Littérature scientifique sur le sujet « MBNH3 »
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Articles de revues sur le sujet "MBNH3"
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Sun, Xueqin, Xinghua Diao, Xiaolin Zhu, Xuexue Yin et Guangying Cheng. « Nanog-mediated stem cell properties are critical for MBNL3-associated paclitaxel resistance of ovarian cancer ». Journal of Biochemistry 169, no 6 (18 février 2021) : 747–56. http://dx.doi.org/10.1093/jb/mvab021.
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Abstract Paclitaxel (PTX) is the standard first-line treatment of ovarian cancer, but its efficacy is limited by multidrug resistance. Therefore, it is crucial to identify effective drug targets to facilitate PTX sensitivity for ovarian cancer treatment. Seventy PTX-administrated ovarian cancer patients were recruited in this study for gene expression and survival rate analyses. Muscleblind-like-3 (MBNL3) gain-of-function and loss-of-function experiments were carried out in ovarian cancer cells (parental and PTX-resistant) and xenograft model. Cancer cell viability, apoptosis, spheroids formation, Nanog gene silencing were examined and conducted to dissect the underlying mechanism of MBNL3-mediated PTX resistance. High expression of MBNL3 was positively correlated with PTX resistance and poor prognosis of ovarian cancer. MBNL3 increased cell viability and decreased apoptosis in ovarian stem-like cells, through upregulating Nanog. This study suggests the MBNL3-Nanog axis is a therapeutic target for the treatment of PTX resistance in ovarian cancer management.
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Holm, 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, no 50 (30 novembre 2015) : 15444–49. http://dx.doi.org/10.1073/pnas.1506943112.
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Formative research suggests that a human embryonic stem cell-specific alternative splicing gene regulatory network, which is repressed by Muscleblind-like (MBNL) RNA binding proteins, is involved in cell reprogramming. In this study, RNA sequencing, splice isoform-specific quantitative RT-PCR, lentiviral transduction, and in vivo humanized mouse model studies demonstrated that malignant reprogramming of progenitors into self-renewing blast crisis chronic myeloid leukemia stem cells (BC LSCs) was partially driven by decreased MBNL3. Lentiviral knockdown of MBNL3 resulted in reversion to an embryonic alternative splice isoform program typified by overexpression of CD44 transcript variant 3, containing variant exons 8–10, and BC LSC proliferation. Although isoform-specific lentiviral CD44v3 overexpression enhanced chronic phase chronic myeloid leukemia (CML) progenitor replating capacity, lentiviral shRNA knockdown abrogated these effects. Combined treatment with a humanized pan-CD44 monoclonal antibody and a breakpoint cluster region - ABL proto-oncogene 1, nonreceptor tyrosine kinase (BCR-ABL1) antagonist inhibited LSC maintenance in a niche-dependent manner. In summary, MBNL3 down-regulation–related reversion to an embryonic alternative splicing program, typified by CD44v3 overexpression, represents a previously unidentified mechanism governing malignant progenitor reprogramming in malignant microenvironments and provides a pivotal opportunity for selective BC LSC detection and therapeutic elimination.
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Guendouz, Dj, Z. Charifi, H. Baaziz, T. Ghellab, N. Arikan, Ş. Uğur et G. Uğur. « Electronic structure, optical and thermodynamic properties of ternary hydrides MBeH3 (M = Li, Na, and K) ». Canadian Journal of Physics 94, no 9 (septembre 2016) : 865–76. http://dx.doi.org/10.1139/cjp-2016-0299.
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Electronic band structure, optical and thermodynamic properties of ternary hydrides MBeH3 (M = Li, Na, and K) were studied using ab initio density functional theory (DFT). The effect of the adopted approximation to the exchange-correlation functional of the DFT is explicitly investigated by considering four different expressions of two different classes (local-density approximation and generalized-gradient approximation). The calculated magnitude of B classifies MBeH3 (M = Li, Na, and K) as easily compressible materials. The bonding interaction in these compounds is quite complicated. The interaction between M and BeH6 is ionic and that between Be and H comprises both ionic and covalent characters. The electronic structure of the complex hydride was investigated by calculating the partial and total densities of states, and electron charge density distribution. Large gaps in the density of states appear at the Fermi energy of LiBeH3, NaBeH3, and KBeH3 indicating that these classes of hydrides are insulators. Optical properties, including the dielectric function, reflectivity, and absorption coefficient, each as a function of photon energy, are calculated and show an optical anisotropy for LiBeH3 and KBeH3. Through the quasi-harmonic Debye model, in which the phononic effects are considered, temperature dependence of volume V(T), bulk modulus B(T), and thermal expansion coefficient α(T), constant-volume and constant-pressure specific heat (Cv and Cp) and Debye temperature ΘD, the entropy S, and the Grüneisen parameter γ were calculated at wide pressure and temperature ranges. The principal aspect of the obtained results is the close similarity of MBeH3 (M = Li, Na, and K) compounds.
