Literatura científica selecionada sobre o tema "MBNH3"
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Artigos de revistas sobre o assunto "MBNH3"
Sun, Xueqin, Xinghua Diao, Xiaolin Zhu, Xuexue Yin e Guangying Cheng. "Nanog-mediated stem cell properties are critical for MBNL3-associated paclitaxel resistance of ovarian cancer". Journal of Biochemistry 169, n.º 6 (18 de fevereiro de 2021): 747–56. http://dx.doi.org/10.1093/jb/mvab021.
Texto completo da fonteHolm, Frida, Eva Hellqvist, Cayla N. Mason, Shawn A. Ali, Nathaniel Delos-Santos, Christian L. Barrett, Hye-Jung Chun et al. "Reversion to an embryonic alternative splicing program enhances leukemia stem cell self-renewal". Proceedings of the National Academy of Sciences 112, n.º 50 (30 de novembro de 2015): 15444–49. http://dx.doi.org/10.1073/pnas.1506943112.
Texto completo da fonteGuendouz, Dj, Z. Charifi, H. Baaziz, T. Ghellab, N. Arikan, Ş. Uğur e G. Uğur. "Electronic structure, optical and thermodynamic properties of ternary hydrides MBeH3 (M = Li, Na, and K)". Canadian Journal of Physics 94, n.º 9 (setembro de 2016): 865–76. http://dx.doi.org/10.1139/cjp-2016-0299.
Texto completo da fonteManesis, Anastasia C., Richard J. Jodts, Brian M. Hoffman e Amy C. Rosenzweig. "Copper binding by a unique family of metalloproteins is dependent on kynurenine formation". Proceedings of the National Academy of Sciences 118, n.º 23 (1 de junho de 2021): e2100680118. http://dx.doi.org/10.1073/pnas.2100680118.
Texto completo da fonteWang, Xianxian, Yanchao Cai, Xiucheng Liu e Cunfu He. "Quantitative Prediction of Surface Hardness in Cr12MoV Steel and S136 Steel with Two Magnetic Barkhausen Noise Feature Extraction Methods". Sensors 24, n.º 7 (23 de março de 2024): 2051. http://dx.doi.org/10.3390/s24072051.
Texto completo da fonteHolm, Frida Linnea, Eva Hellqvist, Cayla N. Mason, Shawn Ali, Nathaniel Delos Santos, Christian Barrett, Hye-Jung Chun et al. "Reversion to an Embryonic Alternative Splicing Program Enhances Leukemia Stem Cell Self-Renewal". Blood 126, n.º 23 (3 de dezembro de 2015): 1227. http://dx.doi.org/10.1182/blood.v126.23.1227.1227.
Texto completo da fonteKanadia, Rahul N., Carl R. Urbinati, Valerie J. Crusselle, Defang Luo, Young-Jae Lee, Jeffrey K. Harrison, S. Paul Oh e Maurice S. Swanson. "Developmental expression of mouse muscleblind genes Mbnl1, Mbnl2 and Mbnl3". Gene Expression Patterns 3, n.º 4 (agosto de 2003): 459–62. http://dx.doi.org/10.1016/s1567-133x(03)00064-4.
Texto completo da fonteLee, Kyung-Soon, Kimberly Smith, Paul S. Amieux e Edith H. Wang. "MBNL3/CHCR prevents myogenic differentiation by inhibiting MyoD-dependent gene transcription". Differentiation 76, n.º 3 (março de 2008): 299–309. http://dx.doi.org/10.1111/j.1432-0436.2007.00209.x.
Texto completo da fonteGrammatikakis, Ioannis, Young-Hwa Goo, Gloria V. Echeverria e Thomas A. Cooper. "Identification of MBNL1 and MBNL3 domains required for splicing activation and repression". Nucleic Acids Research 39, n.º 7 (24 de novembro de 2010): 2769–80. http://dx.doi.org/10.1093/nar/gkq1155.
Texto completo da fonteHelbing, Jan. "Spin state transitions upon visible and infrared excitation of ferric MbN3". Chemical Physics 396 (março de 2012): 17–22. http://dx.doi.org/10.1016/j.chemphys.2011.04.001.
