Relevant bibliographies by topics / Steroid hormones Cellular control mechanisms

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Academic literature on the topic 'Steroid hormones Cellular control mechanisms'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Steroid hormones Cellular control mechanisms"

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Labus, Jennifer S., Emeran A. Mayer, Kjersti Aagaard, Jean Stains, Katarzyna Broniowska, and Andrea Rapkin. "Reduced concentrations of vaginal metabolites involved in steroid hormone biosynthesis are associated with increased vulvar vestibular pain and vaginal muscle tenderness in provoked vestibulodynia: An exploratory metabolomics study." Molecular Pain 17 (January 2021): 174480692110418. http://dx.doi.org/10.1177/17448069211041853.

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Provoked vestibulodynia (PVD) is a chronic vulvar pain disorder characterized by hypersensitivity and severe pain with pressure localized to the vulvar vestibule. Knowledge regarding pathophysiological mechanisms contributing to the etiology and production of symptoms in PVD remains incomplete but is considered multifactorial. Using a cross-sectional observational study design, data from untargeted metabolomic profiling of vaginal fluid and plasma in women with PVD and healthy women was combined with pain testing and brain imaging in women with PVD to test the hypotheses that women with PVD compared to healthy women show differences in vaginal and plasma metabolites involved in steroid hormone biosynthesis. Steroid hormone metabolites showing group differences were correlated with vulvar vestibular pain and vaginal muscle tenderness and functional connectivity of brain regions involved in pain processing in women with PVD to provide insight into the functional mechanisms linked to the identified alterations. Sensitivity analyses were also performed to determine the impact of hormonal contraceptive use on the study findings. Women with PVD compared to healthy controls had significant reductions primarily in vaginal fluid concentrations of androgenic, pregnenolone and progestin metabolites involved in steroidogenesis, suggesting localized rather than systemic effects in vagina and vulvar vestibule. The observed reductions in androgenic metabolite levels showed large effect size associations with increased vulvar vestibular pain and vulvar muscle tenderness and decreases in androgenic and progestin metabolites were associated with decreased connectivity strength in primary sensorimotor cortices. Women with PVD showed symptom-associated reductions in vaginal fluid concentrations of metabolites involved in the biosynthesis of steroid hormones previously shown to affect the integrity of vulvar and vaginal tissue and nociceptive processing. Deficiency of certain steroids may be an important mechanism contributing to the pathophysiology of symptoms in PVD may provide potential diagnostic markers that could lead to new targets for therapeutic intervention.
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Habener, J. F. "Regulation of polypeptide-hormone biosynthesis at the level of the genome." American Journal of Physiology-Cell Physiology 249, no. 3 (September 1, 1985): C191—C199. http://dx.doi.org/10.1152/ajpcell.1985.249.3.c191.

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Understanding of gene control mechanisms has greatly accelerated largely due to the application of recombinant DNA techniques. Polypeptide hormone genes encode multiexonic-intronic transcriptional sequences, the exons of which in turn encode polyprotein precursors or prohormones from which the hormones are cleaved during posttranslational processing of the prohormones. Transcriptional processes are regulated by at least two qualitatively different modes of gene regulation. The first mode includes the factors and structural components of a gene that determine whether a gene can or cannot be expressed in a given tissue when the appropriate inducer is present. The second mode is the physiological induction and regulation of the gene that can normally be expressed in a particular tissue. Both cis and trans regulatory mechanisms appear to operate in both tissue-specific expression and physiological regulation. Tissue-specific enhancer sequences consisting of short nucleotide sequences of from 10 to 50 base pairs have been identified in or around genes that are expressed in specific tissues. In many instances trans-acting DNA binding proteins have been found to repress or activate the transcription of the genes. Physiological regulation of hormone genes involves at least two different classes of macromolecules, steroid hormone receptors and phosphoproteins that are formed in response to the binding of ligands to specific surface-located receptors. Although the precise mechanisms by which information encoded in cellular effectors is coupled to cellular responses is incomplete, continued investigations should lead to a more complete understanding of gene control mechanisms and the eventual ability to alter the expression of specific genes.
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Mullany, Lisa K., Eric A. Hanse, Andrea Romano, Charles H. Blomquist, J. Ian Mason, Bert Delvoux, Chelsea Anttila, and Jeffrey H. Albrecht. "Cyclin D1 regulates hepatic estrogen and androgen metabolism." American Journal of Physiology-Gastrointestinal and Liver Physiology 298, no. 6 (June 2010): G884—G895. http://dx.doi.org/10.1152/ajpgi.00471.2009.

