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Literatura académica sobre el tema "Pou5f1"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 16 de febrero de 2022

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Artículos de revistas sobre el tema "Pou5f1"

Hasegawa, Shun, Isseki Nakao, Yuki Ootani, Ami Ogawa, Miku Takano y Tsutomu Kinoshita. "Identification and characterization of POU class V family genes in Japanese red bellied newt, Cynops pyrrhogaster". Zygote 27, n.º 05 (15 de agosto de 2019): 329–36. http://dx.doi.org/10.1017/s0967199419000339.

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SummaryMammalian Pou5f1 encodes the POU family class V (POU-V) transcription factor which is essential for the pluripotency of embryonic cells and germ cells. In vertebrates, various POU-V family genes have been identified and classified into the POU5F1 family or its paralogous POU5F3 family. In this study, we cloned two cDNAs named CpPou5f1 and CpPou5f3, which encode POU-V family proteins of the Japanese red bellied newt Cynops pyrrhogaster. In the predicted amino acid sequence encoded by CpPou5f1, the typical MAGH sequence at the N-terminus and deletion of arginine at the fifth position of POU-homeodomain were recognized, but not in the sequence encoded by CpPou5f3. Phylogenetic analysis using Clustal Omega software indicated that CpPou5f1 and CpPou5f3 are classified into the clade of the POU5F1 and POU5F3 families, respectively. In a real-time polymerase chain reaction (RT-PCR) analysis, the marked gene expression of CpPou5f1 was observed during oogenesis and early development up to the tail-bud stage, whereas weak gene expression of CpPou5f3 was detected only in the early stages of oogenesis and gastrula. In adult organs, CpPou5f1 was expressed only in the ovary, while gene expression of CpPou5f3 was recognized in various organs. A regeneration experiment using larval forelimb revealed that transient gene expression of CpPou5f1 occurred at the time of wound healing, followed by gene activation of CpPou5f3 during the period of blastema formation. These results suggest that CpPou5f1 and CpPou5f3 might play different roles in embryogenesis and limb regeneration.

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Zheng, Yu, LeAnna J. Phillips, Rachel Hartman, Junhui An y Christina T. Dann. "Ectopic POU5F1 in the male germ lineage disrupts differentiation and spermatogenesis in mice". Reproduction 152, n.º 4 (octubre de 2016): 363–77. http://dx.doi.org/10.1530/rep-16-0140.

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Expression levels of the pluripotency determinant, POU5F1, are tightly regulated to ensure appropriate differentiation during early embryogenesis. POU5F1 is also present in the spermatogonial stem cell/progenitor cell population in mice and it is downregulated as spermatogenesis progresses. To test if POU5F1 downregulation is required for SSCs to differentiate, we produced transgenic mice that ubiquitously express POU5F1 in Cre-expressing lineages. Using a Vasa-Cre driver to produce ectopic POU5F1 in all postnatal germ cells, we found that POU5F1 downregulation was necessary for spermatogonial expansion during the first wave of spermatogenesis and for the production of differentiated spermatogonia capable of undergoing meiosis. In contrast, undifferentiated spermatogonia were maintained throughout adulthood, consistent with a normal presence of POU5F1 in these cells. The results suggest that POU5F1 downregulation in differentiating spermatogonia is a necessary step for the progression of spermatogenesis. Further, the creation of a transgenic mouse model for conditional ectopic expression of POU5F1 may be a useful resource for studies of POU5F1 in other cell lineages, during tumorogenesis and cell fate reprogramming.

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Choi, Y. H., H. D. Harding, D. L. Hartman, A. D. Obermiller, S. Kurosaka, K. J. McLaughlin y K. Hinrichs. "The uterine environment modulates trophectodermal POU5F1 levels in equine blastocysts". REPRODUCTION 138, n.º 3 (septiembre de 2009): 589–99. http://dx.doi.org/10.1530/rep-08-0394.

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The reported patterns of trophectodermal expression of POU5F1 protein in blastocysts vary among species, and are possibly related to the differences in placental growth and function. This study investigated the pattern of embryonic POU5F1 expression in the horse, a species with delayed placental formation. Immature equine oocytes expressed POU5F1 protein in the cytoplasm and nucleus. Staining for POU5F1 protein inin vitro-produced (IVP) embryos decreased to day 5 of culture, then the nuclear staining increased to day 7. IVP day-7 to -11 blastocysts showed POU5F1 staining in nuclei throughout the blastocysts. In contrast,in vivo-produced day-7 to -10 blastocysts showed greatly reduced trophoectodermal POU5F1 protein expression. To determine whether the uterine environment modulates POU5F1 expression, IVP blastocysts were transferred to the uteri of mares, then recovered 2–3 days later (IVP-ET embryos). These embryos showed similar POU5F1 expression as thein vivo-produced embryos. Levels ofPOU5F1,SOX2, andNANOGmRNA in IVP-ET blastocysts were significantly higher in the inner cell mass than in trophectoderm (TE) cells. These data suggest that the differentiation of equine TE, as indicated by loss of POU5F1 expression, is impaired duringin vitroculture, but proceeds normally when the embryos are exposed to the uterine environment. Previously reported differences in trophectodermal expression of POU5F1 among species may thus be in part artifactual, i.e. related toin vitroculture. Failure for correction of such changes by the uterine environment is a potential factor in the placental abnormalities seen after transfer of cultured embryos in some species.

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Gupta, Rangan, Toshihiko Ezashi y R. Michael Roberts. "Squelching of ETS2 Transactivation by POU5F1 Silences the Human Chorionic Gonadotropin CGA Subunit Gene in Human Choriocarcinoma and Embryonic Stem Cells". Molecular Endocrinology 26, n.º 5 (1 de mayo de 2012): 859–72. http://dx.doi.org/10.1210/me.2011-1146.

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Abstract The subunit genes encoding human chorionic gonadotropin, CGA, and CGB, are up-regulated in human trophoblast. However, they are effectively silenced in choriocarcinoma cells by ectopically expressed POU domain class 5 transcription factor 1 (POU5F1). Here we show that POU5F1 represses activity of the CGA promoter through its interactions with ETS2, a transcription factor required for both placental development and human chorionic gonadotropin subunit gene expression, by forming a complex that precludes ETS2 from interacting with the CGA promoter. Mutation of a POU5F1 binding site proximal to the ETS2 binding site does not alter the ability of POU5F1 to act as a repressor but causes a drop in basal promoter activity due to overlap with the binding site for DLX3. DLX3 has only a modest ability to raise basal CGA promoter activity, but its coexpression with ETS2 can up-regulate it 100-fold or more. The two factors form a complex, and both must bind to the promoter for the combination to be transcriptionally effective, a synergy compromised by POU5F1. Similarly, in human embryonic stem cells, which express ETS2 but not CGA, ETS2 does not occupy its binding site on the CGA promoter but is found instead as a soluble complex with POU5F1. When human embryonic stem cells differentiate in response to bone morphogenetic protein-4 and concentrations of POU5F1 fall and hCG and DLX3 rise, ETS2 then occupies its binding site on the CGA promoter. Hence, a squelching mechanism underpins the transcriptional silencing of CGA by POU5F1 and could have general relevance to how pluripotency is maintained and how the trophoblast lineage emerges from pluripotent precursor cells.

