The Experts below are selected from a list of 1985835 Experts worldwide ranked by ideXlab platform
Naihe Jing - One of the best experts on this subject based on the ideXlab platform.
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different transcription factors regulate nestin gene expression during P19 Cell neural differentiation and central nervous system development
Journal of Biological Chemistry, 2009Co-Authors: Wei Bian, Leping Cheng, Guoliang Xu, Yongfeng Chen, Naihe JingAbstract:Nestin is a molecular marker for neural progenitor Cells. Rat and human nestin genes possess a central nervous system-specific enhancer within their second introns. However, the transcription factors that bind to the nestin enhancer have not been fully elucidated. Here, we show that the second intron of the mouse nestin gene is sufficient to drive reporter gene expression in the developing nervous system. The core sequence of this central nervous system-specific enhancer localizes to the 3' 320-bp region. The cis-elements for Sox and POU family transcription factors and the hormone-responsive element are essential for nestin expression during embryonic carcinoma P19 Cell neural differentiation and in the developing chick neural tube. Interestingly, different transcription factors bind to the nestin enhancer at different stages of P19 Cell neural differentiation and central nervous system development. Sox2 and SF1 may mediate basal nestin expression in undifferentiated P19EC Cells, whereas Sox2, Brn1, and Brn2 bind to the enhancer in P19 neural progenitor Cells. Similarly, in vivo, Oct1 binds to the nestin enhancer in embryonic day 8.5 (E8.5) mouse embryos, and Oct1, Brn1, and Brn2 bind to this enhancer in E10.5 and E12.5 mouse embryos. Our studies therefore suggest a temporal coordination of transcription factors in determining nestin gene expression.
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comparative proteomic analysis of proteins involved in Cell aggregation during neural differentiation of P19 mouse embryonic carcinoma Cells
Journal of Proteome Research, 2009Co-Authors: Xia Gao, Naihe Jing, Li Liu, Hongyu Tian, Fukun ZhaoAbstract:Cell-Cell interactions play a crucial role during embryogenesis and are enhanced during Cell aggregation. P19 mouse embryonic carcinoma Cells can differentiate into neural Cells by the addition of retinoic acid (RA) or by overexpression of the Wnt1 gene, with both processes dependent on Cell aggregation. To identify molecules involved in the Cell aggregation process, two-dimensional gel electrophoresis (2DE) was used to establish the Cell aggregation-associated protein profiles. MALDI-TOF/TOF was used to identify 71 protein spots with differential expression patterns. Among these spots, 54 were differentially expressed in both P19 and Wnt1-overexpressing P19 (Wnt1/P19) Cell aggregates, with 42 proteins up-regulated and 12 proteins down-regulated. The other 17 spots were differentially expressed only in Wnt1/P19 Cells. The expression patterns of 5 Cell aggregation-associated proteins, N-myc downstream-regulated gene 1 (NDRG1), 14-3-3 epsilon, 14-3-3 gamma, acid calponin and Cell division control protein 2 homologue (Cdc2), were confirmed by immunoblot and RT-PCR. To further investigate the relationship between Cell aggregation and neural differentiation, NDRG1 expression was inhibited by RNA interference during P19 Cell aggregation. Silencing of NDRG1 reduced the size of Cell aggregates and the expression of N-cadherin, and it also impaired the RA-induced P19 Cell neural differentiation. In conclusion, this study provides new clues for the possible mechanism underlying Cell aggregation during pluripotent stem Cell neural differentiation.
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ADAM23 Plays Multiple Roles in Neuronal Differentiation of P19 Embryonal Carcinoma Cells
Neurochemical Research, 2007Co-Authors: Yaping Sun, Naihe Jing, Yingming Wang, Jing Zhang, Jing Tao, Chen Wang, Kejing Deng, Shouyi QiaoAbstract:ADAM23, belonging to ADAM (A Disintegrin And Metalloprotease) protein family, is mainly expressed in brain. P19 Cells could differentiate into neuroectodermal Cell lineage after Cell aggregates have been induced by retinoic acid (RA). In this report, we show that the post-transcriptional and post-translational processes of ADAM23 are regulated during the differentiation of P19 Cells. In P19-derived neurons, ADAM23 is polarized distributed in the proximal part. To explore the possible roles of ADAM23 during P19 Cell neuronal differentiation, ADAM23-RNAi P19 Cell lines were established. These transfected Cells could differentiate into neurofilament-expression neurons in the absence of RA, whereas wild-type P19 Cell can not. These results suggest ADAM23 may play roles in both early and later stage of neuronal differentiation.