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Cyclin D1 is a cell cycle control protein that plays an important role in regenerating liver and many types of cancer. Previous reports have shown that cyclin D1 can directly enhance estrogen receptor activity and inhibit androgen receptor activity in a ligand-independent manner and thus may play an important role in hormone-responsive malignancies. In this study, we examine a distinct mechanism by which cyclin D1 regulates sex steroid signaling, via altered metabolism of these hormones at the tissue and cellular level. In male mouse liver, ectopic expression of cyclin D1 regulated genes involved in the synthesis and degradation of sex steroid hormones in a pattern that would predict increased estrogen and decreased androgen levels. Indeed, hepatic expression of cyclin D1 led to increased serum estradiol levels, increased estrogen-responsive gene expression, and decreased androgen-responsive gene expression. Cyclin D1 also regulated the activity of several key enzymatic reactions in the liver, including increased oxidation of testosterone to androstenedione and decreased conversion of estradiol to estrone. Similar findings were seen in the setting of physiological cyclin D1 expression in regenerating liver. Knockdown of cyclin D1 in HuH7 cells produced reciprocal changes in steroid metabolism genes compared with cyclin D1 overexpression in mouse liver. In conclusion, these studies establish a novel link between the cell cycle machinery and sex steroid metabolism and provide a distinct mechanism by which cyclin D1 may regulate hormone signaling. Furthermore, these results suggest that increased cyclin D1 expression, which occurs in liver regeneration and liver diseases, may contribute to the feminization seen in these settings.
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Gellersen, B., and J. Brosens. "Cyclic AMP and progesterone receptor cross-talk in human endometrium: a decidualizing affair." Journal of Endocrinology 178, no. 3 (September 1, 2003): 357–72. http://dx.doi.org/10.1677/joe.0.1780357.

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During the menstrual cycle, the ovarian hormones oestradiol and progesterone control the ordered growth and differentiation of uterine cells. This remodelling process is critical for implantation of the developing embryo, the formation of the placenta, and maintenance of pregnancy. Failure of uterine tIssues to respond appropriately to ovarian hormone signalling results in defective placentation, associated with a spectrum of pregnancy disorders such as recurrent miscarriages and preeclampsia. These obstetrical disorders are a major cause of maternal and perinatal morbidity and mortality. Progesterone exerts its action on target cells, at least in part, through binding to the progesterone receptor (PR), a member of the steroid/thyroid hormone receptor superfamily of ligand-activated transcription factors. The mechanism by which progesterone controls the differentiation of human endometrial stromal cells, a process termed decidualization, in the secretory phase of the menstrual cycle is not well understood. Emerging evidence indicates that locally expressed factors and activation of the cAMP second messenger pathway integrate hormonal inputs and confer cellular specificity to progesterone action through the induction of diverse transcription factors capable of modulating PR function.
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Dai, Long-Jun, Gordon Ritchie, Dirk Kerstan, Hyung Sub Kang, David E. C. Cole, and Gary A. Quamme. "Magnesium Transport in the Renal Distal Convoluted Tubule." Physiological Reviews 81, no. 1 (January 1, 2001): 51–84. http://dx.doi.org/10.1152/physrev.2001.81.1.51.