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Castillo-Martín, Miriam, Marc Yeste, Eva Pericuesta, Roser Morató, Alfonso Gutiérrez-Adán y Sergi Bonet. "Effects of vitrification on the expression of pluripotency, apoptotic and stress genes in in vitro-produced porcine blastocysts". Reproduction, Fertility and Development 27, n.º 7 (2015): 1072. http://dx.doi.org/10.1071/rd13405.

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The aims of the present study were to: (1) evaluate the effect of vitrification and warming on quality parameters and expression levels of pluripotency, apoptotic and stress genes in in vitro-produced (IVP) porcine blastocysts; and (ii) determine the correlation between these parameters. To this end, total cell number, DNA fragmentation, peroxide levels and the relative transcript abundance of BCL-2 associated X protein (BAX), BCL2-like 1 (BCL2L1), heat shock protein 70 (HSPA1A), POU class 5 homeobox 1 (POU5F1), superoxide dismutase 1 (SOD1) and superoxide dismutase 2 (SOD2) were analysed in fresh and vitrified IVP blastocysts. The results suggest that vitrification procedures have no effect on total cell number and gene expression of BAX, BCL2L1, SOD1 and SOD2 or the BAX : BCL2L1 ratio. Nevertheless, a significant increase in DNA fragmentation (2.9 ± 0.4% vs 11.9 ± 2.0%) and peroxide levels (80.4 ± 2.6 vs 97.2 ± 3.1) were seen in vitrified compared with Day 7 fresh blastocysts. In addition, after blastocyst vitrification, relative transcript abundance was downregulated for POU5F1 and upregulated for HSPA1A. Finally, there was a significant correlation of POU5F1 and HSPA1A with DNA fragmentation (POU5F1, r = –0.561; HSPA1A, r = 0.604) and peroxide levels (POU5F1, r = –0.590; HSPA1A, r = 0.621). In conclusion, under the conditions of the present study, vitrification and warming of IVP porcine blastocysts resulted in altered expression of POU5F1 and HSPA1A, but had no effect on BAX, BCL2L1, SOD1 and SOD2 expression.

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Stamatiadis, P., A. Boel, G. Cosemans, M. Popovic, B. Bekaert, R. Guggilla, M. Tang et al. "Comparative analysis of mouse and human preimplantation development following POU5F1 CRISPR/Cas9 targeting reveals interspecies differences". Human Reproduction 36, n.º 5 (20 de febrero de 2021): 1242–52. http://dx.doi.org/10.1093/humrep/deab027.

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Abstract STUDY QUESTION What is the role of POU class 5 homeobox 1 (POU5F1) in human preimplantation development and how does it compare with the mouse model? SUMMARY ANSWER POU5F1 is required for successful development of mouse and human embryos to the blastocyst stage as knockout embryos exhibited a significantly lower blastocyst formation rate, accompanied by lack of inner cell mass (ICM) formation. WHAT IS KNOWN ALREADY Clustered regularly interspaced short palindromic repeats—CRISPR associated genes (CRISPR-Cas9) has previously been used to examine the role of POU5F1 during human preimplantation development. The reported POU5F1-targeted blastocysts always retained POU5F1 expression in at least one cell, because of incomplete CRISPR-Cas9 editing. The question remains of whether the inability to obtain fully edited POU5F1-targeted blastocysts in human results from incomplete editing or the actual inability of these embryos to reach the blastocyst stage. STUDY DESIGN, SIZE, DURATION The efficiency of CRISPR-Cas9 to induce targeted gene mutations was first optimized in the mouse model. Two CRISPR-Cas9 delivery methods were compared in the B6D2F1 strain: S-phase injection (zygote stage) (n = 135) versus metaphase II-phase (M-phase) injection (oocyte stage) (n = 23). Four control groups were included: non-injected media-control zygotes (n = 43)/oocytes (n = 48); sham-injected zygotes (n = 45)/oocytes (n = 47); Cas9-protein injected zygotes (n = 23); and Cas9 protein and scrambled guide RNA (gRNA)-injected zygotes (n = 27). Immunofluorescence analysis was performed in Pou5f1-targeted zygotes (n = 37), media control zygotes (n = 19), and sham-injected zygotes (n = 15). To assess the capacity of Pou5f1-null embryos to develop further in vitro, additional groups of Pou5f1-targeted zygotes (n = 29) and media control zygotes (n = 30) were cultured to postimplantation stages (8.5 dpf). Aiming to identify differences in developmental capacity of Pou5f1-null embryos attributed to strain variation, zygotes from a second mouse strain—B6CBA (n = 52) were targeted. Overall, the optimized methodology was applied in human oocytes following IVM (metaphase II stage) (n = 101). The control group consisted of intracytoplasmically sperm injected (ICSI) IVM oocytes (n = 33). Immunofluorescence analysis was performed in human CRISPR-injected (n = 10) and media control (n = 9) human embryos. PARTICIPANTS/MATERIALS, SETTING, METHODS A gRNA-Cas9 protein mixture targeting exon 2 of Pou5f1/POU5F1 was microinjected in mouse oocytes/zygotes or human IVM oocytes. Reconstructed embryos were cultured for 4 days (mouse) or 6.5 days (human) in sequential culture media. An additional group of mouse-targeted zygotes was cultured to postimplantation stages. Embryonic development was assessed daily, with detailed scoring at late blastocyst stage. Genomic editing was assessed by immunofluorescence analysis and next-generation sequencing. MAIN RESULTS AND THE ROLE OF CHANCE Genomic analysis in mouse revealed very high editing efficiencies with 95% of the S-Phase and 100% of the M-Phase embryos containing genetic modifications, of which 89.47% in the S-Phase and 84.21% in the M-Phase group were fully edited. The developmental capacity was significantly compromised as only 46.88% embryos in the S-Phase and 19.05% in the M-Phase group reached the blastocyst stage, compared to 86.36% in control M-Phase and 90.24% in control S-Phase groups, respectively. Immunofluorescence analysis confirmed the loss of Pou5f1 expression and downregulation of the primitive marker SRY-Box transcription factor (Sox17). Our experiments confirmed the requirement of Pou5f1 expression for blastocyst development in the second B6CBA strain. Altogether, our data obtained in mouse reveal that Pou5f1 expression is essential for development to the blastocyst stage. M-Phase injection in human IVM oocytes (n = 101) similarly resulted in 88.37% of the POU5F1-targeted embryos being successfully edited. The developmental capacity of generated embryos was compromised from the eight-cell stage onwards. Only 4.55% of the microinjected embryos reached the late blastocyst stage and the embryos exhibited complete absence of ICM and an irregular trophectoderm cell layer. Loss of POU5F1 expression resulted in absence of SOX17 expression, as in mouse. Interestingly, genetic mosaicism was eliminated in a subset of targeted human embryos (9 out of 38), three of which developed into blastocysts. LIMITATIONS, REASONS FOR CAUTION One of the major hurdles of CRISPR-Cas9 germline genome editing is the occurrence of mosaicism, which may complicate phenotypic analysis and interpretation of developmental behavior of the injected embryos. Furthermore, in this study, spare IVM human oocytes were used, which may not recapitulate the developmental behavior of in vivo matured oocytes. WIDER IMPLICATIONS OF THE FINDINGS Comparison of developmental competency following CRISPR-Cas-mediated gene targeting in mouse and human may be influenced by the selected mouse strain. Gene targeting by CRISPR-Cas9 is subject to variable targeting efficiencies. Therefore, striving to reduce mosaicism can provide novel molecular insights into mouse and human embryogenesis. STUDY FUNDING/COMPETING INTEREST(S) The research was funded by the Ghent University Hospital and Ghent University and supported by the FWO-Vlaanderen (Flemish fund for scientific research, Grant no. G051516N), and Hercules funding (FWO.HMZ.2016.00.02.01). The authors declare no competing interests. TRIAL REGISTRATION NUMBER N/A.