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Cell aggregation-induced FGF8 elevation is essential for P19 Cell neural differentiation.
Molecular biology of the cell, 2006Co-Authors: Chen Wang, Wei Bian, Caihong Xia, Li Liu, Wei Lin, Ye-guang Chen, Siew-lan Ang, Naihe JingAbstract:FGF8, a member of the fibroblast growth factor (FGF) family, has been shown to play important roles in different developing systems. Mouse embryonic carcinoma P19 Cells could be induced by retinoic acid (RA) to differentiate into neuroectodermal Cell lineages, and this process is Cell aggregation dependent. In this report, we show that FGF8 expression is transiently up-regulated upon P19 Cell aggregation, and the aggregation-dependent FGF8 elevation is pluripotent stem Cell related. Overexpressing FGF8 promotes RA-induced monolayer P19 Cell neural differentiation. Inhibition of FGF8 expression by RNA interference or blocking FGF signaling by the FGF receptor inhibitor, SU5402, attenuates neural differentiation of the P19 Cell. Blocking the bone morphogenetic protein (BMP) pathway by overexpressing Smad6 in P19 Cells, we also show that FGF signaling plays a BMP inhibition-independent role in P19 Cell neural differentiation.
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Differential display of proteins involved in the neural differentiation of mouse embryonic carcinoma P19 Cells by comparative proteomic analysis.
Proteomics, 2005Co-Authors: Quan Yuan, Naihe Jing, Chen Wang, Li Liu, Hongyu Tian, K. Tang, Fukun ZhaoAbstract:Mouse embryonic carcinoma P19 Cell has been used extensively as a model to study molecular mechanisms of neural differentiation in vitro. After retinoic acid (RA) treatment and aggregation, P19 Cells can differentiate into neural Cells including neurons and glial Cells. In this study, comparative proteomic analysis is utilized to approach the protein profiles associated with the RA-induced neural differentiation of P19 Cells. Image analysis of silver stained two-dimensional gels indicated that 28 protein spots had significantly differential expression patterns in both quantity and quality. With mass spectrometry analysis and protein functional exploration, many proteins demonstrated an association with distinct aspects of neural differentiation. These proteins were gag polyprotein, rod cGMP-specific 3',5'-cyclic phosphodiesterase, 53 kDa BRG1-associated factor A, N-myc downstream regulated 1, Vitamin D receptor associated factor 1, stromal Cell derived factor receptor 1, phosphoglycerate mutase, Ran-specific GTPase-activating protein, and retinoic acid (RA)-binding protein. While some cytoskeleton-related proteins such as beta cytoskeletal actin, gamma-actin, actin-related protein 1, tropomyosin 1, and cofilin 1 are related to Cell migration and aggregation, other proteins have shown a relationship with distinct aspects of neural differentiation including energy production and utilization, protein synthesis and folding, Cell signaling transduction, and self-protection. The differential expression patterns of these 28 proteins indicate their different roles during the neural differentiation of P19 Cells. As an initial step toward unveiling the regulations involved in the commitment of pluripotent Cells to a neural fate, information from this study may be helpful to uncover the molecular mechanisms of neural differentiation.
Chun Zhu - One of the best experts on this subject based on the ideXlab platform.
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effect of mir 20b on apoptosis differentiation the bmp signaling pathway and mitochondrial function in the P19 Cell model of cardiac differentiation in vitro
PLOS ONE, 2015Co-Authors: Shasha Zhu, Xuehua Liu, Shuping Han, Jingai Zhu, Yuzhu Peng, Chun ZhuAbstract:Objective To explore the effect of miR-20b on apoptosis, differentiation, the BMP signaling pathway and mitochondrial function in the P19 Cell model of cardiac differentiation in vitro.
