Relevant bibliographies by topics / CCNE2

Academic literature on the topic 'CCNE2'

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Published: 1 April 2023

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Journal articles on the topic "CCNE2"

1

Kondo, Yukio, Eric Wieder, Sijie Lu, and 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 (November 16, 2004): 4498. http://dx.doi.org/10.1182/blood.v104.11.4498.4498.

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Abstract Using a similar strategy that successfully identified PR1 as a leukemia-associated antigen (LAA), we identified two homologous HLA-A2-restricted peptides from cyclin E1 (CCNE1) and cyclin E2 (CCNE2) that could be used to elicit peptide-specific CTL from healthy donors in vitro. Two homologous nonameric peptides from CCNE1 (CCNE1144–152) and CCNE2 (CCNE2144–152), which differ by a single amino acid at position 7, have equal binding affinity for HLA-A2 and each elicited peptide-specific CTL with equal efficiency, as measured by specific lysis of T2 cells pulsed with either peptide (CCNE1 59.7% vs CCNE2 72.6% specific lysis, respectively, at E: T 10:1). TCR-Vβ spectratype analysis showed CCNE1-CTL clones to be derived from 3 Vβ families, while CCNE2-CTL clones were derived from a single Vβ family. The CCNE1-CTL and the CCNE2-CTL bound to each of the CCNE1/A2 and CCNE2/A2 tetramers, but staining intensity was greater for the CCNE1-CTL, suggesting greater TCR avidity of the CCNE1-CTL for both peptides. Because each clone cross-recognized the other homologous peptide, we hypothesized that each clone would efficiently kill leukemia that over-expressed either or both CCNE1 and CCNE2 proteins. FACsorted high avidity CTL showed higher specific lysis of peptide-pulsed T2 than did low avidity CTL (38.8% vs 31.9% specific lysis, respectively, at E: T 10:1, p = 0.02). The fluorescence decay of tetramer dissociation (ln (peptide/HLA-A2 tetramer)) over time was linear for each clone, suggesting that avidity was proportional to TCR affinity and tetramer dissociation t1/2 was determined based on first order kinetics. CCNE1-CTL had higher affinity for CCNE1144–152/HLA-A2 (CCNE1/A2, t1/2=84.5min; CCNE2/A2, t1/2=25.3min) and preferentially killed CCNE1144–152-pulsed T2 cells (CCNE1, 56.9% vs CCNE2, 38%, respectively, at E: T 10:1, p = 0.004). Interestingly, CCNE2-CTL also had higher TCR affinity for CCNE1144–152/HLA-A2 (CCNE1/A2, t1/2=29.5min; CCNE2/A2, t1/2=10.7min), but showed only slightly higher specific lysis of CCNE1144–152-pulsed T2 cells (CCNE1 = 49.3% vs CCNE2 = 44.2% specific lysis, respectively, at E: T 10:1, p = 0.33). Each clone specifically lysed HLA-A2+ T-ALL leukemia cells in proportion to both CCNE1 and CCNE2 protein overexpression assessed by Western blot (CCNE1-CTL, R2=0.89; CCNE2-CTL, R2=0.88). In contrast, healthy HLA-A2+ BM cells, which do not overexpress CCNE1 or CCNE2, and control HLA-A2− CML cells that overexpress both proteins, were not lysed. Both the high and low affinity clones showed equal lysis of T-ALL cells that expressed large amounts of each protein (specific lysis = 24.3% by CCNE1-CTL, vs lysis = 23.8% by CCNE2-CTL, at E: T 10:1). However, high affinity CCNE1-CTL killed T-ALL cells significantly better than low affinity CCNE2-CTL (16.8% vs 6.6% lysis, respectively, at E: T 10:1, p =0.02) when the T-ALL expressed a 2.5-fold lower amount of both CCNE1 and CCNE2 proteins. We conclude that the CCNE1 and CCNE2 homologous self-peptides are lymphoid leukemia-associated antigens. Furthermore, while the higher TCR affinity of CCNE1-CTL suggests that the CCNE1 peptide is the more dominant epitope, ultimate target susceptibility is enhanced due to degeneracy of the resulting CTL clones against homologous peptide epitopes.
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Sonntag, 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 (August 27, 2018): 9282–87. http://dx.doi.org/10.1073/pnas.1807155115.

