Relevant bibliographies by topics / Nr5a1

Academic literature on the topic 'Nr5a1'

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Published: 6 July 2024

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Journal articles on the topic "Nr5a1":

1

Shi, Boyang, Huijie Lu, Lihong Zhang, and Weimin Zhang. "Nr5a1b promotes and Nr5a2 inhibits transcription of lhb in the orange-spotted grouper, Epinephelus coioides†." Biology of Reproduction 101, no. 4 (July 17, 2019): 800–812. http://dx.doi.org/10.1093/biolre/ioz121.

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Abstract Nr5a1 (Sf-1) up-regulates lhb expression across vertebrates; however, its regulatory roles on fshb remain to be defined. Moreover, the involvement of Nr5a2 in the regulation of gonadotropin expression is not clear either. In the present study, the involvement of Nr5a1b (a homologue of Nr5a1) and Nr5a2 in the regulation of lhb and fshb expression in the orange-spotted grouper was examined. Dual fluorescent immunohistochemistry using homologous antisera showed that in the pituitary of orange-spotted groupers, Lh cells contain both immunoreactive Nr5a1b and Nr5a2 signals, whereas Fsh cells contain neither of them. In LβT2 cells, Nr5a1b up-regulated basal activities of lhb and fshb promoters possibly via Nr5a sites, and synergistically (on lhb promoter) or additively (on fshb promoter) with forskolin. Surprisingly, Nr5a2 inhibited basal activities of lhb promoter possibly via Nr5a sites and attenuated the stimulatory effects of both forskolin and Nr5a1b. In contrast, Nr5a2 had no effects on fshb promoter. Chromatin immunoprecipitation analysis showed that both Nr5a1b and Nr5a2 bound to lhb promoter, but not fshb promoter in the pituitary of the orange-spotted grouper. The abundance of Nr5a1b bound to lhb promoter was significantly higher at the vitellogenic stage than the pre-vitellogenic stage, whereas that of Nr5a2 exhibited an opposite trend. Taken together, data of the present study demonstrated antagonistic effects of Nr5a1b and Nr5a2 on lhb transcription in the orange-spotted grouper and revealed novel regulatory mechanisms of differential expression of lhb and fshb genes through Nr5a homologues in vertebrates.
2

KUO, Ming-Wei, John POSTLETHWAIT, Wen-Chih LEE, Show-Wan LOU, Woon-Khiong CHAN, and Bon-chu CHUNG. "Gene duplication, gene loss and evolution of expression domains in the vertebrate nuclear receptor NR5A (Ftz-F1) family." Biochemical Journal 389, no. 1 (June 21, 2005): 19–26. http://dx.doi.org/10.1042/bj20050005.

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Fushi tarazu factor 1 (Ftz-F1, NR5A) is a zinc-finger transcription factor that belongs to the nuclear receptor superfamily and regulates genes that are involved in sterol and steroid metabolism in gonads, adrenals, liver and other tissues. To understand the evolutionary origins and developmental genetic relationships of the Ftz-F1 genes, we have cloned four homologous Ftz-f1 genes in zebrafish, called ff1a, ff1b, ff1c and ff1d. These four genes have different temporal and spatial expression patterns during development, indicating that they have distinct mechanisms of genetic regulation. Among them, the ff1a expression pattern is similar to mammalian Nr5a2, while the ff1b pattern is similar to that of mammalian Nr5a1. Genetic mapping experiments show that these four ff1 genes are located on chromosome segments conserved between the zebrafish and human genomes, indicating a common ancestral origin. Phylogenetic and conserved synteny analysis show that ff1a is the orthologue of NR5A2, and that ff1b and ff1d genes are co-orthologues of NR5A1 that arose by a gene-duplication event, probably a whole-genome duplication, in the ray-fin lineage, and each gene is located next to an NR6A1 co-orthologue as in humans, showing that the tandem duplication occurred before the divergence of human and zebrafish lineages. ff1c does not have a mammalian counterpart. Thus we have characterized the phylogenetic relationships, expression patterns and chromosomal locations of these Ftz-F1 genes, and have demonstrated their identities as NR5A genes in relation to the orthologous genes in other species.
3

Suyama, Atsuhito, Nahoko Iwata, Yoshiaki Soejima, Yasuhiro Nakano, Koichiro Yamamoto, Takahiro Nada, and Fumio Otsuka. "Involvement of NR5A1 and NR5A2 in the Regulation of Steroidogenesis by Clock Gene and BMPs by Human Granulosa Cells." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A768. http://dx.doi.org/10.1210/jendso/bvab048.1562.