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over expression of microrna 19 b on P19 Cell through wnt beta catenin pathway
Chinese Journal of Applied Clinical Pediatrics, 2014Co-Authors: Xuehua Liu, Dani Qin, Shasha Zhu, Shuping Han, Jingai Zhu, Chun ZhuAbstract:Objective Previously study indicated that the microRNA(miR)-19b is highly correlated with heart development by chip screening. This study aims to explore the function of miR-19b overexpression on P19 Cells through Wnt/beta-catenin signaling pathway. Methods Potential target gene of miR-19b was predicted by bioinformatics software such as TargetScan on line; Dual luciferase reporter gene system was applied to test whether the the predict target could bind with miR-19b and transfect miR-19b overexpression plasmid or vector into P19 Cells by lipo 2000 and stable Cell lines was selected by Blasticidin; CCK-8 assay was adopted to detect Cell proliferation activityed and Cell apoptosis was detected with Phosphatidylserine eversion analysis.Wnt1 protein expression level and the miR-19b RNA expression levels were detected by Western blot and real-time quantitative PCR. Results Wnt1 was the potential targets of miR-19b in P19 Cells by TargetScan 5.1 software, which was verified by dual luciferase reporter gene; The results of luciferase reporter gene system demonstrats that miR-19b ihibited the activity of Wnt not the Wnt mutation(P<0.05); Overexpression of miR-19b reduced Wnt1 and beta-catenin expression level in the Wnt signaling pathway, respectively(at most point P<0.05). Moreover, miR-19b could promote the proliferation of P19 Cell(at most point P<0.05), and inhibit its apoptosis(P<0.05). Conclusions MiR-19b promotes the P19 Cell proliferation, inhibits its apoptosis.In addition, miR-19b is indirectly interacted with target gene Wnt1 and affects P19 Cell lines through Wnt/beta-catenin signaling pathway. This study shows a new insight of heart development and more efforts are needed on exploring the deep function of heart diseses. Key words: MicroRNA-19b; P19 Cell; Wnt pathway
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Over-expression of MicroRNA-19-b on P19 Cell through Wnt/beta-catenin pathway
Chinese Journal of Applied Clinical Pediatrics, 2014Co-Authors: Xuehua Liu, Dani Qin, Shasha Zhu, Shuping Han, Yu Zhangbin, Zhu Jingai, Chun ZhuAbstract:Objective Previously study indicated that the microRNA(miR)-19b is highly correlated with heart development by chip screening. This study aims to explore the function of miR-19b overexpression on P19 Cells through Wnt/beta-catenin signaling pathway. Methods Potential target gene of miR-19b was predicted by bioinformatics software such as TargetScan on line; Dual luciferase reporter gene system was applied to test whether the the predict target could bind with miR-19b and transfect miR-19b overexpression plasmid or vector into P19 Cells by lipo 2000 and stable Cell lines was selected by Blasticidin; CCK-8 assay was adopted to detect Cell proliferation activityed and Cell apoptosis was detected with Phosphatidylserine eversion analysis.Wnt1 protein expression level and the miR-19b RNA expression levels were detected by Western blot and real-time quantitative PCR. Results Wnt1 was the potential targets of miR-19b in P19 Cells by TargetScan 5.1 software, which was verified by dual luciferase reporter gene; The results of luciferase reporter gene system demonstrats that miR-19b ihibited the activity of Wnt not the Wnt mutation(P
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Effects of miR-19b overexpression on proliferation, differentiation, apoptosis and Wnt/β-catenin signaling pathway in P19 Cell model of cardiac differentiation in vitro.
