular cAMP, and CREB, and transcription of Pomc. Regulation of the activity of CRH by TMEFF2 requires neither the cytoplasmic tail nor the EGF domain, while deletion of the follistatin modules abolishes the inhibitory function of TMEFF2. Moreover, a soluble secreted protein containing the complete extracellular domain is sufficient for inhibition of CRH signaling. TMEFF2-induced inhibition depends on serum components. Furthermore, TMEFF2 regulates the non-canonical activin/BMP4 signaling, PI3K, and Ras/ERK1/2 pathways. Thus, TMEFF2 inhibits the CRH signaling pathway and the PI3K/AKT and Ras/ERK1/2 pathways, contributing to a significant inhibition of transcription of Pomc. We found that expression of TMEFF2 in human Cushing's adenoma is reduced when compared with normal human pituitary, which may indicate that TMEFF2 acts as a tumor suppressor in these adenomas. Furthermore, the overexpression of TMEFF2 decreased proliferation of corticotrope cells. Our results indicate a potential therapeutic use of TMEFF2 or factors that stimulate the activity of TMEFF2 for the treatment of corticotrope tumors in order to reduce their secretion of ACTH and proliferation. © 2015 Society for Endocrinology.
    No preview · Article · Dec 2015 · Journal of Molecular Endocrinology
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    ABSTRACT: The major mission of the ovarian follicle is the timely production of the mature fertilizable oocyte, and this is achieved by gonadotropin-regulated, gap junction-mediated cell-cell communication between the oocyte and surrounding nurturing granulosa cells. We have demonstrated that FSH and transforming growth factor beta 1 (TGFβ1) stimulate Gjal gene-encoded connexin43 (Cx43) gap junction formation/function in rat ovarian granulosa cells is important for their induction of steroidogenesis; additionally, cAMP-protein kinase A (PKA)- and calcium-calcineurin-sensitive cAMP response element-binding (CREB) coactivator CRTC2 plays a crucial role during steroidogenesis. This study was to explore the potential molecular mechanism whereby FSH and TGFβ1 regulate Cx43 synthesis and degradation, particularly the involvement of CRTC2 and ubiquitin ligase Nedd4. Primary culture of granulosa cells from ovarian antral follicles of gonadotropin-primed immature rats was used. At 48 h post-treatment, FSH plus TGFβ1 increased Cx43 level and gap junction function in a PKA- and calcineurin-dependent manner, and TGFβ1 acting through its type I receptor modulated FSH action. Chromatin-immunoprecipitation analysis reveals FSH induced an early-phase (45 min) and FSH+TGFβ1 further elicited a late-phase (24 h) increase in CRTC2, CREB and CBP binding to the Gjal promoter. Additionally, FSH + TGFβ1 increased the half-life of hyper-phosphorylated Cx43 (Cx43-P2). Also, the proteasome inhibitor MG132 prevented the brefeldin A (blocker of protein transport through Golgi)-reduced Cx43-P2 level and membrane Cx43 gap junction plaque. This is associated with FSH + TGFβ1-attenuated Cx43 interaction with Nedd4 and Cx43 ubiquitination. In all, this study uncovers that FSH and TGFβ1 upregulation of Cx43 gap junctions in ovarian granulosa cells critically involves enhancing CRTC2/CREB/CBP-mediated Cx43 expression and attenuating ubiquitin ligase Nedd4-mediated proteosomal degradation of Cx43 protein.
    No preview · Article · Dec 2015 · Journal of Molecular Endocrinology
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    ABSTRACT: Oxidative stress is considered to bean important factor in producing lethal hepatocyte injury associated with nonalcoholic fatty liver disease (NAFLD). Glucose fluctuation, more pronounced in patients with diabetes, has been recognized as an even stronger oxidative stress inducer than the sustained hyperglycemia. Here, we investigated the role of glucose variability in the development of the NAFLD based on hepatocyte apoptosis and possible mechanisms. To achieve this goal we studied C57BL/6J mice that were maintained on a high fat diet (HFD) and injected with glucose (3 g/kg) twice daily to induce intermittent high glucose (IHG). We also studied hepatic L02 cells incubated with palmitic acid (PA) to induce steatosis. The following experimental groups were compared: normal glucose (NG), sustained high glucose (SHG) and IHG with or without PA. We found that, although hepatic enzyme levels and liver lipid deposition were comparable between HFD mice injected with glucose or saline, the glucose injected mice displayed marked hepatocyte apoptosis and inflammation, accompanied by increased lipid peroxide in liver. In vitro, in the presence of PA, IHG increased L02 cell apoptosis and oxidative stress and produced pronounced mitochondrial dysfunction relative to the NG and SHG groups. Furthermore, treatment with the mitochondrial permeability transition (MPT) inhibitor, cyclosporin A (1.5 mmol/l), prevented mitochondrial dysfunction, oxidative stress and hepatocyte apoptosis. Our data suggests that IHG under lipotoxicity might contribute to the development of NAFLD by increasing oxidative stress and hepatocyte apoptosis via MPT and its related mitochondrial dysfunction.