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Abstract We previously reported that the expression levels of Clock gene are linked to the expression levels of steroidogenetic enzymes in human granulosa cells (EJ 2019). However, the downstream molecules of the Clock gene actions in the regulation of ovarian steroidogenesis have yet to be elucidated. In the present study, we investigated the roles of the transcription factors, NR5A1 (also known as SF-1) and NR5A2 (LRH-1), which play key roles in the reproductive function as well as steroidogenesis by focusing on the functional link between Clock gene and bone morphogenetic protein (BMP) signaling using human granulosa KGN cells. First of all, we examined the effects of BMPs/growth differentiation factor (GDF) on forskolin (FSK)-induced steroidogenesis. As a result, FSK-induced mRNA levels of StAR and P450scc, but not P450arom, were potently suppressed by treatments with BMP-6, -9, -15 and GDF-9. The expression levels of NR5A1 and NR5A2 mRNA were also upregulated by FSK treatment, while the BMP-target gene Id-1 mRNA levels were stimulated by the treatment with BMPs. Of interest, treatments with BMPs/GDF increased FSK-induced NR5A1 mRNA levels but suppressed FSK-induced NR5A2 mRNA levels by granulosa cells. The expression levels of NR5A1 mRNA were positively correlated with the changes of P450arom and 3βHSD mRNA, whereas the expression levels of NR5A2 mRNA were correlated with that of StAR and P450scc mRNA. In addition, the expression levels of NR5A1 and NR5A2 mRNAs were positively correlated with the levels of Clock mRNA. In particular, Clock mRNA levels showed highly positive correlation with the levels of NR5A2 mRNA compared with NR5A1 mRNA. Of note, Id-1 mRNA levels were positively correlated with the levels of NR5A1 mRNA, but negatively correlated with that of NR5A2 mRNA. Furthermore, the inhibition of Clock gene expression by siRNA attenuated the expression levels of NR5A1 and NR5A2 mRNA, resulting in decreased mRNA levels of StAR and P450arom in the presence of FSK. Thus, the present results suggested a novel mechanism by which Clock expression is functionally linked to the expression of NR5A1 and NR5A2, the latter of which is further regulated by BMP signaling by granulosa cells. The interaction among Clock, NR5A1/NR5A2 and BMPs may be involved in the fine tuning of steroidogenesis by ovarian follicles.
4

Suzuki, Taiga, Megumi Kasahara, Hidefumi Yoshioka, Ken-ichirou Morohashi, and Kazuhiko Umesono. "LXXLL-Related Motifs in Dax-1 Have Target Specificity for the Orphan Nuclear Receptors Ad4BP/SF-1 and LRH-1." Molecular and Cellular Biology 23, no. 1 (January 1, 2003): 238–49. http://dx.doi.org/10.1128/mcb.23.1.238-249.2003.

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ABSTRACT The orphan receptor Ad4BP/SF-1 (NR5A1) is a constitutive activator, and its activity is repressed by another orphan receptor, Dax-1 (NR0B1). In the present study, we investigated the molecular mechanisms underlying this repression by Dax-1. Yeast two-hybrid and transient-transfection assays confirmed the necessity of three LXXLL-related motifs in Dax-1 for interaction with and repression of Ad4BP/SF-1. In vitro pull-down experiments confirmed that Dax-1 interacts with Ad4BP/SF-1 and also with LRH-1 (NR5A2). The target specificity of the LXXLL-related motifs was indicated by the observations that Ad4BP/SF-1, ERα (NR3A1), LRH-1, ERR2 (NR3B2), and fly FTZ-F1 (NR5A3) interacted through their ligand binding domains with all the LXXLL-related motifs in Dax-1 whereas HNF4 (NR2A1) and RORα (NR1F1) did not. Transcriptional activities of the receptors whose DNA binding domains (DBDs) were replaced by the GAL4 DBD were repressed by Dax-1 to various levels, which correlated with the strength of interaction. Amino acid substitutions revealed that Ad4BP/SF-1 and LRH-1 preferentially interact with L(+1)XXLL-related motifs containing serine, tyrosine, serine, and threonine at positions −2, +2, +3, and +6, respectively. Taken together, our results indicate that the specificities of LXXLL-related motifs in Dax-1 based on their amino acid sequences play an important role in regulation of orphan receptors.
5

Martin, Luc J., and Jacques J. Tremblay. "Glucocorticoids antagonize cAMP-induced Star transcription in Leydig cells through the orphan nuclear receptor NR4A1." Journal of Molecular Endocrinology 41, no. 3 (July 1, 2008): 165–75. http://dx.doi.org/10.1677/jme-07-0145.