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The distal tubule reabsorbs ∼10% of the filtered Mg2+, but this is 70–80% of that delivered from the loop of Henle. Because there is little Mg2+reabsorption beyond the distal tubule, this segment plays an important role in determining the final urinary excretion. The distal convoluted segment (DCT) is characterized by a negative luminal voltage and high intercellular resistance so that Mg2+reabsorption is transcellular and active. This review discusses recent evidence for selective and sensitive control of Mg2+transport in the DCT and emphasizes the importance of this control in normal and abnormal renal Mg2+conservation. Normally, Mg2+absorption is load dependent in the distal tubule, whether delivery is altered by increasing luminal Mg2+concentration or increasing the flow rate into the DCT. With the use of microfluorescent studies with an established mouse distal convoluted tubule (MDCT) cell line, it was shown that Mg2+uptake was concentration and voltage dependent. Peptide hormones such as parathyroid hormone, calcitonin, glucagon, and arginine vasopressin enhance Mg2+absorption in the distal tubule and stimulate Mg2+uptake into MDCT cells. Prostaglandin E2and isoproterenol increase Mg2+entry into MDCT cells. The current evidence indicates that cAMP-dependent protein kinase A, phospholipase C, and protein kinase C signaling pathways are involved in these responses. Steroid hormones have significant effects on distal Mg2+transport. Aldosterone does not alter basal Mg2+uptake but potentiates hormone-stimulated Mg2+entry in MDCT cells by increasing hormone-mediated cAMP formation. 1,25-Dihydroxyvitamin D3, on the other hand, stimulates basal Mg2+uptake. Elevation of plasma Mg2+or Ca2+inhibits hormone-stimulated cAMP accumulation and Mg2+uptake in MDCT cells through activation of extracellular Ca2+/Mg2+-sensing mechanisms. Mg2+restriction selectively increases Mg2+uptake with no effect on Ca2+absorption. This intrinsic cellular adaptation provides the sensitive and selective control of distal Mg2+transport. The distally acting diuretics amiloride and chlorothiazide stimulate Mg2+uptake in MDCT cells acting through changes in membrane voltage. A number of familial and acquired disorders have been described that emphasize the diversity of cellular controls affecting renal Mg2+balance. Although it is clear that many influences affect Mg2+transport within the DCT, the transport processes have not been identified.
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Shramko, S. V., V. N. Zorina, N. A. Zorin, I. A. Botvinyeva, S. V. Arkhipova, and V. V. Likhacheva. "INTERRELATION OF STEROID RECEPTOR GENE EXPRESSION IN UTERINE TISSUES AND SERUM CONCENTRATIONS OF IMMUNOREGULATORY PROTEINS, CYTOKINES, SEX STEROIDS IN PROLIFERATIVE DISEASES." Medical Immunology (Russia) 20, no. 5 (November 6, 2018): 731–38. http://dx.doi.org/10.15789/1563-0625-2018-5-731-738.

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Pathogenetic mechanisms of uterine leiomyoma, adenomyosis and their combination are complicated and poorly understood, a differential diagnosis of leiomyosarcoma of the uterus is difficult. Our study aimed for a comparative analysis of the serum contents of α2-MG, PAG, some cytokines, sex steroids and the expression of steroid receptor genes in the patients with different variants of uterine proliferative diseases, in order to determine their pathological role, diagnostic and prognostic value. Expression of estrogen receptor genes adenomyosis nodes was 1.5 to 2-fold higher than in leiomyoma, the combined pathology showed intermediate values, and expression of ER and PGR genes in leiomyosarcoma was minimal. In cellular leiomyoma, expression of ER receptor genes in the surrounding myometrium was 2 to 3-fold higher than in cases of simple leiomyomas. At the same time, concentration of estrogen and progesterone in the blood is comparable between the groups and control groups. All the patients have a deficiency of immunomodulatory α2-MG (12-13% for leiomyomas, 20% for adenomyosis, and 23% for malignant pathology). The concentration of immunosuppressive PAG is increased in combined conditions and leiomyosarcoma. In addition, the contents of IL-6 and TNFα increase, the VEGF levels exceed normal values 4 to 4.5-fold, in leiomyoma, 5.5-fold, in combined pathology, 6.5, in adenomyosis, and 10-fold, in leiomyosarcoma.The obtained results confirm that immunomodulatory proteins, cytokines and cell-targeting sex hormones exert an interdependent influence upon each other in the studied diseases, and their significant changes may be used in diagnostics and prognosis.
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Parker, Joseph, and Gary Struhl. "Control of Drosophila wing size by morphogen range and hormonal gating." Proceedings of the National Academy of Sciences 117, no. 50 (November 30, 2020): 31935–44. http://dx.doi.org/10.1073/pnas.2018196117.