Cell biochemistry and biophysics, 2013Co-Authors: Dani Qin, Lingmei Qian, Shuping Han, Chun Zhu, Xuejie WangAbstract:MicroRNA (miR)-19b is part of the miR-17–92 cluster associated with cardiac development. Here, we investigated the effects of overexpressing miR-19b on proliferation, differentiation, apoptosis, and regulation of the Wnt/β-catenin signaling pathway in the multipotent murine P19 Cell line that can be induced to undergo cardiogenesis. P19 Cells were transfected with the miR-19b plasmid or empty vector, and miR-19b overexpression was verified by Quantitative Real-Time PCR (qPCR). The miR-19b or vector control stable Cell lines were selected using Blasticidin S HCl, and their proliferation, Cell cycle, and apoptosis levels were analyzed using the Cell Counting Kit-8 and flow cytometry. P19 Cell differentiation markers, apoptosis-related genes (bax, bcl-2), and Wnt/β-catenin signaling pathway-related genes were detected by qPCR, the corresponding proteins by Western blot. Expression of the Wnt pathway and differentiation marker proteins was also verified by immunofluorescence. Morphological changes associated with apoptosis were observed by electron microscopy and Hoechst staining. On the basis of these results, we demonstrated that miR-19b overexpression promoted proliferation and differentiation but inhibited apoptosis in P19 Cells; Wnt and β-catenin expressions were decreased, while that of GSK3β was increased with miR-19b overexpression. Overexpression of miR-19b inhibited activation of the Wnt/β-catenin signaling pathway in P19 Cells, which may regulate cardiomyocyte differentiation. Our findings may bring new insights into the mechanisms underlying cardiac diseases and suggest that miR-19b is a potential new therapeutic target for cardiovascular diseases.
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effects of mir 19b overexpression on proliferation differentiation apoptosis and wnt β catenin signaling pathway in P19 Cell model of cardiac differentiation in vitro
Cell Biochemistry and Biophysics, 2013Co-Authors: Dani Qin, Lingmei Qian, Shuping Han, Chun Zhu, Xuejie WangAbstract:MicroRNA (miR)-19b is part of the miR-17–92 cluster associated with cardiac development. Here, we investigated the effects of overexpressing miR-19b on proliferation, differentiation, apoptosis, and regulation of the Wnt/β-catenin signaling pathway in the multipotent murine P19 Cell line that can be induced to undergo cardiogenesis. P19 Cells were transfected with the miR-19b plasmid or empty vector, and miR-19b overexpression was verified by Quantitative Real-Time PCR (qPCR). The miR-19b or vector control stable Cell lines were selected using Blasticidin S HCl, and their proliferation, Cell cycle, and apoptosis levels were analyzed using the Cell Counting Kit-8 and flow cytometry. P19 Cell differentiation markers, apoptosis-related genes (bax, bcl-2), and Wnt/β-catenin signaling pathway-related genes were detected by qPCR, the corresponding proteins by Western blot. Expression of the Wnt pathway and differentiation marker proteins was also verified by immunofluorescence. Morphological changes associated with apoptosis were observed by electron microscopy and Hoechst staining. On the basis of these results, we demonstrated that miR-19b overexpression promoted proliferation and differentiation but inhibited apoptosis in P19 Cells; Wnt and β-catenin expressions were decreased, while that of GSK3β was increased with miR-19b overexpression. Overexpression of miR-19b inhibited activation of the Wnt/β-catenin signaling pathway in P19 Cells, which may regulate cardiomyocyte differentiation. Our findings may bring new insights into the mechanisms underlying cardiac diseases and suggest that miR-19b is a potential new therapeutic target for cardiovascular diseases.
Ilona S. Skerjanc - One of the best experts on this subject based on the ideXlab platform.
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a P19 cardiac Cell line as a model for evaluating cardiac tissue engineering biomaterials
The Open Tissue Engineering and Regenerative Medicine Journal, 2009Co-Authors: Jennifer Dawson, Ilona S. Skerjanc, Sophie Boisvenue, May GriffithAbstract:Our objective was to develop a suitable cardiomyocyte progenitor Cell line for use in testing biomaterials as potential scaffolds in cardiac tissue engineering. We transfected P19 Cells with the human cardiac -actin promoter driving the gene for puromycin resistance, to create a stable cardiomyocyte-selectable P19 Cell line, termed P19(CA- Puro). Puromycin selection resulted in a 4-10 fold enrichment of cardiac muscle gene expression and a 3-fold enrichment in cardiomyocytes. Morphological, biochemical, and functional analyses were used to evaluate the properties of P19(CA- Puro) cardiomyocytes in the presence and absence of a novel cross-linked collagen-based biomaterial. The collagen-based biomaterial was able to support appropriate viability, gene expression, and cardiomyocyte function. Therefore, P19(CA- Puro) Cells are suitable for examining biomaterials as potential scaffolds and this approach could be used for rapidly screening biomaterials for designing future human embryonic stem Cell therapies.
