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Journal articles on the topic 'Inhibin A'

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Published: 4 June 2021

Last updated: 26 July 2025

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1

Arola, J., J. Liu, P. Heikkila, et al. "Expression of inhibin alpha in adrenocortical tumours reflects the hormonal status of the neoplasm." Journal of Endocrinology 165, no. 2 (2000): 223–29. http://dx.doi.org/10.1677/joe.0.1650223.

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Inhibins are gonadal glycoprotein hormones whose main endocrine function is to inhibit pituitary FSH secretion. In addition to testes and ovaries, other steroid-producing organs are sites of inhibin alpha subunit expression. To study the role of inhibins in human adrenal gland, we screened a panel of 150 adrenals (10 normal adrenals, 25 adrenocortical hyperplasias, 65 adrenocortical adenomas, 30 adrenocortical carcinomas and 20 phaeochromocytomas) for inhibin alpha expression. mRNA levels of inhibin alpha subunit were studied in 57 samples and all tissues were stained immunohistochemically wit

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2

TANAKA, YUMIKO, HIROYUKI TANIYAMA, NOBUO TSUNODA, et al. "The Testis as a Major Source of Circulating Inhibins in the Male Equine Fetus During the Second Half of Gestation." Journal of Andrology 23, no. 2 (2002): 229–36. http://dx.doi.org/10.1002/j.1939-4640.2002.tb02619.x.

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ABSTRACT: Immunolocalization of the inhibin (α) and inhibin/activin (βA and βB) subunit proteins in equine fetal testes was investigated to determine the ability of the fetal testis to produce inhibins at 120, 150, 200, and 250 days of gestation. In addition, concentrations of immunoreactive (ir)‐inhibin, inhibin pro‐αC, and inhibin A in both the maternal and fetal circulation were measured. It was found that plasma concentrations of ir‐inhibin, inhibin pro‐αC, and inhibin A were much higher (P < .05) in the fetal than in the maternal circulation at any stage of gestation examined. Similarl

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3

Vänttinen, Teemu, Tiina Kuulasmaa, Jianqi Liu, and Raimo Voutilainen. "Expression of Activin/Inhibin Receptor and Binding Protein Genes and Regulation of Activin/Inhibin Peptide Secretion in Human Adrenocortical Cells." Journal of Clinical Endocrinology & Metabolism 87, no. 9 (2002): 4257–63. http://dx.doi.org/10.1210/jc.2002-020460.

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Activins and inhibins are glycoprotein hormones produced mainly in gonads but also in other organs. They are believed to be important para/autocrine regulators of various cell functions. We investigated activin/inhibin receptor and binding protein gene expression and the regulation of activin/inhibin secretion in human adrenal cells. RT-PCR revealed inhibin/activin α-, βA/B-subunit, follistatin, activin type I/II receptor, and inhibin receptor (betaglycan and inhibin-binding protein) mRNA expression in fetal and adult adrenals and cultured adrenocortical cells. Cultured cells secreted activin

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4

Robertson, D. M., N. Cahir, J. K. Findlay, H. G. Burger, and N. Groome. "The Biological and Immunological Characterization of Inhibin A and B Forms in Human Follicular Fluid and Plasma1." Journal of Clinical Endocrinology & Metabolism 82, no. 3 (1997): 889–96. http://dx.doi.org/10.1210/jcem.82.3.3801.

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Abstract In a previous study (see Ref. 7), the molecular weight distribution of inhibin activity in fractionated human follicular fluid (hFF) and human male and female plasma/serum was determined by in vitro bioassay using ovine pituitary cells in culture and various specific inhibin A and inhibin α-subunit-directed immunoassays. It was shown, however, that the ovine in vitro bioassay detected inhibin B poorly. These findings are extended in the present study by the determination of the molecular weight profile of in vitro bioactivity using rat pituitary cells, which detects both inhibin A and

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5

Burger, HG, PG Farnworth, JK Findlay, et al. "Aspects of current and future inhibin research." Reproduction, Fertility and Development 7, no. 5 (1995): 997. http://dx.doi.org/10.1071/rd9950997.

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Inhibin was first isolated in 1985. Major progress has been made in defining various aspects of its structure and physiology, using a heterologous radioimmunoassay. Current research is aimed at characterizing the nature of the circulating forms of inhibin and is examining whether there are sex-specific roles for inhibins A and B. It has been recognized that various forms of epithelial and stromal ovarian cancer produce members of the inhibin peptide family but the precise nature of these products is not yet clear. The recognition that the inhibin subunits together with follistatin are expresse

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6

Vanttinen, T., J. Liu, J. Liu, et al. "Regulation of immunoreactive inhibin A and B secretion in cultured human granulosa-luteal cells by gonadotropins, activin A and insulin-like growth factor type-1 receptor." Journal of Endocrinology 167, no. 2 (2000): 289–94. http://dx.doi.org/10.1677/joe.0.1670289.