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It is well established that stress, either physical or psychosocial, causes a decrease in testosterone production by Leydig cells. Glucocorticoids (Gc) are the main mediators of stress response and they convey their repressive effect on Leydig cells through the glucocorticoid receptor (GR). So far, various mechanisms have been proposed to explain the mechanism of action of Gc on Leydig cell steroidogenesis including repression of genes involved in testosterone biosynthesis. Several steroidogenic genes, including steroidogenic acute regulatory (STAR) protein, have been shown to be repressed by Gc in a GR-dependent manner but the underlying mechanisms remain to be fully elucidated. Here, we found that dexamethasone (Dex), a potent synthetic Gc, partly antagonizes the cAMP-dependent stimulation of the mouse Star promoter in MA-10 Leydig cells as revealed by transient transfection assays. This repression requires an element located at −95 bp previously implicated in the activation of the Star promoter by the nuclear receptors, NR4A1 and NR5A1. Dex was found to inhibit NR4A1-dependent transactivation of the Star promoter in Leydig cells by decreasing NR4A1, but not NR5A1, recruitment to the proximal Star promoter as determined by chromatin immunoprecipitation assay. Western blots revealed that Dex did not affect NR4A1 or NR5A1 expression in response to cAMP. These data suggest that NR4A1 would be associated with the GR in a transcriptionally inactive complex as previously demonstrated in pituitary corticotrope cells. Thus, our data provide new molecular insights into the stress-mediated suppression of testosterone production in testicular Leydig cells.
6

Emura, Natsuko, Chiung-Min Wang, William Harry Yang, and Wei-Hsiung Yang. "Steroidogenic Factor 1 (NR5A1) Activates ATF3 Transcriptional Activity." International Journal of Molecular Sciences 21, no. 4 (February 20, 2020): 1429. http://dx.doi.org/10.3390/ijms21041429.

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Steroidogenic Factor 1 (SF-1/NR5A1), an orphan nuclear receptor, is important for sexual differentiation and the development of multiple endocrine organs, as well as cell proliferation in cancer cells. Activating transcription factor 3 (ATF3) is a transcriptional repressor, and its expression is rapidly induced by DNA damage and oncogenic stimuli. Since both NR5A1 and ATF3 can regulate and cooperate with several transcription factors, we hypothesized that NR5A1 may interact with ATF3 and plays a functional role in cancer development. First, we found that NR5A1 physically interacts with ATF3. We further demonstrated that ATF3 expression is up-regulated by NR5A1. Moreover, the promoter activity of the ATF3 is activated by NR5A1 in a dose-dependent manner in several cell lines. By mapping the ATF3 promoter as well as the site-directed mutagenesis analysis, we provide evidence that NR5A1 response elements (−695 bp and −665 bp) are required for ATF3 expression by NR5A1. It is well known that the transcriptional activities of NR5A1 are modulated by post-translational modifications, such as small ubiquitin-related modifier (SUMO) modification and phosphorylation. Notably, we found that both SUMOylation and phosphorylation of NR5A1 play roles, at least in part, for NR5A1-mediated ATF3 expression. Overall, our results provide the first evidence of a novel relationship between NR5A1 and ATF3.
7

Morohashi, Ken-ichirou, Miki Inoue, and Takashi Baba. "Coordination of Multiple Cellular Processes by NR5A1/Nr5a1." Endocrinology and Metabolism 35, no. 4 (December 31, 2020): 756–64. http://dx.doi.org/10.3803/enm.2020.402.

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8

Luppino, Giovanni, Malgorzata Wasniewska, Roberto Coco, Giorgia Pepe, Letteria Anna Morabito, Alessandra Li Pomi, Domenico Corica, and Tommaso Aversa. "Role of NR5A1 Gene Mutations in Disorders of Sex Development: Molecular and Clinical Features." Current Issues in Molecular Biology 46, no. 5 (May 9, 2024): 4519–32. http://dx.doi.org/10.3390/cimb46050274.