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Gil-Kulik, Paulina, Piotr Chomik, Arkadiusz Krzyżanowski, Elżbieta Radzikowska-Büchner, Ryszard Maciejewski, Anna Kwaśniewska, Mansur Rahnama y Janusz Kocki. "Influence of the Type of Delivery, Use of Oxytocin, and Maternal Age on POU5F1 Gene Expression in Stem Cells Derived from Wharton’s Jelly within the Umbilical Cord". Oxidative Medicine and Cellular Longevity 2019 (14 de diciembre de 2019): 1–8. http://dx.doi.org/10.1155/2019/1027106.

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The paper presents an evaluation of the POU5F1 gene expression in mesenchymal stem cells derived from Wharton’s jelly within the umbilical cord, collected from 36 patients during labor. The study is the first one to show that the expression of POU5F1 in mesenchymal stem cells has been dependent on maternal age, birth order, route of delivery, and use of oxytocin. Our research proves that the POU5F1 gene expression in mesenchymal stem cells decreases with each subsequent pregnancy and delivery. Wharton’s jelly stem cells obtained from younger women and during their first delivery, as well as patients treated with oxytocin, show higher POU5F1 gene expression when compared with the subsequent deliveries. This leads to a conclusion that they are characterized by a lower level of differentiation, which in turn results in their greater plasticity and greater proliferative potential. Probably, they are also clinically more useful.

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Liao, Ji, Yikun He y Piroska E. Szabó. "The Pou5f1 distal enhancer is sufficient to drive Pou5f1 promoter-EGFP expression in embryonic stem cells". International Journal of Developmental Biology 57, n.º 9-10 (2013): 725–29. http://dx.doi.org/10.1387/ijdb.120186ps.

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Yamamoto, Yu, Osamu Miura y Takashi Ohyama. "Cruciform Formable Sequences within Pou5f1 Enhancer Are Indispensable for Mouse ES Cell Integrity". International Journal of Molecular Sciences 22, n.º 7 (26 de marzo de 2021): 3399. http://dx.doi.org/10.3390/ijms22073399.

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DNA can adopt various structures besides the B-form. Among them, cruciform structures are formed on inverted repeat (IR) sequences. While cruciform formable IRs (CFIRs) are sometimes found in regulatory regions of transcription, their function in transcription remains elusive, especially in eukaryotes. We found a cluster of CFIRs within the mouse Pou5f1 enhancer. Here, we demonstrate that this cluster or some member(s) plays an active role in the transcriptional regulation of not only Pou5f1, but also Sox2, Nanog, Klf4 and Esrrb. To clarify in vivo function of the cluster, we performed genome editing using mouse ES cells, in which each of the CFIRs was altered to the corresponding mirror repeat sequence. The alterations reduced the level of the Pou5f1 transcript in the genome-edited cell lines, and elevated those of Sox2, Nanog, Klf4 and Esrrb. Furthermore, transcription of non-coding RNAs (ncRNAs) within the enhancer was also upregulated in the genome-edited cell lines, in a similar manner to Sox2, Nanog, Klf4 and Esrrb. These ncRNAs are hypothesized to control the expression of these four pluripotency genes. The CFIRs present in the Pou5f1 enhancer seem to be important to maintain the integrity of ES cells.

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Desmarais, Joëlle A., Simon-Pierre Demers, Joao Suzuki, Simon Laflamme, Patrick Vincent, Sheila Laverty y Lawrence C. Smith. "Trophoblast stem cell marker gene expression in inner cell mass-derived cells from parthenogenetic equine embryos". REPRODUCTION 141, n.º 3 (marzo de 2011): 321–32. http://dx.doi.org/10.1530/rep-09-0536.

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Although putative horse embryonic stem (ES)-like cell lines have been obtained recently from in vivo-derived embryos, it is currently not known whether it is possible to obtain ES cell (ESC) lines from somatic cell nuclear transfer (SCNT) and parthenogenetic (PA) embryos. Our aim is to establish culture conditions for the derivation of autologous ESC lines for cell therapy studies in an equine model. Our results indicate that both the use of early-stage blastocysts with a clearly visible inner cell mass (ICM) and the use of pronase to dissect the ICM allow the derivation of a higher proportion of primary ICM outgrowths from PA and SCNT embryos. Primary ICM outgrowths express the molecular markers of pluripotency POU class 5 homeobox 1 (POU5F1) and (sex determining region-Y)-box2 (SOX2), and in some cases, NANOG. Cells obtained after the passages of PA primary ICM outgrowths display alkaline phosphatase (AP) activity and POU5F1, SOX2, caudal-related homeobox-2 (CDX2) and eomesodermin (EOMES) expression, but may lose NANOG. Cystic embryoid body-like structures expressing POU5F1, CDX2 and EOMES were produced from these cells. Immunohistochemical analysis of equine embryos reveals the presence of POU5F1 in trophectoderm, primitive endoderm and ICM. These results suggest that cells obtained after passages of primary ICM outgrowths are positive for trophoblast stem cell markers while expressing POU5F1 and displaying AP activity. Therefore, these cells most likely represent trophoblast cells rather than true ESCs. This study represents an important first step towards the production of autologous equine ESCs for pre-clinical cell therapy studies on large animal models.

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Tesis sobre el tema "Pou5f1"

Campbell, Pearl. "Pou5f1 Post-translational Modifications Modulate Gene Expression and Cell Fate". Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23607.