    No preview · Article · Dec 2015 · Journal of Molecular Endocrinology
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    Preview · Article · Dec 2015 · Journal of Molecular Endocrinology
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    ABSTRACT: The generation of therapeutic β-cells from human pluripotent stem cells relies on the identification of growth factors that faithfully mimic pancreatic β-cell development in vitro. In this context, the aim of the study was to determine the expression and function of the Glial cell line derived neurotrophic factor receptor α 3 (GFRα3) and its ligand Artemin in islet cell development and function. GFRα3 and Artn expression were characterized by in situ hybridization, immunochemistry and qRT-PCR. We used GFRα3-deficient mice to study GFRα3 function and generated a transgenic mice overexpressing Artn in the embryonic pancreas to study Artn function. We found that GFRα3 is expressed at the surface of a subset of Ngn3-positive endocrine progenitors as well as of embryonic α- and β-cells, while Artn is found in the pancreatic mesenchyme. Adult β-cells lack GFRα3 but α-cells express the receptor. GFRα3 was also found in parasympathetic and sympathetic intra islets neurons as well as in glial cells in the embryonic and adult pancreas. The loss of GFRα3 or overexpression of Artn has no impact on Ngn3- and islet- cells formation and maintenance in the embryo. Islet organisation and innervation as well as glucose homeostasis is normal in GFRα3-deficient mice suggesting functional redundancy.
    No preview · Article · Nov 2015 · Journal of Molecular Endocrinology
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    ABSTRACT: The H295R adrenocortical cell line is widely used for molecular analysis of adrenal functions but is known to have only modest ACTH responsiveness. The lack of ACTH response was linked to low expression of its receptor, melanocortin 2 receptor (MC2R). We hypothesized that increasing MC2R accessory protein (MRAP), which is required to traffic MC2R from the endoplasmic reticulum to the cell surface, would increase ACTH responsiveness. Lentiviral particles containing human MRAP-open reading frame were generated and transduced in H295R cells. Using antibiotic resistance, eighteen clones were isolated for characterization. The most ACTH-responsive steroidogenic clone, H295RA, was used for further experiments. Successful induction of MRAP and increased expression of MC2R in H295RA cells was confirmed by quantitative real time RT-PCR and western blotting. Treatment with ACTH significantly increased aldosterone, cortisol, and dehydroepiandrosterone production in H295RA cells. ACTH also significantly increased transcript levels for all the steroidogenic enzymes required to produce aldosterone, cortisol, and dehydroepiandrosterone, as well as MC2R mRNA. Further analysis using liquid chromatography/tandem mass spectrometry revealed that the main unconjugated steroids produced in H295RA cells were 11-deoxycortisol, cortisol, and androstenedione. Treatment of H295RA cells with ACTH also acutely increased cAMP production and cellular protein levels for total and phosphorylated steroidogenic acute regulatory protein. In summary, through genetic manipulation, we have developed an ACTH-responsive human adrenocortical cell line. The cell line will provide a powerful in vitro tool for molecular analysis of physiologic and pathologic conditions involving the hypothalamic-pituitary-adrenal axis.
    No preview · Article · Nov 2015 · Journal of Molecular Endocrinology
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    ABSTRACT: Inability of pancreatic β-cells to make sufficient insulin to control blood sugar is a central feature of the aetiology of most forms of diabetes. In this review we focus on the deleterious effects of oxidative stress and ER stress on β-cell insulin biosynthesis and secretion, and on inflammatory signalling and apoptosis with a particular emphasis on type 2 diabetes. We argue that oxidative stress and ER stress are closely entwined phenomenon fundamentally involved in β-cell dysfunction, by direct effects on insulin biosynthesis and due to consequences of the ER stress-induced unfolded protein response. We summarise evidence that, although these phenomenon can be driven by intrinsic β-cell defects in rare forms of diabetes, in type 2 diabetes β-cell stress is driven by a range of local environmental factors including increased drivers of insulin biosynthesis, glucolipotoxicity and inflammatory cytokines. We describe our recent findings that a range of inflammatory cytokines contribute to β-cell stress in diabetes, and our discovery that IL-22 protects β-cells from oxidative stress regardless of the environmental triggers, and can correct much of diabetes pathophysiology in animal models. Finally we summarise evidence that β-cell dysfunction is reversible in type 2 diabetes, and discuss therapeutic opportunities for relieving oxidative and ER stress and restoring glycaemic control.