Texto completo da fonteTeses / dissertações sobre o assunto "MBNH3"
Chieh-Wen e 林介玟. "Identification and functional analysis of zebrafish mbnl3". Thesis, 2009. http://ndltd.ncl.edu.tw/handle/35015125149391021434.
Texto completo da fonte中山醫學大學
生物醫學科學學系碩士班
97
Muscleblind-like (MBNL) is a family of proteins that participate in regulation of tissue-specific alternative splicing. In Drosophila, the muscleblind protein was shown to regulate terminal differentiation of photoreceptors and muscles. Three MBNL paralogs have been identified in humans and mice. Previously, we cloned three mbnl genes (zmbnl1 – 3) in zebrafish in order to study their function during fish development. In this study, we focus on zmbnl3. Alternative splicing of the zmbnl3 primary transcripts gives rise to at least 5 protein isoforms. In addition to the characteristic CCCH zinc finger domains, several structural motifs (like LEV box, NGR box, Ser/Thr-rich domain) are also found conserved in zmbnl3. Zmbnl3 is expressed in most adult tissues although the expression of specific spliceforms varies. During embryogenesis, zmbnl3 transcripts are hardly detected until 24hpf. Whole-mount in situ hybridization (WISH) reveals that zmbnl3 expression in the embryo is more ubiquitous rather than specific. zmbnl3 morphants of antisense morpholono knockdown were examined by WISH analysis of several marker genes (wnt1, tnnt2, anxa5), as well as by RT-PCR analysis of the splicing patterns of its suspected targets, clc-1 and tnnt2. The morphants did not show clear difference from WT embryos. However, alcian blue staining revealed overt defects in the pharyngeal arches of zmbnl3 morphants, and myoD expression was also decreased. On the other hand, microinjection of zmbnl3 cRNA into the embryos resulted in defective embryos with crooked body axes and short somites. The defective rate of the injected embryos increased in a dose-dependent manner. WISH analysis of several marker genes (wnt1, pax2.1, myoD, myogenin) revealed that embryos overexpressed with zmbnl3 had disorganized somite formation and abnormal brain development. RT-PCR analysis indicated that the splicing patterns of clc-1 and expression levels of myoD and myogenin were not changed. When introduced into C2C12 cells, zmbnl3 inhibited cell differentiation as judged by lack of cell fusion, change of mef2a splicing pattern and reduction of MHC expression. Dual-luciferase reporter assay further revealed that zmbnl3 down-regulated myoD promoter activity in fish embryos. These data suggest that zmbnl3 may interfere with muscle differentiation through the MyoD-dependent pathway.
Su, Hung-Chi, e 蘇虹綺. "The Effect of MBNL3 Knockdown on Cell Proliferation and Senescence". Thesis, 2013. http://ndltd.ncl.edu.tw/handle/62014042578290292207.
Texto completo da fonte國立中正大學
分子生物研究所
101
Muscleblind-like 3 (MBNL3) belongs to MBNL family that has been implicated in the pathogenesis of myotonic dystrophy type 1 (DM1). Mbnl3 expression is abundant in proliferative tissues and greatly decreases during differentiation. Our laboratory previously found that Mbnl3 knockdown interferes with cell cycle progression and induces senescence through cyclin D1-mediated pathway in C2C12 myoblasts. The first part of my study aimed to confirm the effect of Mbnl3 knockdown on C2C12 cells. My results indicated that (1) both restoration of Mbnl3 and cyclin D1 expression could increase the proliferation rate of Mbnl3 knockdown C2C12 cells, (2) Mbnl3 regulated cyclin D1 transcription possibly through altering Sp1 expression, and (3) the lysosomal content was increased in Mbnl3 knockdown myoblasts, which explains the upregulation of SA--gal activity. These results demonstrated that Mbnl3 may regulate the proliferation and senescence of C2C12 cells through Sp1/cyclin D1 pathway. Recent reports indicate that DM1 patients are at increased risk in developing cancers. The second part of my study aimed to unravel the role of MBNL3 in tumorigenesis. By comparing the RNA level in cancer cells to that in non-tumorigenic counterpart using qRT-PCR, our results revealed that MBNL3 expression was greatly up-regulated in most cancer cell lines examined, including those derived from ovary (6/6), bladder (5/7), oral (1/4), and liver (2/2) cancers. Moreover, knocking down MBNL3 expression severely affected the survival of cancer cells. These results suggest that MBNL3 may play a role in tumorigenesis.