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Disorders/differences of sex development (DSDs) are defined as broad, heterogenous groups of congenital conditions characterized by atypical development of genetic, gonadal, or phenotypic sex accompanied by abnormal development of internal and/or external genitalia. NR5A1 gene mutation is one of the principal genetic alterations implicated in causing DSD. This review outlines the role of NR5A1 gene during the process of gonadal development in humans, provides an overview of the molecular and functional characteristics of NR5A1 gene, and discusses potential clinical phenotypes and additional organ diseases due to NR5A1 mutations. NR5A1 mutations were analyzed in patients with 46,XY DSD and 46,XX DSD both during the neonatal and pubertal periods. Loss of function of the NR5A1 gene causes several different phenotypes, including some associated with disease in additional organs. Clinical phenotypes may vary, even among patients carrying the same NR5A1 variant, indicating that there is no specific genotype–phenotype correlation. Genetic tests are crucial diagnostic tools that should be used early in the diagnostic pathway, as early as the neonatal period, when gonadal dysgenesis is the main manifestation of NR5A1 mutation. NR5A1 gene mutations could be mainly associated with amenorrhea, ovarian failure, hypogonadism, and infertility during puberty. Fertility preservation techniques should be considered as early as possible.
9

Domenice, Sorahia, Aline Zamboni Machado, Frederico Moraes Ferreira, Bruno Ferraz‐de‐Souza, Antonio Marcondes Lerario, Lin Lin, Mirian Yumie Nishi, et al. "Wide spectrum of NR5A1‐related phenotypes in 46,XY and 46,XX individuals." Birth Defects Research Part C: Embryo Today: Reviews 108, no. 4 (December 2016): 309–20. http://dx.doi.org/10.1002/bdrc.21145.

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Steroidogenic factor 1 (NR5A1, SF‐1, Ad4BP) is a transcriptional regulator of genes involved in adrenal and gonadal development and function. Mutations in NR5A1 have been among the most frequently identified genetic causes of gonadal development disorders and are associated with a wide phenotypic spectrum. In 46,XY individuals, NR5A1‐related phenotypes may range from disorders of sex development (DSD) to oligo/azoospermia, and in 46,XX individuals, from 46,XX ovotesticular and testicular DSD to primary ovarian insufficiency (POI). The most common 46,XY phenotype is atypical or female external genitalia with clitoromegaly, palpable gonads, and absence of Müllerian derivatives. Notably, an undervirilized external genitalia is frequently seen at birth, while spontaneous virilization may occur later, at puberty. In 46,XX individuals, NR5A1 mutations are a rare genetic cause of POI, manifesting as primary or secondary amenorrhea, infertility, hypoestrogenism, and elevated gonadotropin levels. Mothers and sisters of 46,XY DSD patients carrying heterozygous NR5A1 mutations may develop POI, and therefore require appropriate counseling. Moreover, the recurrent heterozygous p.Arg92Trp NR5A1 mutation is associated with variable degrees of testis development in 46,XX patients. A clear genotype‐phenotype correlation is not seen in patients bearing NR5A1 mutations, suggesting that genetic modifiers, such as pathogenic variants in other testis/ovarian‐determining genes, may contribute to the phenotypic expression. Here, we review the published literature on NR5A1‐related disease, and discuss our findings at a single tertiary center in Brazil, including ten novel NR5A1 mutations identified in 46,XY DSD patients. The ever‐expanding phenotypic range associated with NR5A1 variants in XY and XX individuals confirms its pivotal role in reproductive biology, and should alert clinicians to the possibility of NR5A1 defects in a variety of phenotypes presenting with gonadal dysfunction. Birth Defects Research (Part C) 108:309–320, 2016. © 2016 The Authors Birth Defects Research Part C: Embryo Today: Reviews Published by Wiley Periodicals, Inc.
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Shima, Yuichi, Kanako Miyabayashi, Takami Mori, Koji Ono, Mizuki Kajimoto, Hae Lim Cho, Hitomi Tsuchida, et al. "Intronic Enhancer Is Essential for Nr5a1 Expression in The Pituitary Gonadotrope and for Postnatal Development of Male Reproductive Organs in a Mouse Model." International Journal of Molecular Sciences 24, no. 1 (December 22, 2022): 192. http://dx.doi.org/10.3390/ijms24010192.