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Canonical Wnt signaling regulates Foxc1/2 expression in P19 Cells.
Differentiation; research in biological diversity, 2009Co-Authors: Josée Savage, Anastassia Voronova, Virja Mehta, Flavia Sendi-mukasa, Ilona S. SkerjancAbstract:Abstract FOXC1 and FOXC2 are forkhead/winged-helix transcription factors expressed in paraxial mesoderm and somites. Emphasizing the importance of FOXC1/2 during embryonic development, double-knockout mice lacking the alleles for both Foxc1 and Foxc2 failed to form segmented somites and undergo myogenesis. The present study aims to determine upstream factors that regulate Foxc1/2 expression during the differentiation of P19 Cells into skeletal muscle. Previous work had shown that dominant-negative forms of β-catenin, Gli2, and Meox1 could inhibit distinct stages of skeletal myogenesis in P19 Cells. In the presence of a dominant-negative β-catenin fusion protein, Foxc1/2 transcripts were not upregulated and neither were markers of somitogenesis/myogenesis, including Meox1, Pax3 and MyoD. Conversely, inhibition of GSK3 by LiCl or overexpression of activated β-catenin in aggregated P19 Cells resulted in enhancement of Foxc1/2 expression, indicating that FOX transcription may be under the control of Wnt signaling. Supporting this hypothesis, β-catenin bound to conserved regions upstream of Foxc1 during P19 Cell differentiation and drove transcription from this region in a promoter assay. In addition, ectopic expression of a dominant-negative Meox1 or Gli2 resulted in decreased Foxc1/2 transcript levels, correlating with inhibition of skeletal myogenesis. Overexpression of Gli2 was also sufficient to upregulate Foxc1/2 transcript levels and induce skeletal myogenesis. In summary, Foxc1/2 expression is dependent on a complex interplay from various signaling inputs from the Wnt and Shh pathways during early stages of in vitro skeletal myogenesis.
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Cross talk between hedgehog and bone morphogenetic proteins occurs during cardiomyogenesis in P19 Cells.
In vitro cellular & developmental biology. Animal, 2009Co-Authors: Peter J. Gianakopoulos, Ilona S. SkerjancAbstract:Hedgehog (Hh) signaling plays a role in heart morphogenesis and can initiate cardiomyogenesis in P19 Cells. To determine if Hh signaling is essential for P19 Cell cardiomyogenesis, we determined which Hh factors are expressed and the effect of Hh signal transduction inhibitors. Here, we find that the Hh gene family and their downstream mediators are expressed during cardiomyogenesis but an active Hh signaling pathway is not essential. However, loss of Hh signaling resulted in a delay of BMP-4, GATA-4, Gli2, and Meox1 expression during cardiomyogenesis. By using Noggin-overexpressing P19 Cells, we determined that Hh signaling was not active during Noggin-mediated inhibition of cardiomyogenesis. Thus, there is cross talk between the Hh and BMP signaling pathways and the Hh pathway appears important for timely cardiomyogenesis.