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Inhibins are gonadal glycoproteins with endocrine effects on pituitary FSH secretion and para/autocrine effects on ovarian and testicular function. The purpose of this study was to investigate the endocrine and para/autocrine regulation of inhibin A and inhibin B secretion in human ovarian granulosa-luteal cells. The cells were obtained from women undergoing in vitro fertilization, and the primary cultures were treated with FSH, LH, human chorionic gonadotropin (hCG), activin A, 8-bromo cyclic AMP (8-BrcAMP), staurosporine (a protein kinase C inhibitor) and an antagonist of IGF action (type-1

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7

Kenny, HA, DJ Bernard, TH Horton, and TK Woodruff. "Photoperiod-dependent regulation of inhibin in Siberian hamsters: I. Ovarian inhibin production and secretion." Journal of Endocrinology 174, no. 1 (2002): 71–83. http://dx.doi.org/10.1677/joe.0.1740071.

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Follicle-stimulating hormone (FSH) stimulates ovarian follicle development and the production of protein hormones including inhibin A and inhibin B. The inhibins are dimeric proteins (alpha-beta(A) or alpha-beta(B)) secreted by growing follicles that suppress FSH in a classical endocrine negative feedback loop. Siberian hamsters, Phodopus sungorus, exhibit seasonal variation in FSH levels. Given the role of inhibin in FSH regulation, we hypothesized that ovarian inhibin expression differs between animals reared in long (16 h light:8 h darkness) and short (6 h light:18 h darkness) photoperiods.

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8

Wiater, Ezra, Kathy A. Lewis, Cynthia Donaldson, Joan Vaughan, Louise Bilezikjian, and Wylie Vale. "Endogenous Betaglycan Is Essential for High-Potency Inhibin Antagonism in Gonadotropes." Molecular Endocrinology 23, no. 7 (2009): 1033–42. http://dx.doi.org/10.1210/me.2009-0021.

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Abstract Inhibins are endocrine hormones that regulate gametogenesis and reproduction through a negative feedback loop with FSH. Inhibin action involves antagonism of signaling by activin or other TGFβ family ligands. In transfection assays, antagonism by inhibin can be potentiated by betaglycan, a coreceptor for selected TGFβ family ligands. We tested whether betaglycan is an obligate inhibin coreceptor through disruption of betaglycan function by RNA interference-mediated knockdown and immunoneutralization. Betaglycan knockdown and anti-betaglycan IgG each independently prevented inhibin-A b

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9

Walton, Kelly L., Emily K. Kelly, Katharine E. Johnson, David M. Robertson, Peter G. Stanton, and Craig A. Harrison. "A Novel, More Efficient Approach to Generate Bioactive Inhibins." Endocrinology 157, no. 7 (2016): 2799–809. http://dx.doi.org/10.1210/en.2015-1963.

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Gonadal-derived inhibins are essential factors in mammalian reproduction, negatively regulating pituitary production of FSH. Interestingly, declines in inhibin levels across the menopause transition correlate with not only an increase in FSH but also a rapid decrease in bone mass. Therefore, inhibins have been touted as potential therapeutics for osteoporosis in postmenopausal women. However, as heterodimeric proteins of α- and β- (βA or βB)-subunits, inhibins are difficult to produce recombinantly, are poorly processed to their mature bioactive forms, and their expression is always accompanie

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10

Imai, M., M. Yamoto, H. Otani, and R. Nakano. "Cytokine modulation of inhibin secretion in cultured rat granulosa cells." Journal of Endocrinology 151, no. 3 (1996): 449–57. http://dx.doi.org/10.1677/joe.0.1510449.

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Abstract In the present study, we examined the effects of tumour necrosis factor α (TNFα) and interleukin-1β (IL-1β) on inhibin secretion by cultured rat granulosa cells using immunoblotting and two-site enzyme immunoassay for inhibin A (α-βA dimer). FSH stimulated the secretion of the inhibin α-βA dimer (32 kDa) by the cells in a dose-dependent manner. In addition to the predominant 32 kDa inhibin α-βA dimer staining, staining of minor immunoreactive bands was also enhanced by FSH. TNFα alone did not have any effect on inhibin secretion. Immunoblot analyses using an antiserum against α-subuni

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11

Farnworth, Paul G., Yao Wang, Pauline Leembruggen, et al. "Rodent adrenocortical cells display high affinity binding sites and proteins for inhibin A, and express components required for autocrine signalling by activins and bone morphogenetic proteins." Journal of Endocrinology 188, no. 3 (2006): 451–65. http://dx.doi.org/10.1677/joe.1.06444.

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Inhibins are expressed in the adrenal cortex, but little is known of their binding or role in the adrenal. The aims of the present study were, first, to establish whether a mouse adrenocortical (AC) cell line expresses inhibins/activins and bone morphogenetic proteins (BMP), along with proteins required for inhibin to antagonise activin and BMP actions and, secondly, to characterise and compare inhibin binding sites and proteins in the rat adrenal gland and AC cells. AC cells were found to: (1) express mRNA for multiple BMPs (BMP-2, -3, -4, -6, -8a), growth/differentiation factors (GDF-1, -3,

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12

Harrison, C. A., E. Wiater, K. A. Lewis, P. C. Gray та W. W. Vale. "125. Identification of a functional binding site on betaglycan for inhibin and TGFβ". Reproduction, Fertility and Development 17, № 9 (2005): 75. http://dx.doi.org/10.1071/srb05abs125.

