Littérature scientifique sur le sujet « CCNE2 »
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Articles de revues sur le sujet "CCNE2"
Kondo, Yukio, Eric Wieder, Sijie Lu et Jeffrey Molldrem. « High Avidity Cyclin E1-Derived Peptide-Specific CTL Kill Lymphoid Leukemia Cells and Cross-Recognize a Homologous Cyclin E2-Derived Peptide. » Blood 104, no 11 (16 novembre 2004) : 4498. http://dx.doi.org/10.1182/blood.v104.11.4498.4498.
Texte intégralSonntag, Roland, Nives Giebeler, Yulia A. Nevzorova, Jörg-Martin Bangen, Dirk Fahrenkamp, Daniela Lambertz, Ute Haas et al. « Cyclin E1 and cyclin-dependent kinase 2 are critical for initiation, but not for progression of hepatocellular carcinoma ». Proceedings of the National Academy of Sciences 115, no 37 (27 août 2018) : 9282–87. http://dx.doi.org/10.1073/pnas.1807155115.
Texte intégralIshiyama, Ken, Yukio Kondo, Eric Wieder, Sijie Lu et Jeffrey Molldrem. « High Avidity Cyclin E-Derived Peptide-Specific CTL Contribute to Induction of Remission after Stem Cell Transplantation without Associated Graft-Versus-Host Disease. » Blood 106, no 11 (16 novembre 2005) : 1424. http://dx.doi.org/10.1182/blood.v106.11.1424.1424.
Texte intégralHe, Hong, Ken Ishiyama, Gheath Alatrash, Yukio Kondo, Sijie Lu et Jeffrey J. Molldrem. « T-Cell Immunity to Two HLA-A2-Restricted Self-Determinants of Cyclin E May Contribute to Remission After Stem Cell Transplantation. » Blood 114, no 22 (20 novembre 2009) : 686. http://dx.doi.org/10.1182/blood.v114.22.686.686.
Texte intégralMartín-Garcia, David, Alba Navarro, Rafael Valdés-Mas, Guillem Clot, Jesús Gutiérrez-Abril, Miriam Prieto, Inmaculada Ribera-Cortada et al. « CCND2 and CCND3 hijack immunoglobulin light-chain enhancers in cyclin D1− mantle cell lymphoma ». Blood 133, no 9 (28 février 2019) : 940–51. http://dx.doi.org/10.1182/blood-2018-07-862151.
Texte intégralWu, Lizheng, Kuan Yang, Yajie Gui et Xiaojing Wang. « Nicotine-upregulated miR-30a arrests cell cycle in G1 phase by directly targeting CCNE2 in human periodontal ligament cells ». Biochemistry and Cell Biology 98, no 3 (juin 2020) : 354–61. http://dx.doi.org/10.1139/bcb-2019-0156.
Texte intégralTao, Kaiyi, JinShi Liu, JinXiao Liang, XiaoFang Xu, LiWei Xu et WeiMin Mao. « Vascular endothelial cell-derived exosomal miR-30a-5p inhibits lung adenocarcinoma malignant progression by targeting CCNE2 ». Carcinogenesis 42, no 8 (15 juin 2021) : 1056–67. http://dx.doi.org/10.1093/carcin/bgab051.
Texte intégralDiab, Sami, Matei P. Socoteanu, Carlos A. Encarnacion, Cynthia R. C. Osborne, Carolyn B. Hendricks, Kristi McIntyre, Vibha Taneja Thomas et al. « High-risk breast cancer genes at 8q22-24 and their role in over 5,000 patients evaluated with the 70-gene risk of recurrence assay. » Journal of Clinical Oncology 38, no 15_suppl (20 mai 2020) : 3569. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.3569.
Texte intégralLee, Christine, Kristine J. Fernandez, Sarah Alexandrou, C. Marcelo Sergio, Niantao Deng, Samuel Rogers, Andrew Burgess et C. Elizabeth Caldon. « Cyclin E2 Promotes Whole Genome Doubling in Breast Cancer ». Cancers 12, no 8 (13 août 2020) : 2268. http://dx.doi.org/10.3390/cancers12082268.
Texte intégralKikuchi, Kei, et Daisuke Kaida. « CCNE1 and E2F1 Partially Suppress G1 Phase Arrest Caused by Spliceostatin A Treatment ». International Journal of Molecular Sciences 22, no 21 (27 octobre 2021) : 11623. http://dx.doi.org/10.3390/ijms222111623.