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Nuclear receptor subfamily 5 group A member 1 (NR5A1) is expressed in the pituitary gonadotrope and regulates their differentiation. Although several regulatory regions were implicated in Nr5a1 gene expression in the pituitary gland, none of these regions have been verified using mouse models. Furthermore, the molecular functions of NR5A1 in the pituitary gonadotrope have not been fully elucidated. In the present study, we generated mice lacking the pituitary enhancer located in the 6th intron of the Nr5a1 gene. These mice showed pituitary gland-specific disappearance of NR5A1, confirming the functional importance of the enhancer. Enhancer-deleted male mice demonstrated no defects at fetal stages. Meanwhile, androgen production decreased markedly in adult, and postnatal development of reproductive organs, such as the seminal vesicle, prostate, and penis was severely impaired. We further performed transcriptomic analyses of the whole pituitary gland of the enhancer-deleted mice and controls, as well as gonadotropes isolated from Ad4BP-BAC-EGFP mice. These analyses identified several genes showing gonadotrope-specific, NR5A1-dependent expressions, such as Spp1, Tgfbr3l, Grem1, and Nr0b2. These factors are thought to function downstream of NR5A1 and play important roles in reproductive organ development through regulation of pituitary gonadotrope functions.
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Journal articles Dissertations / Theses

Dissertations / Theses on the topic "Nr5a1":

1

Fabbri-Scallet, Helena 1987. "Análise molecular do gene NR5A1 em pacientes 46,XY com distúrbios da diferenciação do sexo." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317065.

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Orientador: Marcilda Palandi de Mello
Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-22T17:47:27Z (GMT). No. of bitstreams: 1 Fabbri_HelenaCampos_M.pdf: 5693726 bytes, checksum: f3da0b3f4f94d25ac46393e9f831a748 (MD5) Previous issue date: 2013
Resumo: O termo Distúrbio da Diferenciação do Sexo (DDS) caracteriza-se pelo desenvolvimento genital ou gonadal incompleto ou desordenado. Os DDS com cariótipo 46,XY são caracterizados por genitália externa ambígua ou feminina, em alguns casos com gônadas disgenéticas, e presença ou ausência de derivados de Müller. Os mais frequentes são a insensibilidade androgênica, deficiência da 5-alfa-redutase tipo 2, disgenesia gonadal e DDS ovário-testicular. Vários são os genes que participam dos processos de determinação e diferenciação do sexo. Alterações no gene NR5A1, que codifica o fator de transcrição SF- 1, é responsável por diferentes fenótipos de DDS. A proteína SF-1 é expressa principalmente em tecidos esteroidogênicos (gônadas, adrenais e placenta), nas células de Sertoli, nas células de Leydig e nos ovários; é o principal regulador do metabolismo do colesterol nas células esteroidogênicas. Além disso, regula a atividade de outros genes, como os CYPs, HSD3B, StAR, SOX9, DAX1, entre outros. Na literatura são descritas alterações no gene NR5A1 associadas à DDS 46,XY, anorquia bilateral, amenorréia primária, falência ovariana precoce, hipospádia, infertilidade masculina, e alguns casos de tumores adrenais e endometrioses. Neste trabalho foi realizada a análise molecular do gene NR5A1 em 86 pacientes com DDS 46,XY, incluindo-se disgenesia gonadal completa (n = 7), disgenesia gonadal parcial (n = 18), DDS 46,XY idiopático (n = 41) e outros (n = 20). Doze alterações foram identificadas neste trabalho, sendo: sete na região codificante (p.Ser32Asn, p.Arg39Cis, p.Lis38*, p.Cis65Tir, p.L80Wfs*8, p.Cis247*, and p.Asp364Trefs*18), uma em sítio de splicing (c.1138+1G>T), duas no exon 1 nãocodificante (c.-133G>A e c.-156_-136ins18pb), três na região 5'UTR (c.-413G>A, c.- 208C>A, e c.-762C>T) e uma na região 3'UTR (c.*1286C>T). As variações aqui descritas, não foram identificadas em controles saudáveis. As análises in silico demonstraram o possível efeito deletério de cada alteração e, suas relações com o fenótipo dos indivíduos. Embora estes resultados demonstrem a importância de cada alteração para o fenótipo, haverá ainda a necessidade de se investigar os efeitos funcionais in vitro. As alterações com potencial deletério foram identificadas em maior frequência nos casos dos distúrbios da diferenciação gonadal (20%) e DDS 46,XY idiopático (22%)
Abstract: The term Disorders of Sex Differentiation (DSD) characterize incomplete or disorganized genital or gonadal development. The DSD with 46, XY karyotype may present either ambiguous or female genitalia and also dysgenetic gonads in some cases, with presence or absence of Müllerian derivatives. The most frequent are androgen insensitivity, 5-alpha-reductase type 2 deficiency, gonadal dysgenesis and ovarian-testicular DSD. There are several genes that participate in both sex determination and differentiation processes. Mutations in NR5A1 gene, which encoding SF-1, a transcription factor, are responsible for different phenotypes of DSD. The protein SF-1, which is expressed mainly in steroidogenic tissues (gonads, adrenal glands and placenta), is also express in Sertoli and Leydig cells, in the ovaries, and is the major regulator of cholesterol metabolism in steroidogenic cells. Moreover, it regulates the activity of other genes, such as CYPs, HSD3B, StAR, SOX9, DAX1, among others. The literature describes the association of changes in NR5A1 gene with 46, XY DSD, bilateral anorchia, primary amenorrhea, premature ovarian failure, hypospadias, male infertility, and some cases of adrenal tumors and endometriosis. The present work involved the molecular analysis of NR5A1 gene in 86 patients with 46, XY DSD including complete gonadal dysgenesis (n = 7), partial gonadal dysgenesis (n = 18), idiopathic 46, XY DSD (n = 41) and others (n = 20). Twelve variations had been identified: seven in the coding region (p.Ser32Asn, p.Arg39Cis, p.Lis38*, p.Cis65Tir, p.L80Wfs*8, p.Cis247*, and p.Asp364Trefs*18), one at a splice site (c.1138+1 G>T), two in the noncoding exon 1 (c.-133G>A and c.-156_-136ins18pb), three in the 5'UTR region (c.- 413G>A, c.-208C>A and c.-762C>T) and one in the 3'UTR (c.*1286C>T). The variations herein described, have not been identified in healthy controls. In silico analysis showed possible deleterious effects for each change and its correlations to individual phenotypes. Although those results demonstrate the importance of each change for the phenotype, there in vitro functional effects must be investigated. The potentially deleterious changes were identified more frequently in cases of disorders of gonadal development (20%) and idiopathic 46, XY DSD (22%)
Mestrado
Genetica Animal e Evolução
Mestra em Genética e Biologia Molecular
2