Ke, Wen-Hsing, e 柯雯馨. "Investigation of Effect of MBNL3 Knockdown on Cell Cycle Progression in C2C12 Myoblasts". Thesis, 2011. http://ndltd.ncl.edu.tw/handle/71769638459090265318.
Texto completo da fonte國立中正大學
分子生物研究所
100
Muscleblind-like protein 3 (MBNL3) belongs to MBNL family implicated in the pathogenesis of myotonic dystrophy, the most common neuromuscular disease in adults. MBNL3 expression is abundant in proliferating myoblasts and greatly down-regulated during differentiation. In this study, we have investigated the effect of MBNL3 loss-of-function on C2C12 myoblasts by using lentiviral knockdown system. The results indicated that MBNL3 knockdown cells had lower proliferation rate than scramble control as revealed by cell counting and MTT assay. Propidium iodide staining revealed that myoblasts with MBNL3 knockdown were enriched in G1 population. Consistent with these findings, real-time PCR and western blotting analyses revealed a decrease in cyclin D1 and S780 phosphorylated pRb protein level considered critical for G1 phase progression. In addition, microscopic observation and measurement of the cell size revealed a flattened and enlarge beta morphology, characteristic of senescent cells. Further senescence-associated beta-galactosidase (SA-beta-gal) assay confirmed that a significant portion of MBNL3 knockdown cells entered senescent state prematurely. Overexpression of MBNL3 and cyclin D1 significantly restored the proliferation rate and reduced senescence of these cells. Our findings suggest that MBNL3 may regulate G1 progression and senescence through cyclin D1-mediated pathway in C2C12 myoblasts.
Huang, Shu-Yuan, e 黃淑媛. "Mbnl3 regulates myoblast proliferation and induces senescence through the Sp1/cyclin D1/Rb pathway". Thesis, 2015. http://ndltd.ncl.edu.tw/handle/jx6ny8.
Texto completo da fonte國立中正大學
分子生物研究所
103
Muscleblind-like 3 (MBNL3) belongs to the MBNL family which has been implicated in the pathogenesis of neuromuscular disease myotonic dystrophy. While MBNL3 is barely detectable in adult muscle, it is expressed in proliferative myoblasts and transiently during muscle regeneration. Our previous study found that Mbnl3 knockdown interferes with cell cycle progression and induces senescence through cyclin D1-mediated pathway in C2C12 myoblasts. The first aim of my study is to confirm the effect of Mbnl3 knockdown on C2C12 cells. The result indicated that the effect of shMbnl3 on cyclin D1 expression occurs at the transcriptional level through down-regulation of Sp1 expression. In addition, down-regulation of pRb as well as p16 expression greatly reversed the effect of shMbnl3 on C2C12 cells, and finally Mbnl3 depletion interferes with C2C12 differentiation. These findings provide the first experimental evidence to suggest that Mbnl3 is required for the proliferation and survival of regenerating myoblasts through cyclin D1/pRB pathway. The second aim of my study is to unravel the role of MBNL3 in cancer cells. Previous study showed that MBNL3 was specifically up-regulated in hepatoma cell lines Huh7 and HepG2, and knockdown of MBNL3 severely affected the survival of these cells. In addition, MBNL3 is not overexpression in breast cancer cell lines MCF-7、MDA-MB-231 MBNL3 but knockdown of MBNL3 also severely affects the survival of these cells. Furthermore, down-regulation of pRb expression reversed the effect of Mbnl3 knockdown on hepatoma cells. Finally, non-tumorigenic epithelial cell line MCF-10A depleted with MBNL3 also showed decreased proliferation rate. These results suggest that MBNL3 plays an important role in cell proliferation.