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Embryonic stem cells (ESCs) are characterized by their unlimited capacity for self-renewal and the ability to contribute to every lineage of the developing embryo. The promoters of developmentally regulated loci within these cells are marked by coincident epigenetic modifications of gene activation and repression, termed bivalent domains. Trithorax group (TrxG) and Polycomb Group (PcG) proteins respectively place these epigenetic marks on chromatin and extensively colocalize with Oct4 in ESCs. Although it appears that these cells are poised and ready for differentiation, the switch that permits this transition is critically held in check. The derepression of bivalent domains upon knockdown of Oct4 or PcG underscores their respective roles in maintaining the pluripotent state through epigenetic regulation of chromatin structure. The mechanisms that facilitate the recruitment and retention of Oct4, TrxG, and PcG proteins at developmentally regulated loci to maintain the pluripotent state, however, remain unknown. Oct4 may function as either a transcriptional activator or repressor. Prevailing thought holds that both of these activities are required to maintain the pluripotent state through activation of genes implicated in pluripotency and cell-cycle control with concomitant repression of genes required for differentiation and lineage-specific differentiation. More recent evidence however, suggests that the activator function of Oct4 may play a more critical role in maintaining the pluripotent state (Hammachi et al., 2012). The purpose of the studies described in this dissertation was to clarify the underlying mechanisms by which Oct4 functions in transcriptional activation and repression. By so doing, we wished to contextualize its role in pluripotent cells, and to provide insight into how changes in Oct4 function might account for its ability to facilitate cell fate transitions. As a result of our studies we find that Oct4 function is dependent upon post-translational modifications (PTMs). We find through a combination of experimental approaches, including genome-wide microarray analysis, bioinformatics, chromatin immunoprecipitation, functional molecular, and biochemical analyses, that in the pluripotent state Oct4, Akt, and Hmgb2 participate in a regulatory feedback loop. Akt-mediated phosphorylation of Oct4 facilitates interaction with PcG recruiter Hmgb2. Consequently, Hmgb2 functions as a context dependent modulator of Akt and Oct4 function, promoting transcriptional poise at Oct4 bound loci. Sumoylation of Oct4 is then required to maintain Hmgb2 enrichment at repressed loci and to transmit the H3K27me3 mark in daughter progeny. The expression of Oct4 phosphorylation mutants however, leads to Akt inactivation and initiates the DNA Damage Checkpoint response. Our results suggest that this may subsequently facilitate chromatin reorganization and cell fate transitions. In summary, our results suggest that controlled modulation of Oct4, Akt, and Hmgb2 function is required to maintain pluripotency and for the faithful induction of transcriptional programs required for lineage specific differentiation.

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Le, Rolle Morgane. "Voie de signalisation WNT/ β-catenin et différenciation des cellules germinales chez les mammifères". Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2019. http://theses.univ-cotedazur.fr/2019AZUR6014.

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La préservation de la fertilité suscite une inquiétude croissante. Depuis les dernières décennies, la fertilité a diminué dans les pays industrialisés. En conséquence, un nombre croissant de couples a recours à la procréation médicalement assistée, sans grand succès par manque de connaissances sur les cellules reproductrices (cellules germinales). L’étude de ces cellules constitue un socle essentiel pour des applications médicales, mais jusqu’à présent, les mécanismes moléculaires qui régissent leur développement restent peu compris en raison de l’absence de modèles d'étude physiologiques.Les cellules germinales sont produites au cours du développement embryonnaire, se multiplient pour constituer un stock suffisant, se différencient dans la gonade en fonction du sexe de l'embryon, puis entrent en méiose pour devenir des gamètes fertiles, les ovocytes (femelles) et les spermatozoïdes (mâles). Mon laboratoire d’accueil a démontré que la voie de signalisation canonique WNT/β-catenin est nécessaire au développement de l'ovaire in vivo et qu'en absence d'activation de cette voie dans l'ovaire embryonnaire de souris, la prolifération et la différenciation des cellules germinales primordiales sont perturbées.Tirant partie de notre expertise dans l'analyse de modèles de différenciation gonadique, nous nous sommes intéressés au mécanisme d'action de la voie WNT/β-catenin dans la différenciation des cellules germinales, en analysant au moyen de modèles murins de perte et gain de fonction de β-catenin les conséquences de la modification de son expression dans les cellules de la gonade.Dans un premier temps, nous avons démontré que le maintien, après la naissance, de l'activité de la voie WNT/β-catenin dans les cellules souches spermatogoniales du testicule de souris stimule leur prolifération de manière massive, provoquant un défaut de différenciation en spermatozoïdes. Dans un deuxième temps, nous avons montré que l'ablation génétique du gène Ctnnb1 (codant pour β-catenin) dans les cellules germinales primordiales in vivo entraîne une perte précoce de leur pluripotence et une différenciation prématurée en ovogonies. Nous avons démontré, pour la première fois in vivo, que tandis que le développement ovarien progresse, β-catenin forme des complexes protéiques avec POU5F1 et CDH1 qui transitent du noyau des cellules germinales à leur membrane, permettant ainsi leur sortie de pluripotence et leur différenciation. Nos résultats indiquent que l'E3-ubiquitine ligase ZNRF3 régule la pluripotence des cellules germinales par une boucle de rétroaction négative.Ces données indiquent que dans l'ovaire comme dans le testicule, une régulation fine de l'activité de la voie de signalisation WNT/β-catenin est requise pour déterminer la fenêtre de différenciation des cellules germinales primordiales in vivo. De plus, la voie WNT/β-catenin contrôle la sortie de pluripotence des cellules germinales primordiales via une activité non-transcriptionnelle de β-catenin, permettant à terme de coordonner le développement des cellules somatiques et germinales de la gonade. Dans les années à venir, nos travaux pourraient aider à la génération des gamètes in vitro
Since the last decennials, fertility is decreasing in industrial countries, and nowadays, infertility reaches a prevalence of 9 to 18% of the general population, with a significant proportion of cases being due to defective gametogenesis. Accordingly, fertility preservation raises a growing concern. Nowadays, a growing number of couples undergo Assisted Reproductive Technology with little success due to the lack of knowledge on mechanisms orchestrating germ cell differentiation. Little is known about how primordial germ cells become gametogenesis-competent cells (gonocytes), because of the lack of suitable physiological models. Primordial germ cells give rise to the next generation by differentiating from pluripotent progenitors into highly specialized cells, the gametes, which in turn generate a totipotent zygote after fertilization. After specification in the early embryo, primordial germ cells colonize the gonad, lose pluripotency and gain their capacity for irreversible sexual differentiation. Gonocytes then become either female (oogonia) or male (spermatogonia), and eventually progress into meiotic divisions. So far, the mechanisms of germ cell changes in potency remain largely elusive.My host laboratory has demonstrated that activation of the canonical WNT/β-catenin signalling is required for ovarian development. Thus, absence of WNT/β-catenin activation eventually triggers defects in germ cell proliferation and sexual differentiation. However, genetic models of cell-specific ablation of Ctnnb1 (encoding β-catenin) were still missing to assess the contribution of WNT/β-catenin in the germ cells. We decided to analyse the role of this signalling pathway by generating specific mouse models for β-catenin loss or gain of function and by investigating the consequences of WNT/β-catenin deregulation in either the somatic or the germ cells of the developing gonad. We first demonstrated that WNT/β-catenin regulates spermatogonial stem cell proliferation and differentiation in the post-natal testis, demonstrating that this signalling activity must be finely tuned over time to ensure spermatogenesis.Secondly, we showed that genetic elimination of Ctnnb1 in mouse primordial germ cells in vivo leads to a precocious loss of pluripotency and to premature germ cell differentiation into gonocytes. We demonstrated, for the first time in vivo, that while ovarian development is getting forward, β-catenin forms proteic complexes containing POU5F1 and CDH1 that transit from the nucleus of the germ cells to their membrane, thus allowing primordial germ cells to exit pluripotency and eventually differentiate. Our results also reveal that the ZNRF3 E3-ubiquitine ligase negatively regulates germ cell exit from pluripotency through a negative feedback loop.Collectively, our results show that the WNT/β-catenin signalling is necessary for determining the proper window of differentiation in both somatic and germ cells. Moreover, WNT/β-catenin controls the germ cell exit from pluripotency through β-catenin non-transcriptional activity, eventually coordinating the development of the different cell types of the fetal ovary. In the future, our results might help to recapitulate gametogenesis in vitro