Astudillo, Rebekka Anna-Maria [Verfasser]. "Funktionelle Charakterisierung von heterozygoten Mutationen des Steroidogenetischen Faktors 1 (SF1/NR5A1) bei 46,XY Störungen der Geschlechtsentwicklung / Rebekka Anna-Maria Astudillo." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2021. http://d-nb.info/1241538085/34.

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Köhler, Birgit [Verfasser]. "XY Störungen der Geschlechtsentwicklung (XY DSD) : die Rolle des Wilms-Tumorsuppressorgens (WT1) und des „Steroidogenic Factor 1“ (NR5A1, SF1) sowie Langzeitergebnisse / Birgit Köhler." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1043480951/34.

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Tantawy, Sally [Verfasser]. "Untersuchung des Steroidogenic Factor 1 kodierenden Gens NR5A1 in einer Kohorte von 50 ägyptischen Patienten mit 46,XY Störungen der Geschlechtsentwicklung / Sally Moustafa Elsayed Tantawy." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1133074278/34.

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Tantawy, Sally Moustafa Elsayed [Verfasser]. "Untersuchung des Steroidogenic Factor 1 kodierenden Gens NR5A1 in einer Kohorte von 50 ägyptischen Patienten mit 46,XY Störungen der Geschlechtsentwicklung / Sally Moustafa Elsayed Tantawy." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1133074278/34.

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Garner, Hannah Claire. "The role of Nr4a1 in the development of Ly6Clow monocytes." Thesis, King's College London (University of London), 2016. https://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-nr4a1-in-the-development-of-ly6clow-monocytes(bdc403c1-200f-4b12-8617-4cc23ce46171).html.

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Monocytes are haematopoietic stem cell-derived, immune effector cells. In mice, monocytes consist of two principal subsets: the classical Ly6C-expressing subset and the patrolling Ly6Clow subset. The origin and fate of Ly6Clow monocytes remains a topic of debate, as does their interrelationship with Ly6C+ monocytes. The current model of Ly6Clow monocyte development suggests that Ly6C+ monocytes are the obligate, steady state precursors of the Ly6Clow subset, undergoing conversion or maturation within the blood. However, several studies have reported differing genetic dependencies of monocyte subsets that are in conflict with this model of Ly6Clow monocyte development. To re-investigate monocyte precursor-product relationships, this project combined genetic, kinetic and adoptive transfer studies to probe the interrelationships between bone marrow precursors, blood monocytes and tissue macrophages. This study firstly confirms the existence of a third, minor monocyte subset that expresses MHC II and varying levels of Ly6C and is found in the blood, spleen and bone marrow monocyte compartments. Secondly, this study establishes that all three monocyte subsets arise in the bone marrow from a proliferating common pro-monocyte via two genetically distinct lineages. This study demonstrates that Ly6Clow MHC II- monocytes arise from a novel Nr4a1-dependent, Irf8-independent intermediate population in the bone marrow compartment under steady state conditions, whereas. Thirdly, Nr4a1-dependent monocytes have a long half-life and circulate within the systemic and splenic vasculature, contributing minimally to tissue macrophage populations under steady state conditions. The findings in this thesis clarify and extend our understanding of monocyte genetic and functional heterogeneity.
7

Hofsten, Jonas von. "Developmental and reproductive regulation of NR5A genes in teleosts." Doctoral thesis, Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-374.