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E-type cyclins E1 (CcnE1) and E2 (CcnE2) are regulatory subunits of cyclin-dependent kinase 2 (Cdk2) and thought to control the transition of quiescent cells into the cell cycle. Initial findings indicated that CcnE1 and CcnE2 have largely overlapping functions for cancer development in several tumor entities including hepatocellular carcinoma (HCC). In the present study, we dissected the differential contributions of CcnE1, CcnE2, and Cdk2 for initiation and progression of HCC in mice and patients. To this end, we tested the HCC susceptibility in mice with constitutive deficiency for CcnE1 or CcnE2 as well as in mice lacking Cdk2 in hepatocytes. Genetic inactivation of CcnE1 largely prevented development of liver cancer in mice in two established HCC models, while ablation of CcnE2 had no effect on hepatocarcinogenesis. Importantly, CcnE1-driven HCC initiation was dependent on Cdk2. However, isolated primary hepatoma cells typically acquired independence on CcnE1 and Cdk2 with increasing progression in vitro, which was associated with a gene signature involving secondary induction of CcnE2 and up-regulation of cell cycle and DNA repair pathways. Importantly, a similar expression profile was also found in HCC patients with elevated CcnE2 expression and poor survival. In general, overall survival in HCC patients was synergistically affected by expression of CcnE1 and CcnE2, but not through Cdk2. Our study suggests that HCC initiation specifically depends on CcnE1 and Cdk2, while HCC progression requires expression of any E-cyclin, but no Cdk2.
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Ishiyama, Ken, Yukio Kondo, Eric Wieder, Sijie Lu, and 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 (November 16, 2005): 1424. http://dx.doi.org/10.1182/blood.v106.11.1424.1424.

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Abstract Cyclin E1 (CCNE1) and cyclin E2 (CCNE2) are cell cycle genes that are overexpressed in AML, ALL, and CML, and in solid tumors such as breast cancer, lung cancer, and gastric cancer. We reported that two homologous nonameric peptides from CCNE1 (CCNE1144-152, ILLDWLMEV) and CCNE2 (CCNE2144-152, ILLDWLLEV), which differ by a single amino acid at position 7, have equal binding affinity for HLA-A2 and that CCNE1- and CCNE2- specific CTL elicited from healthy donors kill ALL and CML cells that overexpress CCNE1 and CCNE2. Interestingly, CCNE1/A2 and CCNE2/A2 tetramers bind to both T-cell receptors (TCR), but the longer tetramer dissociation t1/2 of CCNE1/A2 compared with CCNE2/A2 tetramer suggests CCNE1 is the more dominant epitope. To determine the clinical significance of CTL immunity to these self-epitopes, we studied peripheral blood mononuclear cells from 18 patients before and after allogeneic stem cell transplantation (SCT) using CCNE1/A2 and CCNE2/A2 tetramers. An increase in the absolute number of circulating CCNE1- or CCNE2-CTL after SCT was considered evidence of an immune response (IR). Of the18 patients, there were 10 with CML and 8 with ALL, and all were HLA-A2+ and had sufficient blood samples cryopreserved from various time points before SCT and 3–12 months after SCT for analysis. Ten patients, including all 8 ALL patients, were in complete remission (CR) prior to SCT and 5 patients achieved CR after SCT. An IR to CCNE1 was found in 12 of 18 (67%) patients and an IR to CCNE2 was found in 14 of 18 (78%) patients. All 12 patients who had an IR to CCNE1 also had an IR to CCNE2, reflecting possible cross-recognition of both peptides by the same CTL clones. By Chi-square analysis, IR to either CCNE1 or CCNE2 did not correlate with diagnosis (CML vs. ALL), source of the graft (matched related donors vs. mismatched donors), or disease status prior to SCT (remission vs. no remission). Six patients developed acute graft-versus-host disease (aGVHD) and 12 developed chronic graft-versus-host disease (cGVHD). IR to either CCNE1 or CCNE2 occurred more frequently in patients without aGVHD than in the patients with aGVHD (92% vs. 50%, p<0.05), although no significant difference in the IR frequency was observed amongst those who developed cGVHD versus those that did not. Of 8 CML patients who were not in CR prior to SCT, IR to either CCNE1 or CCNE2 occurred more frequently in patients that achieved CR compared to those that did not achieve CR after SCT (100% vs. 33%, respectively; p<0.04). These results provide clinical evidence that both CCNE1 and CCNE2 peptides are novel leukemia-associated antigens, and they justify future clinical trials to determine whether CTL immunity can be enhanced against these antigens in patients with ALL and CML.
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He, Hong, Ken Ishiyama, Gheath Alatrash, Yukio Kondo, Sijie Lu, and 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 (November 20, 2009): 686. http://dx.doi.org/10.1182/blood.v114.22.686.686.