Texte intégralThèses sur le sujet "CCNE2"
Tarr, Joseph Thomas. « CTGF/CCN2 : The Marionettist of Mammalian Palatogenesis ». Diss., Temple University Libraries, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/540676.
Texte intégralPh.D.
The mammalian palate develops early in embryogenesis by way of a carefully orchestrated series of temporally and spatially regulated signaling events. Molecular signaling pathways that have been proven to be vital to the process of palatogenesis include TGF-βs, BMPs, FGFs, EGF, and Wnts. The absence of connective tissue growth factor (CTGF/CCN2) has been shown previously to cause failure of proper palatogenesis, i.e. cleft palate. However, the details about the phenotype of this model of cleft palate were scarce. Additionally, CCN2 is known to interact with TGF-βs, BMPs, FGFs, EGF, and Wnts, though information on how these pathways were impacted in the developing palate lacking CCN2 were also not available. In Chapters 2 and 3, through our use of gross specimen and histological examination combined with cell and organ culture, we produced the most detailed characterization of the CCN2 knockout (KO) model of cleft palate with identification of negatively affected signaling pathways that lead to the clefting phenotype. Collection and examination of gross and histological sections revealed at 100% penetrance of cleft palate in which development is impaired around the phase of palatal shelf elevation. Organ culture also revealed that when artificially apposed, the CCN2 KO model system also suffers from a fusion deficit. Finally, utilizing cells isolated from the developing palates, we found a reduction in proliferation, adhesion, and spreading with an enhanced migratory ability. Addition of recombinant CCN2 was able to rescue cell spreading but not proliferation. CCN2 as an immobilized substrate did not rescue adhesive ability. Decreased adhesion and spreading in the KO cells are attributed to the inability of the KO cells to activate Rac1 and RhoA. Examination of gene expression differences by mRNA-sequencing and qRT-PCR revealed numerous gene expression alterations between the wild type (WT) and the KO palates, most notably FGF4 and EGFR. Addition of FGF4 or EGF to cell culture was unable to promote increased proliferation in the KO cells while producing a response in the WT cells. Examination of downstream signaling revealed highly amplified and prolonged ERK1/2 signaling in the FGF4 treated palate cells indicating that FGF signaling is significantly altered in the absence of CCN2. Treatment of the cells with EGF produced a response proportional to EGFR expression differences indicating that EGFR signaling is not impacted beyond the receptor protein levels. The link between EGFR protein levels and FGF mediated ERK1/2 activation is a protein called Spry2. We found greatly reduced Spry2 mRNA levels in the KO palates and upon FGF4 stimulation at 24 hours of exposure indicating that in the absence of CCN2, proper inhibition of FGF signaling and EGFR degradation is negatively altered. Collectively, the data demonstrate that CCN2 is vital to palatogenesis by impacting proliferation, shelf elevation, and shelf fusion through increased FGF signaling and reduced EGFR signaling resulting partially from reduced Spry2 activity.
Temple University--Theses
Kiwanuka, Elizabeth. « CCN2 – Keratinocyte Interactions In Vitro and In Vivo ». Doctoral thesis, Uppsala universitet, Plastikkirurgi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-213566.
Texte intégralMcLean, Celia. « Investigating the expression and function of CCN2 in articular cartilage ». Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/5289.
Texte intégralNakatani, Kana. « Inhibition of CDK4/6 and autophagy synergistically induces apoptosis in t(8;21) acute myeloid leukemia cells ». Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263584.
Texte intégralWang, Wen. « Investigating the role of CCN1, CCN2, and CCN6 in osteoclast and osteoblast physiology ». Thesis, University of Aberdeen, 2012. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=204059.
Texte intégralHolmes, Alan Matthew. « Regulation of connective tissue growth factor/CCN2 gene expression in systemic sclerosis fibroblasts ». Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445639/.
Texte intégralHendesi, Honey. « CONNECTIVE TISSUE GROWTH FACTOR (CTGF/CCN2) REGULATES OSTEOBLAST CYTOSKELETAL REORGANIZATION AND MOTILITY AND ENHANCES DIFFERENTIATION VIA BINDING TO INTEGRIN RECEPTORS AND ACTIVATION OF DOWNSTREAM SIGNALINGS ». Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/263674.
Texte intégralPh.D.