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Betaglycan is a co-receptor that modulates signaling by TGFβ superfamily members including TGFβs and inhibins. Loss of betaglycan expression, or blocking of betaglycan function, has been implicated in several human diseases and in animal disease models. However, characterization of the superfamily ligands and receptors involved in these disease states is complicated because of the pleiotropic nature of betaglycan co-receptor action. Here we report the identification and characterization of a domain within the extracellular region of betaglycan that binds inhibin-A and TGFβ-1. We show that both

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13

Michel, U., H. Jarry, M. Metten, and W. Wuttke. "Inhibin production by porcine granulosa and luteal cells: development and biological validation of a RIA." Acta Endocrinologica 120, no. 4 (1989): 511–18. http://dx.doi.org/10.1530/acta.0.1200511.

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Abstract. We describe the development and biological validation of a radioimmunoassay for immuno- and bioactive porcine inhibin. A synthetic 1-32 porcine inhibin peptide was used to raise an antiserum and Tyr-1-32 peptide as tracer. As standard we employed porcine follicular fluid calibrated with the 1-32 α-inhibin. Medium obtained from serum-free cultured porcine granulosa cells was chromatographed on Superose S-12 and Mono-Q. Resulting fractions were analysed for inhibin bio- and immunoreactivity. It is shown that granulosa cells produce at least two types of bioactive inhibins, one being al

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14

Vukotić, M., G. Trajković, M. Parlić, A. Ćorac, M. Mirković, and N. Milošević. "INHIBINS INHIBINS - QUALITIES, QUALITIES, SIGNIFICANCE SIGNIFICANCE AND HIS ROLE IN PREGNANCY PREGNANCY." Praxis medica 36, no. 1 (2008): 103–6. http://dx.doi.org/10.70949/pramed200801235v.

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&lt;p&gt;Inhibins are glycoprotein hormones of which there are two molecular forms, inhibin A and inhibin B. Classically, inhibin is known to have a negative feedback effect on pituitary follicle-stimulating hormone secretion. The fetoplacental unit produced inhibin throughout pregnancy. Inhibin Ais the predominant molecular form of inhibin in maternal circulation from 4 week of gestation. Although the precise biological function of inhibin Ain pregnancy is unclear, it is evident from recent studies that inhibin A could be a better marker of placental function than human chorionic gona

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15

Lambert-Messerlian, G. M., J. A. Canick, G. E. Palomaki, A. L. Schneyer та G. M. Lambert-Messerlian. "Second Trimester Levels of Maternal Serum Inhibi A, Total Inhibin, α Inhibin Precursor, and Activin in Down's Syndrome Pregnancy". Journal of Medical Screening 3, № 2 (1996): 58–62. http://dx.doi.org/10.1177/096914139600300202.

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Objective –To determine the levels of various biochemical forms of the placental protein, inhibin (total inhibin, inhibin A, and α inhibin precursor) and activin in maternal serum samples from fetal Down's syndrome, and to determine which of these analytes most effectively identifies samples from affected pregnancies. Methods –Maternal serum samples were collected from 100 unaffected pregnancies and 20 cases of fetal Down's syndrome during gestational weeks 15–20 for routine triple marker screening, and were stored frozen after clinical assay. Levels of inhibin A, total inhibin, α inhibin prec

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16

Ohshima, K., H. Kishi, M. Itoh, et al. "Secretion of inhibin A, inhibin B and inhibin pro-alphaC during the oestrous cycle of the golden hamster (Mesocricetus auratus)." Journal of Endocrinology 162, no. 3 (1999): 451–56. http://dx.doi.org/10.1677/joe.0.1620451.

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Plasma concentrations of inhibin pro-alphaC, inhibin A and inhibin B were determined by enzyme-linked immunosorbent assay at 6 h intervals throughout the 4-day oestrous cycle of the golden hamster. Plasma concentrations of follicle-stimulating hormone (FSH) and oestradiol-17beta were also measured by radioimmunoassay during the oestrous cycle. Plasma concentrations of inhibin A increased from the early morning of day 1 (day 1=day of ovulation) and reached plateau levels at 0500 h on day 2. An abrupt increase in plasma concentrations of inhibin A was found at 1700 h on day 4, when the preovulat

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17

Clifton, RJ, L. O'Donnell, and DM Robertson. "Pachytene spermatocytes in co-culture inhibit rat Sertoli cell synthesis of inhibin beta B-subunit and inhibin B but not the inhibin alpha-subunit." Journal of Endocrinology 172, no. 3 (2002): 565–74. http://dx.doi.org/10.1677/joe.0.1720565.