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Abstract Abstract 686 Cyclin E1 (CCNE1) and cyclin E2 (CCNE2) are tightly regulated cell cycle genes in normal cells but are over-expressed and constitutively active in breast cancer and in the majority of hematological malignances. To validate CCNE as a potential target antigen for T-cells in leukemia, we first confirmed aberrant CCNE1 and CCNE2 protein in PBMC from 26 (93%) of 28 patients (CML = 16; AML = 7; ALL =2; NHL = 3) by Western Blot compared to 4 (33%) of 12 healthy controls (p < 0.0005). Next, we screened the sequences of CCNE1 and CCNE2 for HLA-A*0201 binding motifs and identified a pair of homologous nonameric peptides with highest predicted binding to HLA-A*0201 using an NCBI algorithm. The peptides, denoted CCNE1M (144ILLDWLMEV152) and CCNE2L (144ILLDWLLEV152), differed at P7 (M or L), and both differed from mouse sequence at P1 (V). Synthetic mouse and human peptides were used to confirm high affinity HLA-A2 binding on T2 cells by FACS analysis and peptide-pulsed T2 were used to elicit peptide-specific CTLs from healthy HLA-A2+ PBMC in vitro. CCNE1M-CTL lines specifically lysed both CCNE1M-loaded and CCNE2L-loaded T2 cells, while no CTL could be elicited with mouse peptide. Similarly, CCNE2L-stimulated CTL lines killed CCNE1M-loaded and CCNE2L-loaded T2 cells but not non-loaded T2 cells. Using CCNE1M and CCNE2L HLA-A2 tetramers, we found that either tetramer could bind equally to either the CCNE1M- or CCE2L-derived CTL lines, suggesting that both peptides could be cross-recognized by CTL lines elicited with either peptide. To further study the cross-recognition and potential immune dominance of both peptides and to determine their potential anti-leukemia activity, CCNE1M- and CCNE2L-CTL clones were derived by limiting dilution assay. Two peptide-specific CTL clones from each of the lines showed 25% and 26% specific lysis, respectively, of leukemia cells at E:T 10:1. Neither CCNE-specific CTLs showed lysis of BM cells that were obtained from the same patient during remission, nor HLA-A2+ BM cells from a healthy donor. Next, we compared the T-cell antigen receptor (TCR) avidity of these CCNE1M- and the CCNE2L-CTL clones by measuring tetramer dissociation half-times (t1/2) at 25°C using CCNE1M/HLA-A2 and CCNE2L/HLA-A2 (and control pp65/HLA-A2) tetramers analyzed by flow cytometry. The decay of normalized (to time = 0) tetramer-bound fluorescence versus time was linear for each clone with either tetramer (R2 = 0.85 to 0.91), showing that tetramer binding avidity could be used to proportionally determine TCR affinity. Furthermore, first order kinetics could be used to determine the t1/2 of each of the clones. The t1/2 of CCNE1M/HLA-A2 tetramer was 85 min and 25 min, respectively, while the t1/2of CCNE1L/HLA-A2 was 30 min and 11 min, respectively, for the CCNE1M-CTL and the CCNE2L-CTL. This suggests that while both peptides were cross recognized by unique T-cell clones (with unique TCR, determined by TCR-Vβ sequence comparisons), CCNE1M appeared to be immunodominant. To determine whether immune response (IR) to either peptide occurred in leukemia patients, we studied PBMC from 18 patients (10 CML; 8 ALL) before and 3–6 mo after SCT with CCNE1M/HLA-A2- and CCNE2L/HLA-A2-tetramer assay. The mean number of CCNE1M-CTL and CCNE2L-CTL cells increased after SCT (p< 0.002 in CCNE1M-CTL and CCNE2L-CTL) compared to no change in mean number of pp65-CTL before/after SCT. IR (defined as ≥ 20% increase of specific CTL after SCT) to either CCNE1M or CCNE2L did not correlate with type of leukemia, donor-recipient HLA disparity (matched or mismatched), or disease status prior to SCT by Fisher's exact test. However, in 8 CML patients not in remission prior to SCT, IR to either CCNE1 or CCNE2 occurred more frequently in patients who achieved CR compared to those that did not achieve CR after SCT (100% vs. 33%, respectively; p < 0.04). These findings were confirmed in an additional 25 AML patients with active disease at SCT. To study whether the peptide-specific CTL were functional, we measured IFN-γ and TNF-αa production after peptide stimulation by Luminex bead assay and by intracellular cytokine flow cytometry (CFC). The assays showed production of IFN-γ and TNF-αa cytokines by T-cells after stimulation with CCNE1M or CCNE2Lpeptides. Taken together, these results show that CCNE1M and CCNE2Lself-peptides from constitutively active cell cycle proteins are novel leukemia-associated antigens that could be studied in immunotherapy strategies. Disclosures: No relevant conflicts of interest to declare.
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Martín-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 (February 28, 2019): 940–51. http://dx.doi.org/10.1182/blood-2018-07-862151.