Connective Tissue Growth Factor (CTGF) is a matricellular protein that has been shown to mediate cell adhesion, and as a consequence, it regulates cell proliferation, migration, differentiation and gene transcription. Although previous in vivo and in vitro studies supported the anabolic role of CTGF in skeletogenesis, to date mechanisms of this effect remain unknown. So far, no specific receptor has been identified for CTGF, although previous studies have shown that integrins can serve as functional signaling receptors for CTGF. The CTGF-integrin interaction initiates intracellular signaling cascades that ultimately regulate cell cytoskeleton reorganization, gene transcription and cell function. To study the effect of CTGF on osteoblasts, we first conducted adhesion assays using the MC3T3-E1 osteoblastic cell line. We confirmed that osteoblasts adhere to rCTGF in a concentration-dependent manner and we showed this adhesion has characteristics of integrin mediated adhesions. Next, we used an array of blocking antibodies directed against the individual alpha and beta; integrin subunits that are known to be expressed in osteoblasts. Significant decreases in cell adhesion were observed upon treatment with anti-alpha-v or anti-beta1 blocking antibodies. Subsequent coimmunoprecipitation analyses demonstrated that CTGF interacts with alpha-v and beta1 integrins in osteoblasts. Furthermore, we showed that the specificity of this CTGF-integrin interaction occurs in the C-terminal domain (fourth module) of CTGF. The immunefluorescence staining of cells cultured on substrates of rCTGF, fibronectin (positive control) or BSA (negative control) demonstrated that osteoblast adhesion to rCTGF results in actin cytoskeleton reorganization, focal adhesion formation, enhanced cell spreading and Rac activation. These series of events are necessary for proper cell-matrix interaction and integrins' downstream signaling initiation. Next, through alkaline phosphatase (ALP) staining and activity assays, as well as Alizarin red staining, we demonstrated that osteoblast attachment to CTGF matrix enhances cell maturation, bone nodule formation and matrix mineralization. To investigate whether the effect of CTGF on osteoblast differentiation involves activation of specific signaling molecules, we performed Western blot and chromatin immunoprecipitation (ChIP) assays. Osteoblasts cultured on rCTGF expressed higher levels of both total and phosphorylated forms of focal adhesion kinase (FAK) and extracellular signal-regulated kinase (ERK) compared to the cells cultured on BSA. In addition, these osteoblasts showed an increase in runt-related transcription factor 2 (Runx2) binding to the osteocalcin gene promoter compared to the negative control. These experiments confirmed CTGF's effect on enhancing osteoblast differentiation through regulation of important signaling molecules. In another series of experiments, we used primary osteoblasts isolated from CTGF KO mice, their WT littermates, or WT cells infected to overexpress (OE) CTGF to study the effect of different levels of endogenous CTGF on osteoblast cytoskeleton reorganization and motility. Our assays showed enhanced cell adhesion, spreading and Rac expression in CTGF OE osteoblasts, while in CTGF KO osteoblasts, cell adhesion, spreading and Rac expression were significantly decreased. In contrast, CTGF OE osteoblasts that showed high adhesion and spreading, exhibited diminished cell motility and low levels of RhoA expression, while KO cells migrated quickly and expressed high levels of RhoA. Together, these experiments establish CTGF as an adhesion protein for osteoblasts; they demonstrate that the alpha-v beta1 integrin is a functional signaling receptor for CTGF; they confirm that osteoblast differentiation is enhanced when cultured on CTGF matrix through activation of regulatory signaling molecules; and finally, these experiments establish a role for CTGF in the regulation of small RhoGTPases expression, which in turn implies a significant role for CTGF in cell cytoskeleton reorganization and motility.
Temple University--Theses
Rakijas, Jessica B. « E2Fs and Transcription : New Members Help Answer Old Questions ». The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1492780032915208.
Texte intégralBohr, Wilhelm [Verfasser]. « Expression, Aufreinigung und Charakterisierung von rekombinantem hCTGF (CCN2) und rNOV (CCN3) in einem eukaryontischen Zellsystem / Wilhelm Bohr ». Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2010. http://d-nb.info/1015149219/34.
Texte intégralGonnot, Fabrice. « Relations fonctionnelles entre les régulateurs de pluripotence et le cycle cellulaire dans les cellules souches embryonnaires pluripotentes ». Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1149.