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This study investigates the effects of spermatogenic germ cells on inhibin alpha-subunit and beta B-subunit expression, and inhibin alpha-subunit and inhibin B production by rat Sertoli cells in vitro. Sertoli cells isolated from 19-day-old rats were cultured for 48 h at 32 degrees C, in the presence or absence of FSH (2.3-2350 mIU/ml), and in the presence of pachytene spermatocytes, round spermatids or cytoplasts of elongated spermatids purified from adult rat testis by elutriation and density gradient separation. Sertoli cell secretion of inhibin alpha-subunit and inhibin B, as measured by i

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18

Shou, Weinian, Teresa K. Woodruff, and Martin M. Matzuk. "Role of Androgens in Testicular Tumor Development in Inhibin-Deficient Mice*." Endocrinology 138, no. 11 (1997): 5000–5005. http://dx.doi.org/10.1210/endo.138.11.5499.

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To understand gonadal tumor development, we have previously created a mouse model in which mice deficient in the inhibins develop gonadal sex cord-stromal tumors with essentially 100% penetrance. These tumors develop as early as 4 weeks of age and cause cancer cachexia-like symptoms and subsequent death in the inhibin-deficient mice. Gonadectomized inhibin-deficient mice eventually develop adrenal cortical tumors with nearly 100% penetrance. These studies have identified inhibin as a novel secreted tumor suppressor protein with specificity for the gonads and adrenal glands. Sex steroids have b

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19

van Dijk, S., J. Steenbergen, J. Th Gielen, and F. H. de Jong. "Sexual dimorphism in immunoneutralization of bioactivity of rat and ovine inhibin." Journal of Endocrinology 111, no. 2 (1986): 255–61. http://dx.doi.org/10.1677/joe.0.1110255.

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ABSTRACT Inhibin was partially purified from bovine follicular fluid using chromatography on immobilized Procion Red 3B and anion-exchange chromatography. Ovariectomized Texel ewes were immunized against the inhibin-containing fraction from the Procion Red 3B column and the immune response was subsequently boosted with similar fractions or with the preparation obtained from the anion-exchange column. The potencies of the resulting antisera were evaluated in an invitro bioassay system for estimating inhibin activity, using dispersed rat pituitary cells. The antisera were found to inhibit the bi

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Makanji, Yogeshwar, Jie Zhu, Rama Mishra, et al. "Inhibin at 90: From Discovery to Clinical Application, a Historical Review." Endocrine Reviews 35, no. 5 (2014): 747–94. http://dx.doi.org/10.1210/er.2014-1003.

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When it was initially discovered in 1923, inhibin was characterized as a hypophysiotropic hormone that acts on pituitary cells to regulate pituitary hormone secretion. Ninety years later, what we know about inhibin stretches far beyond its well-established capacity to inhibit activin signaling and suppress pituitary FSH production. Inhibin is one of the major reproductive hormones involved in the regulation of folliculogenesis and steroidogenesis. Although the physiological role of inhibin as an activin antagonist in other organ systems is not as well defined as it is in the pituitary-gonadal

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21

Bernard, Daniel J., Kathleen H. Burns, Bisong Haupt, Martin M. Matzuk, and Teresa K. Woodruff. "Normal Reproductive Function in InhBP/p120-Deficient Mice." Molecular and Cellular Biology 23, no. 14 (2003): 4882–91. http://dx.doi.org/10.1128/mcb.23.14.4882-4891.2003.

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ABSTRACT The inhibins are gonadal transforming growth factor β superfamily protein hormones that suppress pituitary follicle-stimulating hormone (FSH) synthesis. Recently, betaglycan and inhibin binding protein (InhBP/p120, also known as the product of immunoglobulin superfamily gene 1 [IGSF1]) were identified as candidate inhibin coreceptors, shedding light on the molecular basis of how inhibins may affect target cells. Activins, which are structurally related to the inhibins, act within the pituitary to stimulate FSH production. Betaglycan increases the affinity of inhibins for the activin t

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22

Ohshima, K., H. Kishi, M. Itoh, et al. "Secretory pattern of inhibin A, inhibin B and inhibin pro-alpha C during induced follicular atresia and subsequent follicular development in the golden hamster (Mesocricetus auratus)." Journal of Endocrinology 172, no. 3 (2002): 575–81. http://dx.doi.org/10.1677/joe.0.1720575.

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The changes in plasma concentrations of inhibins A, B and pro-alpha C were determined in the cyclic golden hamster during follicular atresia induced with antiserum against luteinizing hormone releasing hormone (LHRH-AS) at 1100 h on day 4 (day 1=day of ovulation). Follicular status in the ovary was also studied by determining the number of follicles ovulating in response to human chorionic gonadotrophin (hCG) injection. The time-courses of changes in plasma concentrations of inhibins A, B and pro-alpha C were different from each other during induced follicular atresia and subsequent follicular

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23

Eede, V., J. A. Muir, A. E. O. 'Connor, W. R. Winnall, A. E. Drummond та M. P. Hedger. "206. Differential regulation of activin and inhibin production by interleukin 1 (IL1), transforming growth factor β1 (TGFβ1) and protein kinase C (PKC) in the Sertoli cell and granulosa cell". Reproduction, Fertility and Development 20, № 9 (2008): 6. http://dx.doi.org/10.1071/srb08abs206.