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The stereotyped dimensions of animal bodies and their component parts result from tight constraints on growth. Yet, the mechanisms that stop growth when organs reach the right size are unknown. Growth of the Drosophila wing—a classic paradigm—is governed by two morphogens, Decapentaplegic (Dpp, a BMP) and Wingless (Wg, a Wnt). Wing growth during larval life ceases when the primordium attains full size, concomitant with the larval-to-pupal molt orchestrated by the steroid hormone ecdysone. Here, we block the molt by genetically dampening ecdysone production, creating an experimental paradigm in which the wing stops growing at the correct size while the larva continues to feed and gain body mass. Under these conditions, we show that wing growth is limited by the ranges of Dpp and Wg, and by ecdysone, which regulates the cellular response to their signaling activities. Further, we present evidence that growth terminates because of the loss of two distinct modes of morphogen action: 1) maintenance of growth within the wing proper and 2) induced growth of surrounding “pre-wing” cells and their recruitment into the wing. Our results provide a precedent for the control of organ size by morphogen range and the hormonal gating of morphogen action.
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Wang, Xun, Yongheng Huang, Shiwen Yuan, Amin Tamadon, Shulan Ma, and Yi Feng. "The Role of Hippocampal Estradiol Receptor-αin a Perimenopausal Affective Disorders-Like Rat Model and Attenuating of Anxiety by Electroacupuncture." Evidence-Based Complementary and Alternative Medicine 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/4958312.

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Hormone replacement therapy is the principal treatment for perimenopausal affective disorders which can cause severe side effects. The present study compared the effects of electroacupuncture (EA) and estradiol treatment on perimenopausal affective disorders at the behavioral and cellular levels. In this randomized experimentalin vivostudy, adult female rats were divided into intact, ovariectomy, chronic unpredictable stress (CUS), and ovariectomy and CUS combination groups. After week 6, all groups were subdivided to three subgroups of control, EA, and estradiol treatment. The behavioral parameters in the open field and the elevated plus maze tests were assessed before and after treatments. Alterations of serum steroid hormones and changes of estradiol receptor-α(ER-α) immunofluorescence neurons in the hippocampus sections were evaluated. EA treatment caused more antianxiety effects than estradiol treatment in CUS group (P<0.05). Notably, estradiol and EA treatments had better significant behavioral effects when the models were not estrogen-deficient. Importantly, within each group, compared to the control group, the numbers of ER-α-positive neurons were significantly larger in EA subgroups. Therefore, EA had antianxiety effects on perimenopausal affective disorders caused by CUS but not by estrogen deficiency and upregulation of hippocampus ER-αneurons may contribute to its mechanism of action.
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Stasinopoulos, Ioannis, Shazia Khan, Logan C. MacKay, Roger W. Brown, Matthew J. Bailey, and Ruth Andrew. "Mapping of Corticosteroids in Murine Kidneys Using Mass Spectrometry Imaging." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A822—A823. http://dx.doi.org/10.1210/jendso/bvab048.1676.

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Abstract Renal sodium reabsorption is important for blood pressure homeostasis and is physiologically regulated by aldosterone; glucocorticoids may also contribute. Abnormal steroid hormone activity within the kidney contributes to hypertension but the mechanisms are not fully defined. Molecular profiling of receptors and metabolising enzymes indicates that steroid hormone action is compartmentalised within the kidney. Ambient steroid concentrations are a critical factor governing bioactivity at a cellular level, but this is largely unknown, and the kidney remains a “black box”. Mass spectrometry imaging (MSI) was applied recently to localise steroids in brain and testes, and here is applied to kidney. Image reconstruction permits characterisation and co-registration of kidney histological regions based on regional markers detectable by MSI. Our aim was to map and quantify glucocorticoids and aldosterone in different histological zones (cortex, medulla) of murine kidneys, using an optimised MSI method. This approach has the potential to map steroids within functional zones of the kidney, providing fundamental new information relevant to hormone action in health and in disease. Cryosections of male C57BL6 mouse kidneys (age 12 weeks, n=6) were subject to MSI following derivatisation using Girard T reagent and α-cyano-4-hydroxycinnamic acid matrix application. Images were reconstructed, and methods optimised to enhance signal and limit diffusion of analytes of interest. Matrix assisted laser desorption/ionisation (MALDI) was used as a sampling method, coupled to Fourier Transform Ion cyclotron mass spectrometry. Ions with m/z 458.3010, 460.3166 and 474.2957 were detected, using MALDI, in renal sections, close to the predicted masses of 458.3013 (Δppm=0.65), 460.3169 (Δppm=0.65), and 474.2962 (Δppm=1.05), for derivatives of 11-dehydrocorticosterone, corticosterone and aldosterone respectively. Untargeted evaluation of ions was conducted to find regional markers that would allow definition of kidney histological zones. The Heat maps generated indicated that corticosterone intensity was higher in the inner cortex area close to the corticomedullary junction than the rest of the kidney. In contrast 11-dehydrocorticosterone was detected mainly in medulla and aldosterone signal was equally strong in medulla and outer cortex. Thus, MSI can be used map the sites where glucocorticoid and mineralocorticoids are most active in regulating renal tubular function. Co-localisation of steroids of interest with zonal markers by MSI permits steroid mapping in functional renal zones of the kidney. This approach provides fundamental new insights into the physiological control of sodium transport by steroids and opens doors to understanding changes in disorders of blood pressure. The project was supported and funded by Kidney Research UK.
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Charlier, Thierry D., Charlotte A. Cornil, and Jacques Balthazart. "Rapid Modulation of Aromatase Activity in the Vertebrate Brain." Journal of Experimental Neuroscience 7 (January 2013): JEN.S11268. http://dx.doi.org/10.4137/jen.s11268.