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Wilcots, Josiah. "Determination of induction of Nur77 (NR4A1), Nor1 (NR4A3), and Nurr1 (NR4A2)." Master's thesis, Mississippi State : Mississippi State University, 2009. http://library.msstate.edu/etd/show.asp?etd=etd-04032009-165154.

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Schwaderer, Juliane [Verfasser]. "LRH-1/NR5a2 in regulation of the immune system / Juliane Schwaderer." Konstanz : Bibliothek der Universität Konstanz, 2017. http://d-nb.info/1140736418/34.

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Edey, Caitlin. "Retinoid-mediated Regulation of NR6A1, Prickle1 and Ror2 During Development of the Mouse Embryo." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23609.

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Abstract:
Vitamin A and its derivatives, collectively termed retinoids, are essential for proper growth and development as well as maintenance of homeostasis in the adult. Retinoic acid (RA), the major biologically active vitamin A metabolite, is well characterized for its crucial roles in gene activation during embryogenesis. Our lab had previously performed a microarray analysis to identify genes induced by exogenous RA in the tailbud of early mouse embryos. Three genes were chosen from the microarray results for further investigation; Germ Cell Nuclear Factor (GCNF/NR6A1), Prickle1 (Pk1) and Ror2, the latter of which are known members of the planar cell polarity (PCP) pathway. These genes were further examined for RA regulation by embryo culture and RT-PCR, which strongly supported a direct regulatory mechanism of NR6A1 by RA. Further analysis aiming to identify a functional response element in the promoter of the targets was attempted, including chromatin immunoprecipitation (ChIP), made possible by the generation and characterization of a highly specific antibody against RARγ. This antibody was used in a ChIP promoter walk, which identified regions on target gene promoters that are occupied by RARγ in vivo, and therefore likely harbor RA response elements.
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Book chapters on the topic "Nr5a1":

1

Grgurevic, Neza, and Gregor Majdic. "NR5a1." In Encyclopedia of Signaling Molecules, 3574–84. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101872.

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Grgurevic, Neza, and Gregor Majdic. "NR5a1." In Encyclopedia of Signaling Molecules, 1–11. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101872-1.

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McElreavey, Ken, and Anu Bashamboo. "Steroidogenic Factor 1 (SF-1; NR5A1)." In Encyclopedia of Endocrine Diseases, 415–20. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-801238-3.65242-x.

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Bashamboo, A., L. Lin, B. Ferraz de Souza, D. Lourenco, D. Montjean, C. Ravel, H. Rouba, J. Achermann, and K. McElreavey. "Mutations in NR5A1 Encoding Steroidogenic Factor 1 Are Associated with Spermatogenic Failure." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P2–367—P2–367. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part2.p8.p2-367.

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Ferraz-de-Souza, B., L. Lin, and JC Achermann. "A Role for Steroidogenic Factor-1 (SF-1, NR5A1, Ad4BP) in Adrenal Angiogenesis." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P1–612—P1–612. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p13.p1-612.

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Franca, Monica Malheiros, Mariza Gerdulo Santos, and Claudimara Ferini Pacicco Lotfi. "Sf-1/NR5A1 and Pod-1/TCF21 Expression in Different Human Adrenocortical Tumor Cell Cultures." In The Endocrine Society's 93rd Annual Meeting & Expo, June 4–7, 2011 - Boston, P1–628—P1–628. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p14.p1-628.

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"SF-1 (Ftz-F1, fushi tarazu factor homolog, nuclear receptor subfamily 5 group A member 1[NR5A1])." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1801. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_15507.

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Lin, Lin, Rahul Parnaik, Bruno Ferraz-de-Souza, and John C. Achermann. "Novel Interacting Proteins for Steroidogenic Factor-1 (SF-1, NR5A1, Ad4BP) in the Developing Human Adrenal Gland." In BASIC/TRANSLATIONAL - Gene Regulation: Inflammation, Stress & Metabolism, P3–85—P3–85. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part3.p21.p3-85.