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Activin and inhibin are gonadal regulatory proteins comprising an α-subunit and either a βA-subunit or βB-subunit (inhibin A or B), or two βA-subunits (activin A). Synthesis of the α-subunit, and the inhibins, is regulated by FSH via cAMP/protein kinase A. Regulation of the β-subunits in the gonads is less well defined, but the IL1/MAP kinase, TGFβ /Smad and PKC pathways have been implicated. Sertoli cells and granulosa cells were isolated from 18–22 day-old Sprague-Dawley rats under standard conditions and cultured with IL1, TGFβ1 and the PKC agonists, gonadotrophin releasing hormone (GnRH) o

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24

Hohmann, Femke P., Joop S. E. Laven, Frank H. de Jong, and Bart C. J. M. Fauser. "Relationship between inhibin A and B, estradiol and follicle growth dynamics during ovarian stimulation in normo-ovulatory women." European Journal of Endocrinology 152, no. 3 (2005): 395–401. http://dx.doi.org/10.1530/eje.1.01871.

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Objective: To investigate the relationship between serum concentrations of inhibin A, inhibin B and estradiol (E2) and the number of developing follicles during the administration of exogenous follicle-stimulating hormone (FSH) in various regimens in normo-ovulatory volunteers and to evaluate if inhibins act as suitable markers for the number of developing follicles during ovarian stimulation. Design and methods: Serial hormone determinations and assessment of follicle numbers were carried out during unstimulated cycles and during various interventions with exogenous FSH. Subjects were randomi

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Campbell, BK, and DT Baird. "Inhibin A is a follicle stimulating hormone-responsive marker of granulosa cell differentiation, which has both autocrine and paracrine actions in sheep." Journal of Endocrinology 169, no. 2 (2001): 333–45. http://dx.doi.org/10.1677/joe.0.1690333.

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The aim of these studies was to examine the origin, control and local actions of inhibin A in monovular species, using the sheep as a model. Experiment 1 examined the pattern of mRNA expression for the inhibin subunits in relation to follicular size and pattern of expression to other differentiative markers in granulosa (P450 aromatase) and thecal cells (P450 17alpha-hydroxylase). Experiment 2 examined the pattern of inhibin A production, in relation to oestradiol, by granulosa cells induced to differentiate in vitro with follicle-stimulating hormone (FSH). Experiment 3 examined possible parac

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Nishi, Yoshihiro, Masafumi Haji, Ryoichi Takayanagi, Toshihiko Yanase, Shoichiro Ikuyama, and Hajime Nawata. "In vivo and in vitro evidence for the production of inhibin-like immunoreactivity in human adrenocortical adenomas and normal adrenal glands: relatively high secretion from adenomas manifesting Cushing's syndrome." European Journal of Endocrinology 132, no. 3 (1995): 292–99. http://dx.doi.org/10.1530/eje.0.1320292.

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Nishi Y, Haji M, Takayanagi R, Yanase T, Ikuyama S, Nawata H. In vivo and in vitro evidence for the production of inhibin-like immunoreactivity in human adrenocortical adenomas and normal adrenal glands: relatively high secretion from adenomas manifesting Cushing's syndrome. Eur J Endocrinol 1995;132:292–9. ISSN 0804–4643 To clarify whether adrenal gland secretes inhibin in vivo in physiological or pathological conditions, we measured the levels of inhibin-like immunoreactivity (inhibin-LI) in adrenal veins (A-vein) and compared them with those in inferior vena cava (IVC) using blood samples o

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Vanttinen, T., J. Liu, T. Kuulasmaa, P. Kivinen, and R. Voutilainen. "Expression of activin/inhibin signaling components in the human adrenal gland and the effects of activins and inhibins on adrenocortical steroidogenesis and apoptosis." Journal of Endocrinology 178, no. 3 (2003): 479–89. http://dx.doi.org/10.1677/joe.0.1780479.

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Activins and inhibins are structurally related glycoprotein hormones modulating pituitary FSH secretion and gonadal steroidogenesis. Activins and inhibins are also produced in the adrenal cortex where their physiological role is poorly known. Hormonally active human adrenocortical tumors express and secrete inhibins, while in mice adrenal inhibins may function as tumor suppressors. To clarify the significance of adrenal activins and inhibins we investigated the localization of activin/inhibin signaling components in the adrenal gland, and the effects of activins and inhibins on adrenocortical

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Li, C. H., and K. Ramasharma. "Inhibin." Annual Review of Pharmacology and Toxicology 27, no. 1 (1987): 1–21. http://dx.doi.org/10.1146/annurev.pa.27.040187.000245.

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Burger, Henry G. "Inhibin." Reproductive Medicine Review 1, no. 1 (1992): 1–20. http://dx.doi.org/10.1017/s0962279900000417.