    Preview · Article · Nov 2015 · Journal of Molecular Endocrinology
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    ABSTRACT: G protein-coupled receptor 120 (GPR120), an adipogenic receptor critical for the differentiation and maturation of adipocytes, plays an important role in controlling obesity in both humans and rodents, and thus is an attractive target of obesity treatment studies. However, the mechanisms that regulate the expression of porcine GPR120 remain unclear. In this study, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) techniques were used to analyze and identify the binding of C/EBPβ (transcription factor CCAAT/enhancer binding protein beta) to the GPR120 promoter. C/EBPβ overexpression and RNA interference studies showed that C/EBPβ regulated GPR120 promoter activity and endogenous GPR120 expression. The binding site of C/EBPβ in GPR120 promoter region from -101 to -87 was identified by promoter deletion analysis and site-directed mutagenesis. Overexpression of C/EBPβ increased endogenous GPR120 expression in pig kidney cells (PK). Furthermore, when endogenous C/EBPβ was knocked down, GPR120 mRNA and protein levels were decreased. The stimulatory effect of C/EBPβ on GPR120 transcription and its ability to bind the transcription factor binding site were confirmed by luciferase, ChIP and EMSA. Moreover, the mRNA and protein expression levels of C/EBPβ were induced by high fat diet-feeding. Taken together, it can be concluded that C/EBPβ plays a vital role in regulating GPR120 transcription, and suggest HFD-feeding induces GPR120 transcription by influencing C/EBPβ expression.
    No preview · Article · Nov 2015 · Journal of Molecular Endocrinology
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    ABSTRACT: The arcuate-nucleus of the hypothalamus is essential for metabolic-homeostasis and responds to leptin by producing several neuropeptides including proopiomelanocortin (POMC). We previously reported that high-dose erythropoietin (Epo)-treatment in mice while increasing hematocrit, reduced body-weight, fat-mass, and food intake, and increased energy-expenditure. Moreover, we showed that mice with Epo receptor (EpoR) restricted to erythroid cells (ΔEpoRE) became obese and exhibited decreased energy-expenditure. Epo/EpoR-signaling was found to promote hypothalamus POMC-expression independently from leptin. Herein we used wild-type (WT) and ΔEpoRE-mice and hypothalamus-derived neural-culture system to study the signaling pathways activated by Epo in POMC neurons. We show that Epo-stimulation activated STAT3-signaling and up-regulated POMC expression in WT neural cultures. ΔEpoRE-mice hypothalamus showed reduced POMC levels, and lower STAT3-phosphorylation, with and without leptin-treatment, compared to in vivo and ex vivo WT controls. Collectively, these data show that Epo regulates hypothalamus POMC-expression via STAT3-activation, and provide a previously unrecognized link between Epo- and leptin-response.
    No preview · Article · Nov 2015 · Journal of Molecular Endocrinology
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    ABSTRACT: The extracellular loop 2 (EL2) of FSH receptor (FSHR) plays a pivotal role in various events downstream of FSH stimulation. Because swapping the six FSHR-specific residues in EL2 (chimeric EL2M) with those from LH/choriogonadotropin receptor resulted in impaired internalization of FSH-FSHR complex and low FSH-induced cAMP production, six substitution mutants of EL2 were generated to ascertain the contribution of individual amino acids to the effects shown by chimeric EL2M. Results revealed that L-501 F mainly and (IV)-V-505 to a lesser extent contribute to the diminished receptor function in chimeric EL2M. HEK293 cells stably expressing WTand chimeric EL2M FSHR were generated to track the fate of the receptors post FSH induction. The chimeric EL2M FSHR stable clone showed weak internalization and cAMP response similar to transiently transfected cells. Furthermore, reduced FSH-induced ERK phosphorylation was also observed. The interaction of activated chimeric EL2M and L 501 F FSHR with b- arrestins was weak compared with WT FSHR, thus explaining the impaired internalization of chimeric EL2M and corroborating the indispensable role of EL2 in receptor function.
    No preview · Article · Jun 2015 · Journal of Molecular Endocrinology