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Manesis, Anastasia C., Richard J. Jodts, Brian M. Hoffman et Amy C. Rosenzweig. « Copper binding by a unique family of metalloproteins is dependent on kynurenine formation ». Proceedings of the National Academy of Sciences 118, no 23 (1 juin 2021) : e2100680118. http://dx.doi.org/10.1073/pnas.2100680118.
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Some methane-oxidizing bacteria use the ribosomally synthesized, posttranslationally modified natural product methanobactin (Mbn) to acquire copper for their primary metabolic enzyme, particulate methane monooxygenase. The operons encoding the machinery to biosynthesize and transport Mbns typically include genes for two proteins, MbnH and MbnP, which are also found as a pair in other genomic contexts related to copper homeostasis. While the MbnH protein, a member of the bacterial diheme cytochrome c peroxidase (bCcP)/MauG superfamily, has been characterized, the structure and function of MbnP, the relationship between the two proteins, and their role in copper homeostasis remain unclear. Biochemical characterization of MbnP from the methanotroph Methylosinus trichosporium OB3b now reveals that MbnP binds a single copper ion, present in the +1 oxidation state, with high affinity. Copper binding to MbnP in vivo is dependent on oxidation of the first tryptophan in a conserved WxW motif to a kynurenine, a transformation that occurs through an interaction of MbnH with MbnP. The 2.04-Å-resolution crystal structure of MbnP reveals a unique fold and an unusual copper-binding site involving a histidine, a methionine, a solvent ligand, and the kynurenine. Although the kynurenine residue may not serve as a CuI primary-sphere ligand, being positioned ∼2.9 Å away from the CuI ion, its presence is required for copper binding. Genomic neighborhood analysis indicates that MbnP proteins, and by extension kynurenine-containing copper sites, are widespread and may play diverse roles in microbial copper homeostasis.
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Wang, Xianxian, Yanchao Cai, Xiucheng Liu et Cunfu He. « Quantitative Prediction of Surface Hardness in Cr12MoV Steel and S136 Steel with Two Magnetic Barkhausen Noise Feature Extraction Methods ». Sensors 24, no 7 (23 mars 2024) : 2051. http://dx.doi.org/10.3390/s24072051.
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The correlation between magnetic Barkhausen noise (MBN) features and the surface hardness of two types of die steels (Cr12MoV steel and S136 steel in Chinese standards) was investigated in this study. Back-propagation neural network (BP-NN) models were established with MBN magnetic features extracted by different methods as the input nodes to realize the quantitative prediction of surface hardness. The accuracy of the BP-NN model largely depended on the quality of the input features. In the extraction process of magnetic features, simplifying parameter settings and reducing manual intervention could significantly improve the stability of magnetic features. In this study, we proposed a method similar to the magnetic Barkhausen noise hysteresis loop (MBNHL) and extracted features. Compared with traditional MBN feature extraction methods, this method simplifies the steps of parameter setting in the feature extraction process and improves the stability of the features. Finally, a BP-NN model of surface hardness was established and compared with the traditional MBN feature extraction methods. The proposed MBNHL method achieved the advantages of simple parameter setting, less manual intervention, and stability of the extracted parameters at the cost of small accuracy reduction.
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Holm, 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, no 23 (3 décembre 2015) : 1227. http://dx.doi.org/10.1182/blood.v126.23.1227.1227.