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Inhibin is a glycoprotein hormone, consisting of two dissimilar, disulphide-linked subunits, termed α (MW 20kD) and β (MW 3-15kD), which inhibits the production and/or secretion of pituitary gonadotrophins, preferentially follicle stimulating hormone (FSH). The most widely studied inhibin molecule has a molecular weight of 31-32kD, as purified and cloned from bovine, porcine, ovine, rat and human sources. Higher molecular weight forms have been identified in ovarian follicular fluids and in culture media of granulosa and Sertoli cells, and generally differ from the 31kD form in having larger α

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30

de Kretser, David M. "Inhibin." Molecular and Cellular Endocrinology 69, no. 2-3 (1990): C17—C20. http://dx.doi.org/10.1016/0303-7207(90)90001-o.

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31

De Jong, F. H. "Inhibin." Physiological Reviews 68, no. 2 (1988): 555–607. http://dx.doi.org/10.1152/physrev.1988.68.2.555.

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Inhibin has been defined as a gonadal hormone that exerts a specific negative feedback action on the secretion of FSH from the gonadotropic cells of the pituitary gland. The existence of inhibin was postulated as early as 1923 (250). However, only after reliable and sensitive bioassay systems for the detection and estimation of inhibin had been developed and an ample source of inhibin was found in the form of ovarian follicular fluid has progress been made in the isolation and characterization of the hormone. It is apparent now that inhibin, which itself consists of a dimer of two different su

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McNeilly, A. S., C. G. Tsonis, and D. T. Baird. "Inhibin." Human Reproduction 3, no. 1 (1988): 45–49. http://dx.doi.org/10.1093/oxfordjournals.humrep.a136650.

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33

Robertson, DM, LM Foulds, Vos F. de, L. Leversha, and Kretser DM de. "Identification of inhibin and inhibin-related proteins in human follicular fluid." Reproduction, Fertility and Development 2, no. 4 (1990): 327. http://dx.doi.org/10.1071/rd9900327.

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Inhibin-related proteins were identified in human follicular fluid following fractionation by gel permeation chromatography under neutral and acidic conditions, reversed-phase high performance liquid chromatography (HPLC) and preparative polyacrylamide gel electrophoresis. A number of molecular mass forms of inhibin (30-36 and 59-66 kDa) based on their in vitro biological and immunological activities were identified, of which 59-66 kDa inhibin was the predominant form. Bioactive fractions devoid of inhibin immunoactivity were also identified with molecular masses of 46 and 55 kDa. Based on the

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34

CHRISTENSEN, RICHARD B., ROBERT G. FORAGE, ROBERT A. STEINER, and WILLIAM J. BREMNER. "Effects of Castration and Recombinant Human Inhibin Administration on Circulating Levels of Inhibin and Gonadotropins in Adult Male Monkeys." Journal of Andrology 15, no. 2 (1994): 125–31. http://dx.doi.org/10.1002/j.1939-4640.1994.tb00415.x.

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ABSTRACT: Inhibin has been suggested to play a role in gonadal feedback regulation of follicle‐stimulating hormone (FSH) secretion; however, neither the half‐life nor the time course of action of recombinant inhibin has been reported in any primate species. We sought to determine the disappearance half‐life of circulating endogenous inhibin following castration in adult male monkeys, Macaca fascicularis, and to determine the half‐life of administered recombinant human inhibin A and its effect on bioactive FSH and luteinizing hormone (LH) levels in castrate monkeys. Endogenous inhibin fell from

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Munro, LM, A. Kennedy, and AM McNicol. "The expression of inhibin/activin subunits in the human adrenal cortex and its tumours." Journal of Endocrinology 161, no. 2 (1999): 341–47. http://dx.doi.org/10.1677/joe.0.1610341.

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Inhibins and activins are dimeric proteins of the transforming growth factor-beta superfamily which have been shown to be expressed in the adrenal cortex. Recent studies have suggested a role for these peptides in the pathogenesis and/or function of adrenal tumours. To investigate further their physiological and pathological roles, we have documented immunoreactivity for inhibin alpha, betaA and betaB subunits in normal adult and fetal human adrenals, in hyperplastic adrenals and in adrenal tumours. In the normal and hyperplastic adult gland, diffuse immunopositivity was demonstrated for beta

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Farnworth, P. G., Y. Wang, G. T. Ooi, and J. K. Findlay. "125. Differential regulation of inhibin binding via betaglycan expression in several mouse cell lines." Reproduction, Fertility and Development 16, no. 9 (2004): 125. http://dx.doi.org/10.1071/srb04abs125.