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Hedgehog Signaling Induces Cardiomyogenesis in P19 Cells
The Journal of biological chemistry, 2005Co-Authors: Peter J. Gianakopoulos, Ilona S. SkerjancAbstract:Abstract Sonic Hedgehog (Shh) is a critical signaling factor for a variety of developmental pathways during embryogenesis, including the specification of left-right asymmetry in the heart. Mice that lack Hedgehog signaling show a delay in the induction of cardiomyogenesis, as indicated by a delayed expression of Nkx2-5. To further examine a role for Shh in cardiomyogenesis, clonal populations of P19 Cells that stably express Shh, termed P19(Shh) Cells, were isolated. In monolayer P19(Shh) cultures the Shh pathway was functional as shown by the up-regulation of Ptc1 and Gli1 expression, but no cardiac muscle markers were activated. However, Shh expression induced cardiomyogenesis following Cellular aggregation, resulting in the expression of factors expressed in cardiac muscle including GATA-4, MEF2C, and Nkx2-5. Furthermore, aggregated P19 Cell lines expressing Gli2 or Meox1 also up-regulated the expression of cardiac muscle factors, leading to cardiomyogenesis. Meox1 up-regulated the expression of Gli1 and Gli2 and, thus, can modify the Shh signaling pathway. Finally, Shh, Gli2, and Meox1 all up-regulated BMP-4 expression, implying that activation of the Hedgehog pathway can regulate bone morphogenetic protein signals. Taken together, we propose a model in which Shh, functioning via Gli1/2, can specify mesodermal Cells into the cardiac muscle lineage.
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β-Catenin Is Essential and Sufficient for Skeletal Myogenesis in P19 Cells
The Journal of biological chemistry, 2002Co-Authors: Helen Petropoulos, Ilona S. SkerjancAbstract:Wnt1 and Wnt3a are signaling factors known to play a role in the induction of myogenesis in the myotome of the differentiating somite. Both factors may transduce their signal by a conserved pathway that leads to transcriptional regulation by -catenin/Lef1. -Catenin and Lef1 are found in the myotome prior to MyoD expression. We have utilized the P19 Cell system to study the mechanisms by which Wnt3a may activate MyoD expression and subsequent skeletal muscle development. We have isolated P19 Cell lines that stably express either Wnt3a or activated -catenin and found that aggregation of these Cells results in the induction of myogenesis compared with control Cells. Pax3, Gli2, Mox1, and Six1 were expressed during Wnt3a and -catenin-induced differentiation prior to MyoD expression. Furthermore, we have shown that the nuclear function of -catenin was essential for skeletal myogenesis in P19 Cells by overexpression of a dominant negative -catenin/engrailed chimera. Primitive streak factors were present, but expression of Pax3, Mox1, Gli2, and Six1 was lost in these Cells, indicating that nuclear -catenin is essential for specification of mesodermal precursors to the myogenic lineage. Therefore, Wnt signaling, acting via -catenin, is necessary and sufficient for skeletal myogenesis in P19 Cells.
Stéphane Deschamps - One of the best experts on this subject based on the ideXlab platform.
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zfpip zfp462 is involved in P19 Cell pluripotency and in their neuronal fate
Experimental Cell Research, 2011Co-Authors: Julie Massé, Justine Viet, Daniel Guerrier, Isabelle Pellerin, Claire Piquetpellorce, Stéphane DeschampsAbstract:The nuclear zinc finger protein ZFPIP/Zfp462 is an important factor involved in Cell division during the early embryonic development of vertebrates. In pluripotent P19 Cells, ZFPIP/Zfp462 takes part in Cell proliferation, likely via its role in maintaining chromatin structure. To further define the function of ZFPIP/Zfp462 in the mechanisms of pluripotency and Cell differentiation, we constructed a stable P19 Cell line in which ZFPIP/Zfp462 knockdown is inducible. We report that ZFPIP/Zfp462 was vital for mitosis and self-renewal in pluripotent P19 Cells. Its depletion induced substantial decreases in the expression of the pluripotency genes Nanog, Oct4 and Sox2 and was associated with the transient expression of specific neuronal differentiation markers. We also demonstrated that ZFPIP/Zfp462 expression appears to be unnecessary after neuronal differentiation is induced in P19 Cells. Taken together, our results strongly suggest that ZFPIP/Zfp462 is a key chromatin factor involved in maintaining P19 pluripotency and in the early mechanisms of neural differentiation but that it is dispensable in differentiated P19 Cells.