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Numerous steroid hormones, including 17β-estradiol (E2), activate rapid and transient cellular, physiological, and behavioral changes in addition to their well-described genomic effects. Aromatase is the key-limiting enzyme in the production of estrogens, and the rapid modulation of this enzymatic activity could produce rapid changes in local E2 concentrations. The mechanisms that might mediate such rapid enzymatic changes are not fully understood but are currently under intense scrutiny. Recent studies in our laboratory indicate that brain aromatase activity is rapidly inhibited by an increase in intracellular calcium concentration resulting from potassium-induced depolarization or from the activation of glutamatergic receptors. Phosphorylating conditions also reduce aromatase activity within minutes, and this inhibition is blocked by the addition of multiple protein kinase inhibitors. This rapid modulation of aromatase activity by phosphorylating conditions is a general mechanism observed in different cell types and tissues derived from a variety of species, including human aromatase expressed in various cell lines. Phosphorylation processes affect aromatase itself and do not involve changes in aromatase protein concentration. The control of aromatase activity by multiple kinases suggests that several amino acids must be concomitantly phosphorylated to modify enzymatic activity but site-directed mutagenesis of several amino acids alone or in combination has not to date revealed the identity of the targeted residue(s). Altogether, the phosphorylation processes affecting aromatase activity provide a new general mechanism by which the concentration of estrogens can be rapidly altered in the brain.
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Dissertations / Theses on the topic "Steroid hormones Cellular control mechanisms"

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Witcher, Michael. "Interaction of the anti-apoptotic protein BAG-1 with the vitamin D receptor." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0010/MQ52698.pdf.

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Pelletier, Diane Beatrice. "Identification and partial biological characterization of autocrine growth inhibitory activity in Nb2 lymphoma cell conditioned medium." Diss., The University of Arizona, 1990. http://hdl.handle.net/10150/185002.

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The purpose of these studies was to determine whether lactogen-dependent Nb2-11c cells and lactogen-independent Nb2-SP cells differ with respect to morphology and autocrine growth control. To this end, the ultrastructural and surface morphology of both Nb2 cell lines was analyzed and the autocrine growth modulatory activity of Nb2 cell conditioned medium (Nb2-CM) was determined. The autocrine growth inhibitory activity of Nb2-CM was biologically characterized and attempts were made to biochemically characterize and purify the Nb2 cell autocrine growth inhibitor as well as to determine its mechanism of action. Quantitative analysis of transmission electron micrographs reveals that the ultrastructural morphology of lactogen-dependent Nb2-11c cells differs from that of lactogen-independent Nb2-SP cells. Nb2-11c cells exhibit a greater incidence and volume density of nuclear pockets, whereas the incidence and volume density of lipid droplets is greater in the Nb2-SP cell line. Surface feature of Nb2-11c and Nb2-SP cells, as examined with scanning electron microscopy, and indistinguishable. Nb2-11c and Nb2-SP cells share a common mode of growth control in the form of constitutive secretion of an autocrine inhibitory factor. Medium conditioned by either Nb2-11c or Nb2-SP cells inhibits the growth of both cell lines. Nb2-CM-mediated growth inhibition is dose-dependent and reversible. Nb2-CM does not induce quiescence or cell death, but rather, causes a delay in the progression of cells through all phases of the cell cycle. Nb2 cell proliferation stimulated by a variety of mitogens is inhibited by Nb2-CM. Nb2-CM also has the ability to inhibit the growth of normal rat splenocytes as well as MCF-7 human breast cancer cells. Biochemical analysis of Nb2-CM was equivocal; however, indirect evidence suggests that the autocrine growth inhibitory factor produced by Nb2 cells may be a prostaglandin or another arachadonic acid metabolite since the growth inhibitory activity of Nb2-CM is reduced when CM is prepared in the presence of indomethacin. Interestingly, levels of prostaglandin F₁(α) are elevated in CM-treated culture supernatants. Examination of other signal transduction systems in Nb2 cells suggests that neither cAMP activation, polyamine biosynthesis, nor protein kinase C activation mediate or influence the inhibitory effect of Nb2-CM.
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Books on the topic "Steroid hormones Cellular control mechanisms"