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Abstract Mantle cell lymphoma (MCL) is characterized by the t(11;14)(q13;q32) translocation resulting in overexpression of cyclin D1. However, a small subset of cyclin D1− MCL has been recognized, and approximately one-half of them harbor CCND2 translocations while the primary event in cyclin D1−/D2− MCL remains elusive. To identify other potential mechanisms driving MCL pathogenesis, we investigated 56 cyclin D1−/SOX11+ MCL by fluorescence in situ hybridization (FISH), whole-genome/exome sequencing, and gene-expression and copy-number arrays. FISH with break-apart probes identified CCND2 rearrangements in 39 cases (70%) but not CCND3 rearrangements. We analyzed 3 of these negative cases by whole-genome/exome sequencing and identified IGK (n = 2) and IGL (n = 1) enhancer hijackings near CCND3 that were associated with cyclin D3 overexpression. By specific FISH probes, including the IGK enhancer region, we detected 10 additional cryptic IGK juxtapositions to CCND3 (6 cases) and CCND2 (4 cases) in MCL that overexpressed, respectively, these cyclins. A minor subset of 4 cyclin D1− MCL cases lacked cyclin D rearrangements and showed upregulation of CCNE1 and CCNE2. These cases had blastoid morphology, high genomic complexity, and CDKN2A and RB1 deletions. Both genomic and gene-expression profiles of cyclin D1− MCL cases were indistinguishable from cyclin D1+ MCL. In conclusion, virtually all cyclin D1− MCLs carry CCND2/CCND3 rearrangements with immunoglobulin genes, including a novel IGK/L enhancer hijacking mechanism. A subset of cyclin D1−/D2−/D3− MCL with aggressive features has cyclin E dysregulation. Specific FISH probes may allow the molecular identification and diagnosis of cyclin D1− MCL.
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Wu, Lizheng, Kuan Yang, Yajie Gui, and 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 (June 2020): 354–61. http://dx.doi.org/10.1139/bcb-2019-0156.

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The consumption of nicotine via smoking tobacco has been reported to stimulate the occurrence and progression of periodontitis. Many studies have demonstrated that nicotine prevents the regeneration of periodontal tissues primarily by inhibiting the proliferation of human periodontal ligament (PDL) cells. However, the mechanisms underlying this process are still unclear. Therefore, we investigated whether nicotine-upregulated miR-30a inhibited the proliferation of human PDL cells by downregulating cyclin E2 (CCNE2), in vitro. Quantitative real-time PCR analysis revealed that nicotine upregulated the expression of miR-30a in human PDL cells. In addition, nicotine inhibited the proliferation of human PDL cells by inducing cell cycle arrest. To support this hypothesis, we showed that nicotine downregulated the expression of CCNE2 in human PDL cells, whereas inhibition of miR-30a restored CCNE2 expression that had been downregulated by nicotine. Furthermore, using luciferase reporter assays, we found that miR-30a directly interacts with the CCNE2 3′UTR. In conclusion, these findings indicate that nicotine-upregulated miR-30a inhibits the proliferation of human PDL cells by downregulating the expression of CCNE2.
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Tao, Kaiyi, JinShi Liu, JinXiao Liang, XiaoFang Xu, LiWei Xu, and WeiMin Mao. "Vascular endothelial cell-derived exosomal miR-30a-5p inhibits lung adenocarcinoma malignant progression by targeting CCNE2." Carcinogenesis 42, no. 8 (June 15, 2021): 1056–67. http://dx.doi.org/10.1093/carcin/bgab051.