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Jiang, Hongmei. "THE ROLE OF POU5F1B IN PROSTATE CANCER". OpenSIUC, 2014. https://opensiuc.lib.siu.edu/dissertations/910.

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Accounting for 14% of all new cancer diagnosis in the United States, prostate cancer is the most commonly diagnosed cancer and the second leading cause of cancer related death in the United States. Prognosis for patients diagnosed with metastatic disease is especially poor, since no effective treatments have been developed (1). In this study, we examined the expression and function of POU5F1B, a protein-encoding pseudogene of the homeodomain transcription factor Oct4, in prostate cancer. POU5F1B is located at 8q24, a "gene desert" containing numerous alleles associated with prostate cancer risk. A recent study has indicated that a number of these risk alleles are correlated with POU5F1B expression and prostate cancer susceptibility. The role of POU5F1B in prostate cancer carcinogenesis and progression, however, is not known. In our study, we found that POU5F1B expression is upregulated in prostate cancers and highly overexpressed by high grade (Gleason ≥8) and metastatic prostate cancers. We cloned POU5F1B from prostate cancer cell lines, which contains prostate cancer risk associated SNPs, including a missense mutation inside the homeobox DNA binding domain, to study the functional effects of POU5F1B overexpression in prostate cancers. Here, we report that POU5F1B from prostate tumor encodes functional proteins that exhibit gene transactivation activity comparable to its parent gene, Oct4. Further, we report that POU5F1B overexpression in prostate cancer cell lines increases prostate cancer cell proliferation, migration, anchorage independent growth, and drug resistance in vitro and tumor xenograft growth in vivo. Conversely, shRNA mediated knockdown of endogenous POU5F1B expression in prostate cancer cells inhibit cell proliferation in vitro and tumor growth in vivo, as well as prolong tumor free survival in animal models. The data provide compelling evidence that POU5F1B is an important mediator of prostate cancer progression. We further examined the molecular mechanism behind POU5F1B driven prostate cancer progression. Our studies found that POU5F1B overexpression suppresses E-Cadherin expression at both mRNA and protein levels. Our studies further found POU5F1B overexpression in prostate cancer cells increases Wnt1, TCF1, and TCF4 expression, as well as increased Wnt/β-Catenin signaling - indicating the induction of epithelial-to-mesenchymal transition (EMT) in POU5F1B overexpressing cells(2). Consistently, qPCR analysis found that POU5F1B overexpression significantly increased the expressions of numerous EMT related genes and prostate cancer stem cell markers. Functional studies further confirmed that the transactivation activity of Nanog, another stem cell related transcription factor, is dramatically increased in POU5F1B overexpressing cells. Taken together, our data strongly suggests that POU5F1B overexpression drives prostate cancer progression through the induction of EMT and conferment of stem-cell properties to tumor cells. In summary, our data demonstrated that POU5F1B is overexpressed in prostate tumors, especially high-grade and metastatic tumors, and is a functional driver of prostate cancer progression by inducing EMT in prostate cancer cells. Our study also showed that POU5F1B can potentially be targeted to treat prostate cancer. Based on our findings, depletion of POU5F1B may reduce the risk of metastatic disease or tumor recurrence when used with concurrent therapies in early state tumors and may attenuate treatment resistance in diseases at advanced stages.

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Doretto, Lucas Benites. "Caracterização de marcadores de espermatogônias tronco e sua regulação endócrina e parácrina em zebrafish (Danio rerio)". Botucatu, 2018. http://hdl.handle.net/11449/180640.

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Orientador: Rafael Henrique Nóbrega
Resumo: As células tronco são classificadas em dois grandes grupos de acordo com sua origem e capacidade de diferenciação. Células tronco embrionárias (CTE) são originadas do zigoto, e podem ser classificadas como totipotentes, isto é, capazes de originar um indivíduo inteiro, ou pluripotentes, quando originam os três folhetos embrionários (ecto, meso e endoderme). As células tronco adultas (CTA) são as células tronco encontradas nos tecidos fetais e adultos; classificadas como uni, oligo ou multipotentes dependendo da variedade de tecidos originados a partir delas. Marcadores de células tronco, como antígenos de superfície específicos, fatores de trancrição como OCT4 e NANOG são expressos em CTE e algumas CTA, mas são rapidamente reprimidos à medida que as células se diferenciam. O presente trabalho tem como objetivo identificar marcadores de células tronco e com isso, os efeitos do hormônio endócrino Fsh e do fator parácrino GDNF na atividade proliferativa e gênica dessas populações de células e também de células de Sertoli. Foi observado que os marcadores Pou5f3 e Gfra1a são principalmente expressos em espermatogônias tronco indiferenciadas e que sua expressão reduz significativamente sob efeito do recombinante zebrafish Fsh. Por outro lado, genes como o igf3, nanos3 e nanog tiveram sua expressão aumentada significativamente. O recombinante humano GDNF não altera significativamente a expressão desses genes, porém estimula a proliferação de espermatogônias tipo Aund e Adiff e célul... (Resumo completo, clicar acesso eletrônico abaixo)
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Perez, Christelle. "Contribution à l'étude des bases moléculaires des maladies de la croissance et du mécanisme de régulation du gène GH chez l'homme". Paris 6, 2012. http://www.theses.fr/2012PA066041.