Texte intégralMouse embryonic stem cells (mESCs) display an unorthodox cell cycle characterised by the lack of a functional Rb pathway and robust expression of cyclin E during all cell cycle phases. Therefore, mESCs are constitutively primed for DNA replication. To understand how cyclin E, a key regulator of the G1-to-S phase transition, is regulated in mESCs, we analysed the transcriptional regulation of Ccne1 by transcription factors of the naive pluripotency network. We observed that Esrrb, Klf4 and Tfcp2l1 bound the Ccne1 promoter region on multiple sites between 0 and 1kb upstream transcription start site. Disrupting the binding sites reduced or abolished transcriptional activity in a luciferase assay. Moreover, the doxycyclin-inducible expression of Essrb, Klf4 and Tfcp2l1 up-regulated the Ccne1 mRNA level. Taken together, these results strongly suggest that Essrb, Klf4 and Tfcp2l1 control Cyclin E expression and highlight a direct connection between the naïve pluripotency network and regulation of the mitotic cycle in mESCs. We used the FUCCI reporter system to study cell-cycle dependent expression of the transcription factors that form the naïve pluripotency network. Esrrb, Klf4, Tfcp2l1 and Nanog expression oscillated during the cell cycle with a down-regulated expression between the early G1-phase and the beginning of S-phase, and then up-regulated expression between the beginning of S-phase and the G2/M-phase. These results suggest that the naive pluripotency network is destabilized transiently during the transition from the G1-phase to the S-phase of the cell cycle
Livres sur le sujet "CCNE2"
Inc, Syngress Media, dir. CCNE Cisco certified network associate study guide : (exam 640-407). Berkeley, Calif : Osborne/McGraw-Hill, 1998.
Trouver le texte intégralFay W. Whitney School of Nursing. Commission on Collegiate Nursing Education (CCNE) accreditation review : On-site evaluation, October 18-20, 2010. Laramie, Wyo.?] : University of Wyoming, College of Health Sciences, 2010.
Trouver le texte intégralNA. Cnap Networkg Ccna1& Routrs Ccna2& CCNA Commd. Addison Wesley Longman, 2006.
Trouver le texte intégralClarke. Novell's Ccne Update Netware 6-apdf. Wiley & Sons, Incorporated, John, 2003.
Trouver le texte intégralNA. Cnap Routers Ccna2 Comp& Lab& Sg& Quick Ref Pk. Addison Wesley Longman, 2006.
Trouver le texte intégralNA. Cnap Routrs Ccna2 & Ccna1& 2 Eng Jrnl REV Pk. Addison Wesley Longman, 2006.
Trouver le texte intégralCCNB1, CCNB2, CCNA1, CCNA2, SYT1, SYT2, CKS2, CKS1B, CCNB3, SKP1, CDK1, RPS23, RPS27A, ZFAND4, RPS27, RPS27l, BUB1, BUB1B Could Play Significant Roles in the Aetiology of Schizophrenia by Acting As Points of Contact Between ALDH18A1 and SEC23IP (COP2). Lulu Press, Inc., 2017.
Trouver le texte intégralChapitres de livres sur le sujet "CCNE2"
van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis et al. « CCNA2 ». Dans Encyclopedia of Signaling Molecules, 282. New York, NY : Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100188.
Texte intégralLeask, Andrew. « CCN2 in Skin Fibrosis ». Dans Methods in Molecular Biology, 417–21. New York, NY : Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6430-7_34.
Texte intégralLuo, Chao, Xiaojie Li, Yucheng Chen, Xi Wu, Jia He et Jiliu Zhou. « CCNET : Cascading Convolutions for Cardiac Segmentation ». Dans Lecture Notes in Computer Science, 3–11. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24265-7_1.
Texte intégralLiu, Gang, Jing Ming, Xinyun Wu et Rifeng Jiang. « CCNet : Unpaired Keypoints for Skull Fracture Detection ». Dans Exploration of Novel Intelligent Optimization Algorithms, 189–201. Singapore : Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-4109-2_18.
Texte intégralOrtega, John E., Iria de-Dios-Flores, José Ramom Pichel et Pablo Gamallo. « Revisiting CCNet for Quality Measurements in Galician ». Dans Lecture Notes in Computer Science, 407–12. Cham : Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-98305-5_38.
Texte intégralKawata, Kazumi, Satoshi Kubota et Masaharu Takigawa. « Analysis of Transcytosis of CCN2 by Chondrocytes ». Dans Methods in Molecular Biology, 405–13. New York, NY : Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6430-7_33.
Texte intégralNishida, Takashi, Satoshi Kubota et Masaharu Takigawa. « Production of Recombinant CCN2 Protein by Mammalian Cells ». Dans Methods in Molecular Biology, 95–105. New York, NY : Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6430-7_10.