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Abstract This study tried to explore the molecular mechanism underlying progression of lung adenocarcinoma (LUAD) and discuss the extracellular communication between cancer cells and vascular endothelial cells. Roughly, differential analysis was carried out to note that miR-30a-5p was lowly expressed in LUAD, whereas CCNE2 was highly expressed. Cell functional experiments demonstrated that overexpressed miR-30a-5p led to suppressed cell abilities in proliferation, migration and invasion. Dual-luciferase reporter gene assay and RNA immunoprecipitation verified the binding of miR-30a-5p and CCNE2, as well as decreased mRNA and protein expression of CCNE2 with miR-30a-5p overexpression. Simultaneous up-regulation of miR-30a-5p and CCNE2 reversed the promotion of CCNE2 on malignant behaviors of LUAD cells. In vivo mice experiments exhibited that high miR-30a-5p expression hindered tumor growth. Additionally, miR-30a-5p was localized on the Extracellular Vesicles microRNA (EVmiRNA) database. MiR-30a-5p was abundant in exosomes derived from vascular endothelial cells. To validate that miR-30a-5p could be delivered to LUAD cells via exosomes and then make an effect, exosomes from vascular endothelial cells were first extracted and identified by transmission electron microscopy and detection of exosomal marker proteins (Alix, CD63, TSG101). Sequentially, the extracted exosomes were labeled with DIO to note that exosomes could be internalized by cancer cells. Further experiments indicated that miR-30a-5p was increased in cancer cells co-cultured with exosomes, which in turn suppressed cell malignant behaviors and made cell cycle arrest. In all, our findings clarified that exosomes derived from vascular endothelial cells delivered miR-30a-5p to LUAD cells to affect tumor malignant progression via the miR-30a-5p/CCNE2 axis.
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Diab, 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 (May 20, 2020): 3569. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.3569.

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3569 Background: Previous studies have shown that CCNE2 expression is higher in patients’ cancers resistant to CDK4/6 inhibitors. Increased expression of CCNE2, MTDH, or TSPYL5, genes contained within the 70-gene risk of distant recurrence signature (70GS), has also been implicated in breast oncogenesis, poor prognosis, and chemoresistance. These genes are located on chromosome region 8q22.1, one of the most recurrently amplified regions out of all 70GS genes in breast tumors (Fatima et al. 2017). MYC, located on 8q24, is overexpressed in 40% of all breast cancers (BC). Here we examined the expression of CCNE2, MTDH, and TSPYL5 in relation to 70GS risk and the 80-gene molecular subtype signature (80GS), and their correlation with MYC expression in early stage BC patients. Methods: CCNE2, MTDH, TSPYL5, and MYC mRNA expression was measured in 5022 BC samples sent to Agendia (Irvine, CA) for 70GS and 80GS testing, which included FFPE microarray full-transcriptome data. 70GS was used to stratify patients into Ultra Low Risk (UL), Low Risk (LR), High Risk (HR), and Ultra High Risk (UH). Both 70GS and 80GS were used to classify patient samples into Luminal A, Luminal B, HER2, or Basal type. Wilcoxon rank sum test was used to assess expression differences. Results: The expression of CCNE2, MTDH, and TSPYL5 significantly correlated with each other and was higher in HR patients compared to LR patients (p < 0.001) and higher in UH patients compared to HR patients (p < 0.001). Expression of these genes was highest in Basal type tumors, 83% of which were UH, followed by Luminal B type tumors, and lowest in Luminal A type tumors. CCNE2 and MYC expression was elevated in LR compared to UL patients (p < 0.001 and p = 0.0043). There was no difference in MYC expression between HR vs. LR or UH vs. HR. Lastly, there was no association between the expression of 8q22.1 genes and MYC in any 70GS subgroup. Conclusions: Within the 70GS, CCNE2, MTDH, and TSPYL5 have similar expression patterns and when overexpressed may identify an UH cohort of BC. This observation, in addition to their physical proximity at 8q22.1 suggests a possible amplicon in this region. The highest expression of CCNE2, MTDH, and TSPYL5 associated with UH patients and is concordant with previous studies that support the role of these genes in BC metastasis. Furthermore, this analysis suggests MYC may not stratify patients based on metastatic potential. These data may be clinically relevant for stratifying patients in ongoing clinical trials evaluating response and resistance to targeted therapies in early stage BC.
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Lee, Christine, Kristine J. Fernandez, Sarah Alexandrou, C. Marcelo Sergio, Niantao Deng, Samuel Rogers, Andrew Burgess, and C. Elizabeth Caldon. "Cyclin E2 Promotes Whole Genome Doubling in Breast Cancer." Cancers 12, no. 8 (August 13, 2020): 2268. http://dx.doi.org/10.3390/cancers12082268.