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Chez la souris, Six6 et Lhx2 sont exprimés dans l’œil et la glande pituitaire en développement. Par une approche "gènes candidats", les ADN de patients avec un phénotype proche de celui de souris invalidées pour ces gènes ont été séquencés. Aucune mutation a été mise en évidence pour SIX6. Deux variations hétérozygotes faux-sens de LHX2 ont été identifiées mais n’ont pas d'effet (tests in vitro). LHX2 a un rôle régulateur transcriptionnel in vitro sur deux gènes pituitaires (PRL, POU1F1), et en action synergique avec POU1F1. Deux mutations hétérozygotes composites de LHX3 chez un patient non consanguin ont permis d’assigner à ce gène un syndrome décrit uniquement chez des patients consanguins. Une de ces mutations a un effet dominant négatif. POU1F1, impliqué dans la différenciation pituitaire terminale, est associé en pathologie humaine à un déficit en hormone de croissance (GH), PRL et TSHβ. L’expression de GH est régulée par la fixation de POU1F1 sur son promoteur et sur un « Locus Control Region » mais ses cofacteurs ne sont pas connus. Deux mutations faux-sens identifiées dans le domaine de transactivation (TAD) de POU1F1 sont associées à un déficit isolé en GH. La résonnance plasmonique de surface a permis de définir les interactions de POU1F1 (normal et mutés) sur ses séquences cibles ; des extraits nucléaires sont passés avec POU1F1 (normal et mutés) afin d’identifier (par spectrométrie de masse) ses partenaires au locus GH. Une cristallographie du TAD a débuté pour analyser sa structure tridimensionnelle qui est probablement altéré par les mutations identifiées
In mice, Six6 and Lhx2 were shown to be expressed in developing eye and pituitary gland. Using a candidate gene approach, DNA from patients with phenotypic features reminiscent of those reported in invalidated mice were sequenced. Any mutation was identified in SIX6 gene. Two LHX2 heterozygous missense variations were identified but are not deleterious (in vitro tests). A transcriptional regulator role of LHX2 was shown in vitro on two pituitary genes (PRL, POU1F1), and a synergic action with POU1F1 on these promoters. Two compound heterozygous LHX3 mutations in a non consanguineous patient permitted us to implicate this gene in syndrome described in other consanguineous patients. A dominant negative effect of one of these mutations was shown. POU1F1, implicated in terminal pituitary differentiation is associated, in human pathology, with growth hormone (GH), PRL and TSHβ deficiencies. GH expression is regulated by POU1F1 binding on its promoter and on a locus control region but its co-factors are not known. Two new missense mutations located in the POU1F1 transactivation domain (TAD) were identified and associated with isolated growth hormone deficiency. Surface plasmon resonance permitted us to define interaction properties between POU1F1 (wild-type and mutated) on its target sequences. Nuclear extracts from pituitary cell lines are used with POU1F1 (wild-type and mutated) to identified (by mass spectrometry) co-factors at GH locus. A crystallographic study was started to determine the TAD tridimensional structure which is probably altered by the identified mutations

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Ubhi, Kirenjeet. "The POU-domain transcription factor, POU3f1, in neurodevelopment, psychiatric disorders and brain injury". Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431674.

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Roche, Catherine. "Thérapies alternatives des adénomes somatotropes et lactotropes résistants : implication du facteur de transcription POU1F1 et du récepteur SST2". Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM5067.

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A ce jour, un certain nombre d'adénomes hypophysaires somatotropes échappent encore au contrôle de la maladie. Il reste nécessaire d'étudier plus finement les différentes voies de contrôle de la sécrétion hormonale et de la prolifération tumorale afin d'identifier des traitements alternatifs susceptibles de contrôler ces symptômes tumoraux. De même, un certain nombre de patients porteurs de prolactinomes (environ 10%), à l'origine de dysfonctionnement gonadique et sexuels, échappent au contrôle de l'hypersécrétion de prolactine par les traitements actuels. Pour ces deux types de tumeurs, s'ajoutent des complications neurologiques consécutives à l'accroissement des volumes tumoraux. Dans une perspective de contrôle de l'hypersécrétion tumorale nous nous sommes intéressés à deux stratégies faisant intervenir un transfert de gènes dans les cellules. POU1F1 est un facteur de transcription crucial pour le développement et le maintien des lignages somatotrope, lactotrope et thyréotrope et son expression est retrouvée dans les adénomes hypophysaires. De plus, des mutations de ce gène, notamment le mutant dominant négatif R271W, ont été identifiés chez des patients présentant des déficits hypophysaires combinés en GH, en PRL et en TSH. Une première partie de ma thèse a donc porté sur l'étude du transfert du mutant dominant négatif de POU1F1 par un vecteur lentiviral dans les tumeurs hypophysaires somatotropes et lactotropes afin d'évaluer son impact sur la sécrétion hormonale et sur la viabilité cellulaire. Nous avons montré que l'inactivation de ce facteur de transcription entrainait une diminution de la viabilité cellulaire et de la sécrétion de toutes les tumeurs testées
To this date, some somatotroph adenomas do not respond to the current treatment of pituitary tumors. It still necessary to study the different ways to control the hormonal secretion and the tumor progression to identify alternate therapy capable to manage these symptoms. Likewise, some patient with prolactinomas (about 10%) responsible of gonad and sexual dysfunction do not respond to the control of prolactin hypersecretion. In addition, some neurological complications are finding due to the neighboring structures compression for both of these tumors. To better control the hormonal secretion we investigate two different strategies involving a gene transfer in the cells. POU1F1 is a major transcription factor involved in the pituitary development and the management of somatotroph, thyreotroph and lactotroph cell lines. Its expression is found in pituitary adenomas belonging of these 3 cell lines. Moreover some mutations like the R271W mutant are identified in patients with combined pituitary hormonal deficiency (CPHD). In the first part of my thesis we transfer this dominant negative mutant via a lentiviral transfer in the somatotroph and lactotroph adenomas to evaluate its impact on hormonal secretion and cell viability. We show an inhibitory effect of the POU1F1 inactivation on the secretion and the cell viability of all our tumors. Somatostatin analogs are the major medical therapy for somatotroph adenomas and control GH secretion in 60% of these patients. Octreotide resistance is highly correlated to a low expression of the sst2 receptor

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Pérez, Christelle. "Contribution à l'étude des bases moléculaires des maladies de la croissance et du mécanisme de régulation du gène GH chez l'homme". Phd thesis, Université Pierre et Marie Curie - Paris VI, 2012. http://tel.archives-ouvertes.fr/tel-00834281.

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Chez la souris, Six6 et Lhx2 sont exprimés dans l'œil et la glande pituitaire en développement. Par une approche "gènes candidats", les ADN de patients avec un phénotype proche de celui de souris invalidées pour ces gènes ont été séquencés. Aucune mutation a été mise en évidence pour SIX6. Deux variations hétérozygotes faux-sens de LHX2 ont été identifiées mais n'ont pas d'effet (tests in vitro). LHX2 a un rôle régulateur transcriptionnel in vitro sur deux gènes pituitaires (PRL, POU1F1), et en action synergique avec POU1F1. Deux mutations hétérozygotes composites de LHX3 chez un patient non consanguin ont permis d'assigner à ce gène un syndrome décrit uniquement chez des patients consanguins. Une de ces mutations a un effet dominant négatif. POU1F1, impliqué dans la différenciation pituitaire terminale, est associé en pathologie humaine à un déficit en hormone de croissance (GH), PRL et TSHβ. L'expression de GH est régulée par la fixation de POU1F1 sur son promoteur et sur un " Locus Control Region " mais ses cofacteurs ne sont pas connus. Deux mutations faux-sens identifiées dans le domaine de transactivation (TAD) de POU1F1 sont associées à un déficit isolé en GH. La résonnance plasmonique de surface a permis de définir les interactions de POU1F1 (normal et mutés) sur ses séquences cibles ; des extraits nucléaires sont passés avec POU1F1 (normal et mutés) afin d'identifier (par spectrométrie de masse) ses partenaires au locus GH. Une cristallographie du TAD a débuté pour analyser sa structure tridimensionnelle qui est probablement altéré par les mutations identifiées

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Fujita, R. "Analysing the effect of co-expression of Brn-3a/POU4F1 transcription factor with p53 family proteins in the heart". Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1403064/.