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Abstract Background Formative research suggests that a human embryonic stem cell-specific alternative splicing gene regulatory network, which is repressed by Muscleblind-like (MBNL) RNA binding proteins, is involved in cell reprogramming. However, its role in malignant reprogramming of progenitors into self-renewing leukemia stem cells (LSCs) had not been established. Methods Whole transcriptome RNA sequencing (RNA-seq) was performed on FACS purified progenitors from normal, chronic phase and blast crisis chronic myeloid leukemia samples and analyzed using Cuff-links, GSEA and IPA software. Splice isoform specific qRT-PCR, confocal microscopy, lentiviral overexpression and shRNA knockdown experiments were performed according to published methods (Jamieson NEJM 2004; Geron et al Cancer Cell 2008; Goff et al Cell Stem Cell 2013). Results We performed LSC RNA-seq, lentiviral overexpression and knockdown and discovered that decreased expression of MBNL3, a repressor of an embryonic alternative splicing program and reprogramming, activated a pluripotency network and increased expression of a pro-survival isoform of CD44v3, which is more commonly expressed in human embryonic stem cells. This resulted in malignant reprogramming of progenitors in blast crisis CML endowing them with unbridled survival and self-renewal capacity. This is the first description of MBNL3 downregulation as a mechanism of reversion to an embryonic alternative splicing program, which elicits malignant progenitor reprogramming of progenitors into self-renewing leukemia stem cells. While isoform specific lentiviral CD44v3 overexpression enhanced chronic phase CML progenitor replating capacity, lentiviral shRNA knockdown abrogated these effects. In keeping with activation of a stem cell reprogramming network, CD44v3 upregulation was associated with increased expression of pluripotency transcription factors, including OCT4, SOX2 and b-catenin in addition to the pro-survival long isoforms of MCL1 and BCLX resulting in increased self-renewal and apoptosis resistance. Conclusion In summary, MBNL3 downregulation activates an embryonic alternative splicing program, typified by CD44v3 overexpression, and represents a novel mechanism governing LSC generation in malignant microenvironments. Reversal of malignant reprogramming by epigenetic modulation of embryonic alternative splicing or via monoclonal antibody targeting of CD44v3 splice isoform may represent a pivotal opportunity for selective BC LSC eradication. Disclosures Jamieson: Johnson & Johnson: Research Funding; GlaxoSmithKline: Research Funding.
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Kanadia, Rahul N., Carl R. Urbinati, Valerie J. Crusselle, Defang Luo, Young-Jae Lee, Jeffrey K. Harrison, S. Paul Oh et Maurice S. Swanson. « Developmental expression of mouse muscleblind genes Mbnl1, Mbnl2 and Mbnl3 ». Gene Expression Patterns 3, no 4 (août 2003) : 459–62. http://dx.doi.org/10.1016/s1567-133x(03)00064-4.
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Lee, Kyung-Soon, Kimberly Smith, Paul S. Amieux et Edith H. Wang. « MBNL3/CHCR prevents myogenic differentiation by inhibiting MyoD-dependent gene transcription ». Differentiation 76, no 3 (mars 2008) : 299–309. http://dx.doi.org/10.1111/j.1432-0436.2007.00209.x.
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Grammatikakis, Ioannis, Young-Hwa Goo, Gloria V. Echeverria et Thomas A. Cooper. « Identification of MBNL1 and MBNL3 domains required for splicing activation and repression ». Nucleic Acids Research 39, no 7 (24 novembre 2010) : 2769–80. http://dx.doi.org/10.1093/nar/gkq1155.
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Helbing, Jan. « Spin state transitions upon visible and infrared excitation of ferric MbN3 ». Chemical Physics 396 (mars 2012) : 17–22. http://dx.doi.org/10.1016/j.chemphys.2011.04.001.
Texte intégralThèses sur le sujet "MBNH3"
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Chieh-Wen et 林介玟. « Identification and functional analysis of zebrafish mbnl3 ». Thesis, 2009. http://ndltd.ncl.edu.tw/handle/35015125149391021434.
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碩士中山醫學大學
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.
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Su, Hung-Chi, et 蘇虹綺. « The Effect of MBNL3 Knockdown on Cell Proliferation and Senescence ». Thesis, 2013. http://ndltd.ncl.edu.tw/handle/62014042578290292207.
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碩士國立中正大學
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.
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Ke, Wen-Hsing, et 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.
Texte intégralRésumé :
碩士國立中正大學
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.
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Huang, Shu-Yuan, et 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.
Texte intégralRésumé :
碩士國立中正大學
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.