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Genome doubling is an underlying cause of cancer cell aneuploidy and genomic instability, but few drivers have been identified for this process. Due to their physiological roles in the genome reduplication of normal cells, we hypothesised that the oncogenes cyclins E1 and E2 may be drivers of genome doubling in cancer. We show that both cyclin E1 (CCNE1) and cyclin E2 (CCNE2) mRNA are significantly associated with high genome ploidy in breast cancers. By live cell imaging and flow cytometry, we show that cyclin E2 overexpression promotes aberrant mitosis without causing mitotic slippage, and it increases ploidy with negative feedback on the replication licensing protein, Cdt1. We demonstrate that cyclin E2 localises with core preRC (pre-replication complex) proteins (MCM2, MCM7) on the chromatin of cancer cells. Low CCNE2 is associated with improved overall survival in breast cancers, and we demonstrate that low cyclin E2 protects from excess genome rereplication. This occurs regardless of p53 status, consistent with the association of high cyclin E2 with genome doubling in both p53 null/mutant and p53 wildtype cancers. In contrast, while cyclin E1 can localise to the preRC, its downregulation does not prevent rereplication, and overexpression promotes polyploidy via mitotic slippage. Thus, in breast cancer, cyclin E2 has a strong association with genome doubling, and likely contributes to highly proliferative and genomically unstable breast cancers.
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Kikuchi, Kei, and Daisuke Kaida. "CCNE1 and E2F1 Partially Suppress G1 Phase Arrest Caused by Spliceostatin A Treatment." International Journal of Molecular Sciences 22, no. 21 (October 27, 2021): 11623. http://dx.doi.org/10.3390/ijms222111623.

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The potent splicing inhibitor spliceostatin A (SSA) inhibits cell cycle progression at the G1 and G2/M phases. We previously reported that upregulation of the p27 cyclin-dependent kinase inhibitor encoded by CDKN1B and its C-terminal truncated form, namely p27*, which is translated from CDKN1B pre-mRNA, is one of the causes of G1 phase arrest caused by SSA treatment. However, the detailed molecular mechanism underlying G1 phase arrest caused by SSA treatment remains to be elucidated. In this study, we found that SSA treatment caused the downregulation of cell cycle regulators, including CCNE1, CCNE2, and E2F1, at both the mRNA and protein levels. We also found that transcription elongation of the genes was deficient in SSA-treated cells. The overexpression of CCNE1 and E2F1 in combination with CDKN1B knockout partially suppressed G1 phase arrest caused by SSA treatment. These results suggest that the downregulation of CCNE1 and E2F1 contribute to the G1 phase arrest induced by SSA treatment, although they do not exclude the involvement of other factors in SSA-induced G1 phase arrest.
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Dissertations / Theses on the topic "CCNE2"

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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.

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Biomedical Sciences
Ph.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
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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.

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Cutaneous wound healing is a complex process involving the migration of inflammatory cells to the wound site, deposition of extracellular matrix, and the reestablishment of an intact epithelial barrier. Re-epithelialization depends on the proliferation and directional migration of keratinocytes from the wound edges. Initially, keratinocytes migrate over a provisional wound matrix that is rich in fibronectin, and as the wound heals the provisional matrix becomes replaced by one consisting of collagen and proteoglycans. Re-epithelialization is tightly regulated by a variety of peptides such as growth factors, cytokines and proteases, and abnormalities may result in chronic non-healing wounds or hypertrophic scars. CCN2 (Connective Tissue Growth Factor) is a multifunctional protein with effects on cells and their interactions with the connective tissue. CCN2 is expressed in a variety of cell types and regulates numerous cell functions including proliferation, differentiation, adhesion, migration and stimulation of collagen production. While the importance of CCN2 for the fibrotic response has been well studied, its involvement in keratinocyte function has not yet been fully explored. Using an in vivo wound model, the expression of CCN2 was captured at the leading keratinocyte edge during re-epithelialization. In vitro, exogenous addition of CCN2 to human keratinocyte cultures promoted keratinocyte migration. Subsequently, integrin a5b1 was identified as an important mediator of CCN2 enhancement of keratinocyte adhesion to fibronectin. CCN2 activated the FAK-MAPK signaling pathway, and pretreatment with MEK1 specific inhibitor PD98059 markedly reduced CCN2-promoted keratinocyte migration. In vitro, CCN2 expression was induced by TGF-β1. Compared with inhibiting the SMAD pathway, blocking MAPK was more effective in reducing TGF-β1-induced CCN2 mRNA and protein expression. In addition, CCN2-induced keratinocyte spreading required FAK. Treatment with CCN2 led to actin disassembly and altered the activity of the Rho proteins and p190RhoGAP in keratinocytes. Furthermore, Cdc42 mediated CCN2-induced cell polarity. In conclusion, using in vivo and in vitro models, CCN2 was shown to regulate keratinocyte function by promoting keratinocyte adhesion, spreading and migration. A complete understanding of CCN2 expression in keratinocytes is crucial in order to develop novel therapies for wound healing.
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McLean, Celia. "Investigating the expression and function of CCN2 in articular cartilage." Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/5289.