Texte intégralAoyama, Eriko, Takako Hattori, Satoshi Kubota et Masaharu Takigawa. « Production of Recombinant CCN2 Protein in Escherichia coli ». Dans Methods in Molecular Biology, 77–84. New York, NY : Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6430-7_8.
Texte intégralHattori, Takako, Mitsuhiro Hoshijima et Masaharu Takigawa. « Protein Imaging of CCN2 and CCN3 in Living Cells ». Dans Methods in Molecular Biology, 211–15. New York, NY : Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6430-7_20.
Texte intégralShimo, Tsuyoshi, Hiroaki Takebe, Saki Fujii et Akihiro Hosoya. « Immunohistochemical Analysis of CCN2 in Experimental Fracture Healing Models ». Dans Methods in Molecular Biology, 335–42. New York, NY : Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2744-0_23.
Texte intégralActes de conférences sur le sujet "CCNE2"
Lathrop, Scott. « CCNet ». Dans the 1995 ACM/IEEE conference. New York, New York, USA : ACM Press, 1995. http://dx.doi.org/10.1145/224170.285578.
Texte intégralHuang, Zilong, Xinggang Wang, Lichao Huang, Chang Huang, Yunchao Wei et Wenyu Liu. « CCNet : Criss-Cross Attention for Semantic Segmentation ». Dans 2019 IEEE/CVF International Conference on Computer Vision (ICCV). IEEE, 2019. http://dx.doi.org/10.1109/iccv.2019.00069.
Texte intégralTaylor-Harding, Barbie, Hasmik Agadjanian, Paul Joseph Aspuria, Takako Mizuno, Dong-Joo Cheon, Sandra Orsulic, Beth Karlan, Christine Walsh et Wolf Ruprecht Wiedemeyer. « Abstract B48 : Targeting chemo-resistance in CCNE1-amplified ovarian cancer ». Dans Abstracts : AACR Special Conference on Advances in Ovarian Cancer Research : From Concept to Clinic ; September 18-21, 2013 ; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1078-0432.ovca13-b48.
Texte intégralMartinez-Soria, N., L. McKenzie, S. Nakjang, V. Forster, A. Isa, HJ Blair et O. Heidenreich. « CCND2 is a RUNX1/ETO target required for leukaemic propagation ». Dans 30. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch-onkologische Forschung. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1602192.
Texte intégralBai, Shoumei, et Ronald J. Buckanovich. « Abstract 2060 : Therapeutic approaches for CCNE1-amplified HR-proficient ovarian cancer ». Dans Proceedings : AACR Annual Meeting 2021 ; April 10-15, 2021 and May 17-21, 2021 ; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2060.
Texte intégralDoberstein, Kai, Alison Karst, Paul T. Kroeger, Paul Jones, William Hahn et Ronny Drapkin. « Abstract PR01 : Cyclin E : Targeting cell cycle dependencies in CCNE1-amplified tumors ». Dans Abstracts : AACR Special Conference : Addressing Critical Questions in Ovarian Cancer Research and Treatment ; October 1-4, 2017 ; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-pr01.
Texte intégralYue, Taotao, Wenming Yang et Qingmin Liao. « CCNET : Cross Coordinate Network for Joint Diabetic Retinopathy and Diabetic Macular Edema Grading ». Dans 2022 44th Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2022. http://dx.doi.org/10.1109/embc48229.2022.9871284.
Texte intégralAmrish, Amrish, et Shwetank Shwetank. « HRD-GKV-CCNet : A Deep Learning-based Multitask Method for Human Crowd Management ». Dans 2022 2nd International Conference on Emerging Smart Technologies and Applications (eSmarTA). IEEE, 2022. http://dx.doi.org/10.1109/esmarta56775.2022.9935448.
Texte intégralJonathan Weber, Lukas, Alice Kirchheim et Axel Zimmermann. « W&G-Bert : A Concept for a Pre-Trained Automotive Warranty and Goodwill Language Representation Model for Warranty and Goodwill Text Mining ». Dans 9th International Conference on Computer Networks & Communications (CCNET 2022). Academy and Industry Research Collaboration Center (AIRCC), 2022. http://dx.doi.org/10.5121/csit.2022.120304.
Texte intégralCao, Harry, Yu Sun et Ariel Jiang. « An Application to Provide Translated Subtitles and Pictures for Youth English Learners using Speech-to-Text and Nlp Techniques ». Dans 9th International Conference on Computer Networks & Communications (CCNET 2022). Academy and Industry Research Collaboration Center (AIRCC), 2022. http://dx.doi.org/10.5121/csit.2022.120303.
Texte intégral