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ZFPIP/Zfp462 is involved in P19 Cell pluripotency and in their neuronal fate
Experimental cell research, 2011Co-Authors: Julie Massé, Claire Piquet-pellorce, Justine Viet, Daniel Guerrier, Isabelle Pellerin, Stéphane DeschampsAbstract:The nuclear zinc finger protein ZFPIP/Zfp462 is an important factor involved in Cell division during the early embryonic development of vertebrates. In pluripotent P19 Cells, ZFPIP/Zfp462 takes part in Cell proliferation, likely via its role in maintaining chromatin structure. To further define the function of ZFPIP/Zfp462 in the mechanisms of pluripotency and Cell differentiation, we constructed a stable P19 Cell line in which ZFPIP/Zfp462 knockdown is inducible. We report that ZFPIP/Zfp462 was vital for mitosis and self-renewal in pluripotent P19 Cells. Its depletion induced substantial decreases in the expression of the pluripotency genes Nanog, Oct4 and Sox2 and was associated with the transient expression of specific neuronal differentiation markers. We also demonstrated that ZFPIP/Zfp462 expression appears to be unnecessary after neuronal differentiation is induced in P19 Cells. Taken together, our results strongly suggest that ZFPIP/Zfp462 is a key chromatin factor involved in maintaining P19 pluripotency and in the early mechanisms of neural differentiation but that it is dispensable in differentiated P19 Cells.
Julie Massé - One of the best experts on this subject based on the ideXlab platform.
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zfpip zfp462 is involved in P19 Cell pluripotency and in their neuronal fate
Experimental Cell Research, 2011Co-Authors: Julie Massé, Justine Viet, Daniel Guerrier, Isabelle Pellerin, Claire Piquetpellorce, Stéphane DeschampsAbstract:The nuclear zinc finger protein ZFPIP/Zfp462 is an important factor involved in Cell division during the early embryonic development of vertebrates. In pluripotent P19 Cells, ZFPIP/Zfp462 takes part in Cell proliferation, likely via its role in maintaining chromatin structure. To further define the function of ZFPIP/Zfp462 in the mechanisms of pluripotency and Cell differentiation, we constructed a stable P19 Cell line in which ZFPIP/Zfp462 knockdown is inducible. We report that ZFPIP/Zfp462 was vital for mitosis and self-renewal in pluripotent P19 Cells. Its depletion induced substantial decreases in the expression of the pluripotency genes Nanog, Oct4 and Sox2 and was associated with the transient expression of specific neuronal differentiation markers. We also demonstrated that ZFPIP/Zfp462 expression appears to be unnecessary after neuronal differentiation is induced in P19 Cells. Taken together, our results strongly suggest that ZFPIP/Zfp462 is a key chromatin factor involved in maintaining P19 pluripotency and in the early mechanisms of neural differentiation but that it is dispensable in differentiated P19 Cells.
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ZFPIP/Zfp462 is involved in P19 Cell pluripotency and in their neuronal fate
Experimental cell research, 2011Co-Authors: Julie Massé, Claire Piquet-pellorce, Justine Viet, Daniel Guerrier, Isabelle Pellerin, Stéphane DeschampsAbstract:The nuclear zinc finger protein ZFPIP/Zfp462 is an important factor involved in Cell division during the early embryonic development of vertebrates. In pluripotent P19 Cells, ZFPIP/Zfp462 takes part in Cell proliferation, likely via its role in maintaining chromatin structure. To further define the function of ZFPIP/Zfp462 in the mechanisms of pluripotency and Cell differentiation, we constructed a stable P19 Cell line in which ZFPIP/Zfp462 knockdown is inducible. We report that ZFPIP/Zfp462 was vital for mitosis and self-renewal in pluripotent P19 Cells. Its depletion induced substantial decreases in the expression of the pluripotency genes Nanog, Oct4 and Sox2 and was associated with the transient expression of specific neuronal differentiation markers. We also demonstrated that ZFPIP/Zfp462 expression appears to be unnecessary after neuronal differentiation is induced in P19 Cells. Taken together, our results strongly suggest that ZFPIP/Zfp462 is a key chromatin factor involved in maintaining P19 pluripotency and in the early mechanisms of neural differentiation but that it is dispensable in differentiated P19 Cells.