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The pericellular matrix (PCM) is a distinct zone of matrix that surrounds individual chondrocytes throughout articular cartilage. Although not much is known about its function, our group has shown that it has a role in mechanotransduction by controlling the bioavailability of perlecan-bound FGF-2. The aim of this project was to determine the other structural components of the PCM, and to search for other heparin binding growth factors which might be sequestered in the matrix. By confocal microscopy I confirmed that the PCM was rich in type VI collagen and perlecan, although devoid of type II collagen and aggrecan. Isolation of individual chondrons (the chondrocyte together with its PCM) was performed by partial digestion of the matrix using dispase and collagenase, and proteomic analysis using mass spectrometry was performed to identify new proteins. As this method was only partially successful I looked for the presence of a known heparin binding growth factor, connective tissue growth factor (CCN2), in chondron preparations. CCN2, which is an abundant secreted protein of articular cartilage, was present in both the chondron preparation by western blot, and was visualised in the PCM of porcine and human articular cartilage by confocal microscopy. CCN2 is not commercially available so His-tagged recombinant protein was stably expressed and purified using nickel affinity chromatography. Biological activity of the purified protein was investigated in a number of established assays. No biological activity was demonstrated when purified CCN2 was used alone on murine mesenchymal stem cells, but was evident when assayed in combination with low dose TGF-β. The effect of exogenous CCN2 on fibroblasts was limited by the significant release of endogenous CCN2. High constitutive expression of CCN2 in articular cartilage may limit the effects seen by exogenous CCN2. However, the results presented in this thesis support the role of CCN2 as a modulator of TGF beta signalling, and suggest that, through potentiating TGF beta it may regulate matrix turnover in articular cartilage.
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Nakatani, 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.

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Wang, 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.

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CCN protein family members (CYR61, CTGF, Nov, Wisp-1, Wisp-2 and Wisp-3) have important roles in many different processes including angiogenesis, inflammation, remodelling of extracellular matrix and tumorigenesis. In bone, CCN1 increases osteoblastogenesis via Wnt3A signalling and activation of -catenin which, in turn, upregulates CCN1 expression. The exact role of CCN1, CCN2, and CCN6 in osteoclast physiology are not known but we have recently shown that recombinant human (rh)CCN1 inhibits osteoclastogenesis in vitro. The aim of this study was to determine: 1) the expressions of all six members of the CCN protein family in osteoblasts and osteoclasts; 2) the functions of recombinant human CCN2, CCN6 in osteoclastogenesis; 3) whether osteoblast-derived CCN1 may mediate the effect of CCN1 on osteoclast formation and the roles of osteoblast-derived CCN1 and/or osteoclast-derived CCN1 in osteoblast and/or osteoclast differentiation; 4) which signalling pathways are involved in the function of CCN1 in osteoclasts and osteoblasts. We found CCN1-5 but not CCN6 expressed in murine osteoclasts and osteoblasts. All six members were expressed in human OA osteoblasts but only CCN1-3 were detected in human osteoclasts using quantitative RT-PCR. rhCCN1 (in agreement with our previous observations), and also 2 and 6 inhibited human and mouse osteoclast formation in a concentration-dependent manner. We generated and validated an expression construct to specifically overexpress CCN1 in osteoblasts. Incorporation of CCN1-specific siRNA reduced CCN1 expression to between 12.5% and 50% of control osteoblast cultures. In both co-cultures with direct contact between osteoblasts and osteoclast co-cultures as well as Transwell cultures, overexpression of CCN1 in osteoblasts decreased the formation of TRAP positive multinucleated osteoclast-like cells, while siRNA mediated knockdown of CCN1 in the osteoblasts resulted in increased osteoclast-like cell formation. These data suggest that osteoblast-derived CCN1 is a secreted negative regulator of osteoclastogenesis. Moreover, overexpression or knockdown of CCN1 in osteoclast precursors inhibited or increased osteoclast differentiation whilst overexpression or knockdown CCN1 in osteoblasts increased or inhibited osteoblast mineralization respectively. Further investigation found that CCN1 increased Wnt and MAPK signalling in osteoblasts cultured in mineralization medium and inhibited Wnt and IGF-1 signalling during osteoclast differentiation. In conclusion, paracrine and autocrine effects of CCN1 have been demonstrated in osteoclasts and osteoblasts in this study and Wnt, MAPK, amd IGF-1 signalling pathways, may be involved in these effects.
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Holmes, 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/.