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Inserm European Symposium on Hormones and Cell Regulation. (15th 1990 Mont Sainte-Odile, France). Hormones and cell regulation: Hormones et régulation cellulaire : proceedings of the 15th INSERM European Symposium on Hormones and Cell Regulation, held at Mont Sainte-Odile (France), September 24-27, 1990. Paris: Éditions INSERM, 1990.

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INSERM European Symposium on Hormones and Cell Regulation (15e 1990 Sainte-Odile, France). Hormones and cell regulation. Paris: INSERM, 1990.

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Inserm, European Symposium on Hormones and Cell Regulation (14th 1989 Sainte-Odile France). Hormones and cell regulation =: Hormones et régulation cellulaire ; proceedings of the 14th INSERM European Symposium on Hormones and Cell Regulation, held at Mont Sainte-Odile (France) ; sponsored by the Institut National de la Sainté et de la Recherche Médicale (INSERM). Paris: INSERM, 1989.

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Ernesto, Carafoli, Dumont Jacques E. 1931-, King R. J. B, Nunez J, and Institut national de la santé et de la recherche médicale (France), eds. Hormones and cell regulation: Hormones et régulation cellulaire : proceedings of the 10th INSERM European Symposium on Hormones and Cell Regulation, held at Sainte Odile, France, 29 September - 3 October, 1985. London: Libbey, 1986.

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Inserm European Symposium on Hormones and Cell Regulation (10th 1985 Sainte Odile). Hormones and cell regulation =: Hormones et régulation cellulaire ; proceedings of the 10th INSERM European Symposium on Hormones and Cell Regulation, held at Sainte Odile (France), 29 September - 3 October, 1985 ; sponsored by the Institut national de la santé et de la recherche médicale. Paris: INSERM, 1986.

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Inserm, European Symposium on Hormones and Cell Regulation (12th 1987 Mont Sainte-Odile France). Hormones and cell regulation =: Hormones et régulation cellulaire : proceedings of the 12th INSERM European Symposium on Hormones and Cell Regulation, held at Mont Sainte-Odile (France) ; sponsored by the Institut National de la Santé et de la Recherche Médicale (INSERM). London: Libbey, 1988.

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Inserm, European Symposium on Hormones and Cell Regulation (11th 1986 Sainte Odile France). Hormones and cell regulation =: Hormones et Regulation Cellulaire: Proceedings of the 11th INSERM European Symposium on Hormones and Cell Regulation, held at Sainte-Odile (France), 29 September-2 October, 1986. Paris: INSERM, 1987.

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1931-, Dumont Jacques E., Nunez J, and Institut national de la santé et de la recherche médicale (France), eds. Hormones and cell regulation =: Hormones et Regulation Cellulaire: Proceedings of the 14th INSERM European Symposium on Hormones and Cell Regulation, held at Mont Sainte-Odile (France), September 25-28, 1989. London: Libbey, 1989.

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Inserm European Symposium on Hormones and Cell Regulation (11th 1986 Sainte-Odile, France). Hormones and cell regulation =: Hormones et régulation cellulaire ; proceedings of the 11th INSERM European Symposium on Hormones and Cell Regulation, held at Sainte-Odile, (France), 29 September - 2 October 1986 ; sponsored by the Institute National de la Santé et de la Recherche. Paris: INSERM, 1987.

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Inserm European Symposium on Hormones and Cell Regulation (13th 1988 Sainte-Odile, France). Hormones and cell regulation. London: Paris : INSERM, 1989.