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El-Khairi, Ranna, Alejandro Martinez-Aguayo, Bruno Ferraz-de-Souza, Lin Lin, and John C. Achermann. "Role of DAX-1 (NR0B1) and Steroidogenic Factor-1 (NR5A1) in Human Adrenal Function." In Pediatric Adrenal Diseases, 38–46. S. Karger AG, 2010. http://dx.doi.org/10.1159/000321213.

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Demura, Masashi, Fen Wang, Takashi Yoneda, Shigehiro Karashima, Shunsuke Mori, Masashi Oe, Mitsuhiro Kometani, et al. "Multiple Noncoding Exons 1 of Nuclear Receptors NR4A Family (NGFIB,NURR1,NOR1) and NR5A1 (SF1) in Human Vascular and Adrenal Tissues." In BASIC - Regulation of Nuclear Receptors & Gene Expression, P2–8—P2–8. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p21.p2-8.

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Conference papers on the topic "Nr5a1":

1

Wang, Chiung-Min, Victoria Brennan, Ninoska Gutierrez, Xirui Wang, Lizhong Wang, and Wei-Hsiung Yang. "Abstract 763A: SUMOylation of ATF3 alters MC2R, NR5A1, STAR, and TP53 gene activities." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-763a.

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MAIA DE SOUSA, LIZANDRA, MARICILDA PALANDI DE MELLO, and Luiz Filipe Barbosa-Martins. "BUSCA DE NOVAS MUTAÇÕES NO GENE NR5A1 EM UM GRUPO DE HOMENS INFÉRTEIS." In XXIV Congresso de Iniciação Científica da UNICAMP - 2016. Campinas - SP, Brazil: Galoa, 2016. http://dx.doi.org/10.19146/pibic-2016-50634.

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Jin, Jingling, Roma Patel, Nan Ge Jin, Yan Shi, Wenjing Sun, Jianhua Yang, Jed G. Nuchtern, and Sanjeev A. Vasudevan. "Abstract B16: NR5A2 as a potential therapeutic target for hepatoblastoma." In Abstracts: AACR Special Conference: Advances in Pediatric Cancer Research: From Mechanisms and Models to Treatment and Survivorship; November 9-12, 2015; Fort Lauderdale, Florida. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.pedca15-b16.

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Nissim, Sahar, Julia Wucherpfennig, Xiao-Xu Wang, Alec Kimmelman, and Wolfram Goessling. "Abstract 1953: The role of NR5a2 in pancreas development and carcinogenesis." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1953.

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Nissim, Sahar, Julia Wucherpfennig, Xiao-Xu Wang, Alec Kimmelman, and Wolfram Goessling. "Abstract 2657: The role of NR5A2 in pancreas development and oncogenesis." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2657.

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Beeghly-Fadiel, Alicia, Dajah Chase, Johnathan Cooks, Marta Crispens, Dineo Khabele, and Andrew J. Wilson. "Abstract A42: TR3/NR4A1 as a therapeutic target for ovarian cancer." In Abstracts: AACR Special Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; October 1-4, 2017; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-a42.

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Nissim, Sahar, Olivia Weeks, John Hedgepeth, Julia Wucherpfennig, Xiao-Xu Wang, Alec Kimmelman, and Wolfram Goessling. "Abstract 5148: NR5A2 is essential for pancreas development and affects pancreas carcinogenesis." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5148.

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Beeghly-Fadiel, Alicia, Johnathan Cooks, Dajah Chase, Marta Crispens, Dineo Khabele, and Andrew J. Wilson. "Abstract NT-088: PROGNOSTIC SIGNIFICANCE OF NR4A1/TR3 EXPRESSION IN OVARIAN CANCER." In Abstracts: 12th Biennial Ovarian Cancer Research Symposium; September 13-15, 2018; Seattle, Washington. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1557-3265.ovcasymp18-nt-088.

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Mohankumar, Kumaravel, Keshav Karki, Stephen Safe, and Maen Abdelrahim. "Abstract 1149: Nuclear receptor 4A1 (NR4A1) antagonists target PD-L1 in colon cancer." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1149.

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Karki, Keshav, Gus Wright, Jin Un-Ho, Kumaravel Mohankumar, Xing Zhang, and Stephen Safe. "Abstract B41: Bis-indole derived NR4A1 antagonist induces PD-L1 degradation and enhances antitumor immunity." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-b41.

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