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Inhibin A, a member of the transforming growth factor (TGF)-β superfamily, binds to mouse adrenocortical (AC), Leydig (TM3) and Sertoli (TM4) cell lines with high affinity via at least eight membrane protein species, two of which are forms of betaglycan. Inhibin A has been proposed to inhibit the actions of activin and BMP by sequestering their type II receptors in high affinity complexes with betaglycan (1). We previously found that BMPs appear to counteract inhibin action in AC cells by selectively suppressing the expression of endogenous betaglycan, consequently reducing inhibin binding. In

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Yamaguchi, M., K. Tasaka, K. Ogura, M. Sakata, J. Mizuki, and A. Miyake. "Activin inhibits but inhibin activates mouse placental lactogen-II secretion." Journal of Endocrinology 146, no. 3 (1995): 469–74. http://dx.doi.org/10.1677/joe.0.1460469.

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Abstract The regulation of mouse placental lactogen (mPL)-I and mPL-II secretion by activin and inhibin and the expression of activin and inhibin subunit mRNAs in the mouse decidua were examined. Activin-A at a concentration of 10 nm/l significantly inhibited mPL-II secretion by placental cells from days 9 and 12 of pregnancy. However, activin-A did not affect mPL-I secretion by cells from days 7 and 9 of pregnancy nor mPL-II secretion by cells from day 7 of pregnancy. By contrast, 10 nm/l inhibin activated mPL-II secretion by cells from day 12 of pregnancy. These effects of activin and inhibi

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Risbridger, G. P., T. Thomas, C. J. Gurusinghe, and J. R. McFarlane. "Inhibin-related proteins in rat prostate." Journal of Endocrinology 149, no. 1 (1996): 93–99. http://dx.doi.org/10.1677/joe.0.1490093.

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Abstract Inhibin and activin are members of the transforming growth factor β (TGFβ) family which can regulate cell proliferation in a number of tissues. The presence of inhibins and the related proteins, activins, in the prostate has been implicated by the detection of activin type II receptors. The aim of this study was to determine whether or not immunoactive (ir) inhibin and ir-activin are present in the rat prostate and to study the acute regulation by androgens. The results showed that mRNAs for the α and β inhibin subunits were detected in rat prostate by reverse transcription-PCR togeth

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Xu, Huitao, Adnan Khan, Shanjiang Zhao, et al. "Effects of Inhibin A on Apoptosis and Proliferation of Bovine Granulosa Cells." Animals 10, no. 2 (2020): 367. http://dx.doi.org/10.3390/ani10020367.

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Inhibin A is well known for its inhibitory properties against follicle-stimulating hormone (FSH), released through a pituitary–gonadal negative feedback loop to regulate follicular development. Ovarian folliculogenesis, hormonal biosynthesis, and gametogenesis are dependent on inhibins, playing vital roles in promoting or inhibiting cell proliferation. The present study explored the physiological and molecular response of bovine granulosa cells (GCs) to different concentrations of inhibin A in vitro. We treated the primary GCs isolated from ovarian follicles (3–6 mm) with different levels of i

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Buzzard, Jeremy J., Kate L. Loveland, Moira K. O’Bryan, et al. "Changes in Circulating and Testicular Levels of Inhibin A and B and Activin A During Postnatal Development in the Rat." Endocrinology 145, no. 7 (2004): 3532–41. http://dx.doi.org/10.1210/en.2003-1036.

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Abstract This study describes the testicular levels of inhibin/activin subunits by Northern analysis and in situ hybridization and serum and testicular levels of inhibins A and B and activin A by enzyme linked immunosorbent assays (ELISA) during postnatal development in the rat. We show that serum inhibin A levels are less than 4 pg/ml throughout postnatal life. Serum inhibin B levels peak at 572 ± 119 pg/ml (mean ± se) at d 40 post partum (pp) before falling to 182 ± 35 pg/ml in mature males. Serum activin A decreases from 294 ± 29 pg/ml at d 6 to 132 ± 27 pg/ml at maturity. Within the testis

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Escalona, R., Y. Wang, G. T. Ooi, J. K. Findlay, and P. G. Farnworth. "118. Regulation of inhibin binding and action via betaglycan expression in mouse Leydig-like TM3 cells." Reproduction, Fertility and Development 17, no. 9 (2005): 73. http://dx.doi.org/10.1071/srb05abs118.

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The actions of inhibin and transforming growth factor (TGF)-β2 are enhanced when their respective target cells express the TGF-β/inhibin co-receptor, betaglycan. In the present studies, we investigated the effects of multiple members of the TGF-β superfamily on betaglycan expression, and examined the consequences of such regulation for inhibin binding, and inhibin and TGF-β actions in mouse Leydig-like TM3 cells. Isoforms of activin (A and B), TGF-β (1 and 2) and BMP (2, 6 and 7) each suppressed the level of betaglycan mRNA in TM3 cells to 43–46%, 26–39% and 50–71% of control, respectively, du

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Young, J. M., S. Henderson, C. Souza, H. Ludlow, N. Groome, and A. S. McNeilly. "Activin B is produced early in antral follicular development and suppresses thecal androgen production." REPRODUCTION 143, no. 5 (2012): 637–50. http://dx.doi.org/10.1530/rep-11-0327.