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Book chapters on the topic "Steroid hormones Cellular control mechanisms"

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Simpson, Paul C., Ken-ichi Kariya, Larry R. Karns, Carlin S. Long, and Joel S. Karliner. "Adrenergic hormones and control of cardiac myocyte growth." In Molecular Mechanisms of Cellular Growth, 35–43. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3886-8_5.

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"Hormones in Salmon." In Physiological Aspects of Imprinting and Homing Migration in Salmon, 20–48. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-7998-2054-3.ch002.

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Hormones are important signaling molecules produced and secreted in the endocrine system that show interesting close similarities between humans and salmon. They are transported to target organs where they bind to their receptors and control physiological regulation and behavioral activity to maintain homeostasis via feedback mechanisms. Various hormones control freshwater and seawater adaptations to maintain water and salt balances. The juvenile imprinting migration and adult homing migration of salmon are mainly controlled by the brain (thyrotropin-releasing hormone)-pituitary (thyrotropin)-thyroid (thyroid hormones) axis and the brain (gonadotropin-releasing hormone)-pituitary (gonadotropin)-gonad (steroid hormones) axis, respectively. This chapter describes hormone species and actions, hormonal control of freshwater and seawater adaptations, and hormonal changes during juvenile imprinting migration and adult homing migration in salmon.
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Hammes, Stephen R., and Carole R. Mendelson. "Mechanisms of Hormone Action." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0006.

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The capacity of a cell to respond to a particular hormone depends on the presence of cellular receptors specific for that hormone. After binding hormone, the receptor is biochemically and structurally altered, resulting in its activation; the activated receptor then mediates all of the actions of the hormone on the cell. The steroid and thyroid hormones as well as retinoids and 1,25-dihydroxyvitamin D3 diffuse freely through the lipophilic plasma membrane of the cell and interact with receptors that are primarily within the nucleus. On activation, the receptors alter the transcription of specific genes, resulting in changes in the levels of specific messenger RNAs (mRNAs), which are in turn translated into proteins. Hormones that are water soluble, such as the peptide and polypeptide hormones, catecholamines, and other neurotransmitters, as well as the relatively hydrophobic prostaglandins, interact with receptors in the plasma membrane. After hormone binding, the activated membrane receptors initiate signal transduction cascades that result in changes in enzyme activities and alterations in gene expression. In this chapter, the properties of various classes of receptors that are localized within the plasma membranes of target cells and the signal transduction mechanisms that mediate interactions with their ligands will first be addressed. This will be followed by consideration of the structural properties of the nuclear hormone receptors, the events that result in their activation, and the mechanisms whereby the activated nuclear receptors alter the expression of specific genes. Finally, a number of endocrine disorders that are caused by alterations in the number and/or function of plasma membranes and nuclear receptors will be reviewed. The function of a receptor is to recognize a particular hormone among all the molecules in the environment of the cell at a given time and, after binding the hormone, to transmit a signal that ultimately results in a biological response. Hormones are normally present in the circulation in extremely low concentrations, ranging from 10 –9 to 10 –11 M.
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Conference papers on the topic "Steroid hormones Cellular control mechanisms"

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Polstein, Lauren R., and Charles A. Gersbach. "Photoregulated Gene Expression in Human Cells With Light-Inducible Engineered Transcription Factors." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80573.

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Systems for controlling gene expression in mammalian cells have a wide range of applications in medicine, biotechnology and basic science. An ideal gene regulatory system would allow for precise and specific control over the magnitude and kinetics of gene expression in space and time, while also exerting minimal influence on other genes and cellular components. Several gene regulatory systems have been developed in which orthogonal transcription machinery from prokaryotes or insects has been imported into mammalian cells and used to control the expression of a specific gene. Despite the transformative impact of these systems in biomedical and biological research, several limitations of these technologies restrict the scope of possible applications. For example, gene expression in these systems is controlled by a freely diffusible small molecule, such as an antibiotic or steroid. Consequently, it is not possible to achieve spatial control over gene expression within cell culture, tissues, or whole organisms. This is in contrast to natural mechanisms of biological regulation in which spatial control is critical, such as developmental patterning and tissue morphogenesis. Second, dynamic gene regulation requires the removal of these small molecules, which may be slow, laborious, and/or impractical for a particular application. To overcome these limitations, we have engineered an optogenetic system in which the magnitude of gene expression in human cells can be finely tuned by photoregulated synthetic transcription factors.
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