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The fate of cells is determined by a distinct group of transcription factors (TFs) which control the target gene expression in response to cellular stimuli during development and after injury. Moreover, TFs can physically interact with each other, thereby modifying target gene transcription for the fine‐-tuning of cell fate determination depending on the specific cellular signals. The Brn‐-3 family of TFs, B rn‐-3aand Brn-‐3b, was o riginallyisolated and characterised in the neurons of the central and peripheral nervous system, where they play a critical role in differentiation and cell survival during the nervous development. Studies have since shown that Brn‐- 3TFs are expressed in the murine heart during cardiac development, however, the roles of these TFs in the heart following injury are yet to be elucidated. Further to the direct control of gene transcription, Brn-‐3a also physically interacts with p53 and alters cellular response by modifying p53 target gene expression. Thus, up onco-‐expression with p53, Brn -‐3 aprotects neuronal cells from apoptosis and enhances survival by inhibiting p53‐-mediated transcription of pro-¬‐ apoptotic prot einsBax and Noxa, while increasing expression of cell cycle arrest gene p21cip1/waf1 In this study, we investigated the potential role for Brn‐-3a in protecting cardiomyocytes from p53-‐mediated apoptosis following injurious stimuli such as ischemia. W efound that p53 a ndit spr o-‐apoptotic target g enesBax, Noxa and Puma were markedly induced in the infarcted m yocardiumof the injured mouse heart by 1 week after permanent ischemia. In contrast, pro‐-survival Brn-‐3 awas upregulated in the non-‐infarct, remote area of the heart, but interestingly, Brn-‐3a was found to be downregulated in the infarcted tissues where upregulation of the pro-‐apoptotic proteins was most evident. Importantly, immunostaining analysis revealed that Brn‐-3a was co-¬‐ localised with p53 in a distinct region of myocardium bordering th einfarct and non‐- infarct areas. Moreover, transfection studies indicated that Brn‐-3a enhanced activity of p53 to activate thep21cip1/waf1 promoter in H9c2 cells. In conclusion, our results suggest that Brn‐-3a is co‐-expressed with p53 in a subpopulation o fcardiomyocytes following ischemic injury and that this pro-‐survival TF may play a role in protecting cardiomyocytes from ischemia‐-induced apoptosis through modulation of p53‐-dependent transcription of apoptosis‐-associated genes.

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Cosse-Etchepare, Camille. "Étude du rôle des facteurs de transcription pou3f au cours du développement rénal". Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066283/document.

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Chez le xénope, le pronéphros constitue le rein fonctionnel du têtard. Le sang est filtré par le glomus et l'urine est modifiée lors de son transit dans le tubule. Au cours de ma thèse, nous avons analysé l'expression des quatre membres de la famille pou3f au cours du développement embryonnaire chez le xénope. Nous avons montré que leur expression neurale, otique ou encore épidermique est conservée entre le xénope et la souris, de même que l'expression rénale de pou3f3. Nous avons également mis en évidence une expression pronéphrique de pou3f4. Nous avons ensuite analysé le rôle de Pou3f4 au cours du développement du pronéphros. La perte de fonction de Pou3f4 entraine des défauts de différenciation terminale du tubule intermédiaire et distal. Sa surexpression aboutit au contraire à une augmentation de l'expression des marqueurs de différenciation slc12a1 et clcnkb1. Les morphants Pou3f4 présentent aussi des défauts de morphogenèse du tubule intermédiaire caractérisés par des circonvolutions réduites. Nos résultats montrent que Pou3f4 contrôle l'expression de l'ephrine efnA3 dans le tubule pronéphrique. La perte de fonction d'EfnA3 conduit à des défauts de morphogenèse du tubule, suggérant que Pou3f4, par la régulation de l'expression d'efnA3, est impliqué dans les mouvements cellulaires nécessaires à l'élongation antérieure du tubule. Enfin, nous avons observé que pou3f3 et pou3f4 ne se régulent pas l'un de l'autre. Nous avons en revanche mis en évidence une redondance fonctionnelle de ces gènes dans la morphogenèse et la différenciation du tubule puisque la perte de fonction combinée de Pou3f3 et Pou3f4 entraine un phénotype plus sévère que chaque simple perte de fonction
In Xenopus, pronephros is the functional kidney at tadpole stage. The blood is filtrated by the glomus and the urine is modifed all along the tubule. Pou3f3 is required for intermediate and distal tubule formation in mouse. During my PhD, we have analyzed the expression of the four pou3f genes during Xenopus embryonic development. We found that neural, otic, or epidermic expression of the various pou3f genes is conserved between Xenopus and mouse. Pou3f3 expression in the pronephros is similar to that observed in mouse. We futher showed for the first time pou3f4 expression in the developping kidney. Then, we analyzed the role of Pou3f4 during pronephros development. Pou3f4 depletion inhibits the expression of terminal differentiation marker genes in the intermediate and distal tubule. Pou3f4 upregulates the expression of slc12a1 and clcnkb1 in the tubule. Moreoer, we found that Pou3f4 loss of function leads to intermediate tubule morphogenesis defects. While ephrin signaling pathway is largely described as playing crucial role in cellular movement, Pou3f4 controls efnA3 expression in the intermediate and distal tubule. EfnA3 depletion phenocopies Pou3f4 loss of function, suggesting that Pou3f4, by regulationg efnA3 expression, is implicated in cell movements necessary for anterior elongation of the tubule. Finally, we find that pou3f3 and pou3f4 do not regulate each other expression. However, they act redundantly in pronephros development since the combined Pou3f3 and Pou3f4 loss of function results in a more severe phenotype than each loss of function alone

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Libros sobre el tema "Pou5f1"

Lynn, Pat. Easy stitch pouff quilt. Lancaster, Ca: Pouff Quilt International, 1994.

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Gilman, Susan Jane. Hypocrite in a Pouffy White Dress. New York: Grand Central Publishing, 2007.

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Pouf et Youpi boxeurs. [Paris]: Hachette jeunesse, 1992.

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Crowning glories: 21 bridal & communion headpieces, hats, poufs & veils. Canby, Ore: Hot Off The Press, 1994.

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Gilman, Susan Jane. Hypocrite in a pouffy white dress: Tales of growing up groovy and clueless. New York: Warner Books, 2005.

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Hypocrite in a pouffy white dress: Tales of growing up groovy and clueless. New York: Warner Books, 2005.

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Hypocrite in a Pouffy White Dress {Unabridged Audio}. Books on Tape, Inc., 2005.

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Ponti, Claude. Petit prince Pouf. Ecole des loisirs, 2002.

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Perfectionist's How to Book Iii, Window Specialties (Romans, Austrians, Balloons, Pouffs). Lederer Enterprises, 1985.