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Little is known about the role of activin B during folliculogenesis. This study investigated the expression levels of activin/inhibin subunits (βA, βB, and α), steroid enzyme, and gonadotrophin receptors in theca (TC) and granulosa cells (GC) by QPCR and activin A and B and inhibin A protein levels in follicular fluid (FF) of developing sheep follicles during estrus and anestrus. The effect of activin B on androgen production from primary TC cultures in vitro was also assessed. During folliculogenesis, in anestrus and estrus, FF activin B concentrations and thecal and GC activin βB mRNA levels

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Jones, R. L., P. Paiva, T. J. Kaitu'u, and L. A. Salamonsen. "249.Activin A upregulates endometrial metalloproteases: potential mechanisms for promotion of decidualisation and implantation." Reproduction, Fertility and Development 16, no. 9 (2004): 249. http://dx.doi.org/10.1071/srb04abs249.

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Activin and inhibin subunits are co-expressed by human endometrial epithelial and decidualised stromal cells. Activin A is a potent stimulator of decidualisation in vitro, but the mechanisms are unknown. Matrix metalloproteases (MMPs) are known to be important during decidualisation, as administration of a broad spectrum MMP inhibitor in the rat results in reduced decidualisation. Transforming Growth Factor(TGF)-βs are closely related to activins and inhibit MMP production in endometrial epithelial cells. We hypothesised that activins regulate MMP production during decidualisation and/or troph

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Abdulkadyrova, Zarina K., Maria I. Yarmolinskaya, Alexander M. Gzgzyan, Lyailya Kh Dzhemlikhanova, and Elena I. Abashova. "Inhibin as a reproductive biomarker part 2. Clinical significance of inhibins in reproductive medicine." Journal of obstetrics and women's diseases 68, no. 5 (2019): 91–106. http://dx.doi.org/10.17816/jowd68591-106.

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In the early 2000s, the determination of inhibin levels was used actively for the diagnosis of ovarian tumors, as a diagnostic marker for prenatal screening of Down syndrome, as well as a prognostic marker for ovarian reserve when conducting assisted reproductive technologies. However, to date, inhibin is rarely used as a marker for reproductive function. At the same time, numerous studies of recent years indicate the crucial role of inhibin in folliculogenesis and spermatogenesis, as well as in implantation and placentation. This allows to significantly expand the diagnostic spectrum of inhib

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Jaatinen, Risto, Jonas Bondestam, Taneli Raivio та ін. "Activation of the Bone Morphogenetic Protein Signaling Pathway Induces Inhibin βB-Subunit mRNA and Secreted Inhibin B Levels in Cultured Human Granulosa-Luteal Cells". Journal of Clinical Endocrinology & Metabolism 87, № 3 (2002): 1254–61. http://dx.doi.org/10.1210/jcem.87.3.8314.

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During the human menstrual cycle the circulating levels of inhibin B, a dimer of inhibin α- and βB-subunits, fluctuate in a fashion distinct from that of inhibin A, the α-βA-subunit dimer. This suggests that human inhibin subunits are each regulated in a distinct manner in human ovarian granulosa cells by endocrine and local factors. We have previously shown using cultures of human granulosa-luteal (hGL) cells that gonadotropins stimulate the steady state mRNA levels of inhibin α- and βA-subunits, but not those of the βB-subunit, which, on the other hand, are up-regulated by, for instance, act

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Risbridger, Gail P., Jacqueline F. Schmitt, and David M. Robertson. "Activins and Inhibins in Endocrine and Other Tumors." Endocrine Reviews 22, no. 6 (2001): 836–58. http://dx.doi.org/10.1210/edrv.22.6.0450.

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Abstract Inhibin and activin are members of the TGFβ superfamily of growth and differentiation factors. They were first identified as gonadal-derived regulators of pituitary FSH and were subsequently assigned multiple actions in a wide range of tissues. More recently, the inhibin α subunit was considered as a tumor suppressor based on functional studies employing transgenic mouse models. This review evaluates the functional and molecular evidence that the inhibin α subunit is a tumor suppressor in endocrine cancers. The evaluation highlights the discrepant results from the human and mouse stud

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Hofmann, Glen E., Douglas R. Danforth, and David B. Seifer. "Inhibin-B." Obstetrical & Gynecological Survey 53, no. 8 (1998): 488–89. http://dx.doi.org/10.1097/00006254-199808000-00019.

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Segal, Shimon, Chista Safajou, Steven Karp, Ray Mercado, Korina Veenstra, and Benjamin Rivnay. "Inhibin-A." Obstetrics & Gynecology 107, Supplement (2006): 35S. http://dx.doi.org/10.1097/00006250-200604001-00081.

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Hogan, Brigid L. M. "Inhibiting inhibin." Current Biology 3, no. 3 (1993): 170–72. http://dx.doi.org/10.1016/0960-9822(93)90263-n.

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Fetsch, Patricia A., Celeste N. Powers, Maureen F. Zakowski, and Andrea Abati. "Anti-?-inhibin." Cancer 87, no. 3 (1999): 168–72. http://dx.doi.org/10.1002/(sici)1097-0142(19990625)87:3<168::aid-cncr11>3.0.co;2-v.

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