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Pouf Pieces (Hanuman, Book No. 35). Hanuman Books, 1990.

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Capítulos de libros sobre el tema "Pou5f1"

Garcia, Thomas y Marie-Claude Hofmann. "Isolation of Undifferentiated and Early Differentiating Type A Spermatogonia from Pou5f1-GFP Reporter Mice". En Methods in Molecular Biology, 31–44. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-436-0_3.

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Pf�ffle, R., O. Blankenstein, S. W�ller, K. Heimann y G. Heimann. "Pituitary Transcription Factors, POU1F1 and PROP1 Defects". En Hypothalamic-Pituitary Development, 61–76. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000060863.

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Gottfried, I., P. L. M. Huygen y K. B. Avraham. "The Clinical Presentation of DFNA15/POU4F3". En Advances in Oto-Rhino-Laryngology, 92–97. Basel: KARGER, 2002. http://dx.doi.org/10.1159/000066819.

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"POU5F1". En Encyclopedia of Signaling Molecules, 4111. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_103016.

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"Focus: Mutations of the Brn4/Pou3f4 Locus". En Handbook of Mouse Auditory Research, 631–34. CRC Press, 2001. http://dx.doi.org/10.1201/9781420038736-47.

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Gaxie, Daniel, Jérôme Heurtaux y Anne-France Taiclet. "6. « Nabot ! » « Gros pouf ! »". En Les sens du vote, 153–77. Presses universitaires de Rennes, 2016. http://dx.doi.org/10.4000/books.pur.73673.

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Kremer, Hannie, Cor W. R. J. Cremers, Erwin Van Wijk y Frans P. M. Cremers. "POU3F4 and Mixed Deafness With Temporal Bone Defect (DFNX2)". En Epstein's Inborn Errors of Development, 875–79. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199934522.003.0129.

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Le Theule, Marie-Astrid. "DES FICELLES, DES POUFS ET UN ART DU SENS :". En L’art du sens dans les organisations, 27–38. Presses de l'Université Laval, 2019. http://dx.doi.org/10.2307/j.ctv1h0p25s.4.

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Strub, Thomas, Dominique Kobi, Dana Koludrovic y Irwin Davidso. "A POU3F2-MITF-SHC4 Axis in Phenotype Switching of Melanoma Cells". En Research on Melanoma - A Glimpse into Current Directions and Future Trends. InTech, 2011. http://dx.doi.org/10.5772/19769.

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Majdoub, Hussein, Serge Amselem, Marie Legendre, Shoshana Rath, Dani Bercovich y Yardena Tenenbaum-Rakover. "Extreme Short Stature and Severe Neurological Impairment in a 17-Year-Old Male with Untreated Combined Pituitary Hormone Deficiency Due to POU1F1 Mutation". En Prime Archives in Endocrinology. Vide Leaf, Hyderabad, 2020. http://dx.doi.org/10.37247/paendo.1.2020.6.

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Actas de conferencias sobre el tema "Pou5f1"

Miyoshi, Norikatsu, Shiki Fujino, Masaru Sasaki, Kazuhiro Saso, Hidekazu Takahashi, Naotsugu Haraguchi, Taishi Hata et al. "Abstract 3687: Colorectal cancer stem cell expressing POU5F1 promotes liver metastasis". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3687.

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Miyoshi, Norikatsu, Shiki Fujino, Masaru Sasaki, Takayuki Ogino, Hidekazu Takahashi, Mamoru Uemura, Chu Matsuda, Tsunekazu Mizushima, Hidetoshi Eguchi y Yuichiro Doki. "Abstract 4962: Tumor heterogeneity driven by cancer stem cell expressing POU5F1". En Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4962.

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Maskell, L., K. Qamar, TA Hawkins y VS Budhram-Mahadeo. "P23 Essential but partially redundant roles for POU4F1/BRN-3A and POU4F2/BRN-3B transcription factors in the developing heart". En British Society for Cardiovascular Research, Autumn Meeting 2017 ‘Cardiac Metabolic Disorders and Mitochondrial Dysfunction’, 11–12 September 2017, University of Oxford. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bscr.28.

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Jiang, Hongmei, Man-Tzu Wang y Daotai Nie. "Abstract 4970: The role of POU5F1B in prostate cancer". En 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.am2014-4970.

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Jiang, Hongmei, Man-Tzu Wang y Daotai Nie. "Abstract LB-281: The role of POU5F1B in prostate cancer." En 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-lb-281.

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Breyer, Joan P. y Jeffrey R. Smith. "Abstract 2568: Genetic association of POU5F1B at 8q24 with prostate cancer." En 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.am2013-2568.

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Tsou, Ann-Ping, Yu-Lun Liao, Yi-Ming Sun, Jorng-Tzong Horng y Michael Hsiao. "Abstract 3109: SOX4 and POU2F1 synergistically regulate metastasis-associated NRP1 in HCC metastasis." En 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.am2013-3109.

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Huang, Yuan-Ling, Wen-Cheng Chou, Chia-Ni Hsiung, Ling-Yueh Hu, Hou-Wei Chu y Chen-Yang Shen. "Abstract 2156: FGFR2 regulates Mre11 expression and double-strand break repair via the MEK-ERK-POU1F1 pathway in breast tumorigenesis". En 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.am2015-2156.

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Li, Q., N. Omote, Z. Chen, G. DeIuliis, Z. Zhu, E. Herzog, A. Shakya, D. Tantin, J. D. Herazo-Maya y N. Kaminski. "Deletion of Pou2af1 in Type II Alveolar Epithelial Cells Augments Bleomycin-Induced Pulmonary Fibrosis". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5407.

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Martin, Kathi, Nick Jushchyshyn y Claire King. Christian Lacroix Evening gown c.1990. Drexel Digital Museum, 2017. http://dx.doi.org/10.17918/wq7d-mc48.

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The URL links to a website page in the Drexel Digital Museum (DDM) fashion image archive containing a 3D interactive panorama of an evening gown by French fashion designer Christian Lacroix with related text. This evening gown by Christian Lacroix is from his Fall 1990 collection. It is constructed from silk plain weave, printed with an abstract motif in the bright, deep colors of the local costumes of Lacroix's native Arles, France; and embellished with diamanté and insets of handkerchief edged silk chiffon. Ruffles of pleated silk organza in a neutral bird feather print and also finished with a handkerchief edge, accentuate the asymmetrical draping of the gown. Ruching, controlled by internal drawstrings and ties, creates volume and a slight pouf, a nod to 'le pouf' silhouette Lacroix popularized in his collection for Patou in 1986. Decorative boning on the front of the bodice reflects Lacroix's early education as a costume historian and his sartorial reinterpretation of historic corsets. It is from the private collection of Mari Shaw. The panorama is an HTML5 formatted version of an ultra-high resolution ObjectVR created from stitched tiles captured with GigaPan technology. It is representative the ongoing research of the DDM, an international, interdisciplinary group of researchers focused on production, conservation and dissemination of new media for exhibition of historic fashion.

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