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Systemic sclerosis (Scleroderma, SSc) is a chronic, connective tissue disease of unknown etiology, characterised by vascular dysfunction, iriflarnmation and organ fibrosis. Involving both genetic and environmental components, the specific mechanisms which result in fibrosis remain largely unknown. A cardinal feature of SSc is increased synthesis of extracellular matrix (ECM). Dermal fibroblasts cultured from SSc patients maintain many of the abnormal properties seen in vivo, including excess production of collagen type I, and growth factors such as connective tissue growth factor (CTGF/CCN2). CTGF, like many genes dysregulated in SSc, is induced by TGF- p in normal fibroblasts. The overall aim of my studies was to determine the mechanism(s) controlling CTGF over-expression in SSc dermal fibroblasts (SDF). Induction of CTGF by TGF-p was found to be dependent upon elements in the proximal portion of the CTGF promoter, distinct from those of the previously characterised TGF- P response element (TRE). The TRE acts, in NIH/3T3 and HFF cells, as a regulator of basal expression, and is not essential for TGF-P induction of CTGF. Instead TGF-p induces CTGF expression via a Smad3 complex, binding to a bona fide SMAD transcription factor binding site. Over-expression CTGF in SDF is independent of autocrine expression of TGF-P and the SMAD binding element and rather dependent on a functional Sp-binding site. Inhibition of Spl-like DNA binding reduces excessive CTGF expression in SDF. Consistent with this Spl-DNA binding activity is elevated in SDF nuclear extracts. Investigation of the mechanism of elevated Spl-like binding found that SDF exhibited constitunVely active ERK1/2 and JNK1. Inhibition of ERK1/2 repressed elevated Sp-binding and CTGF over-expression observed in SDF. In summary, the data presented in this thesis provide evidence that dysregulation of ERK1/2 in SDF is involved in CTGF over-expression via a Spl-like DNA binding. Thus repression of ERK may represent a candidate in targeting fibrosis in SSc.
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Hendesi, 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.

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Cell Biology
Ph.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
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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.

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Bohr, 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.

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Gonnot, 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.

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Les cellules souches embryonnaires de souris (mESC) présentent un cycle cellulaire atypique caractérisé par l'absence d'une voie Rb fonctionnelle et la forte expression de la cycline E pendant toutes les phases du cycle cellulaire. En conséquence, les mESC sont constitutivement amorcées pour la réplication de l'ADN. Pour comprendre comment la cycline E, un régulateur clé de la transition de la phase G1 à S, est régulée dans les mESC, nous avons analysé la régulation transcriptionnelle de son gène Ccne1 par des facteurs de transcription du réseau de pluripotence naïve. Nous avons observé que les facteurs Esrrb, Klf4 et Tfcp2l1 se lient à la région du promoteur de Ccne1 sur plusieurs sites situés entre 0 et 1kb en amont du site d'initiation de la transcription. Un test luciférase nous a permis de monter qu'une mutation de ces sites de liaison diminue ou abolie l'activité transcriptionnelle du promoteur. De plus, la surexpression inductible à la doxycycline des facteurs Esrrb, Klf4 et Tfcp2l1 augment le niveau d'expression d'ARNm de Ccne1. Ces résultats suggèrent que Esrrb, Klf4 et Tfcp2l1 contrôlent l'expression de la cycline E. Ils mettent en évidence un lien direct entre le réseau de pluripotence naïve et la régulation du cycle mitotique dans les mESC. Nous avons utilisé le système rapporteur FUCCI pour étudier en fonction du cycle cellulaire l'expression des facteurs de transcription qui forment le réseau de pluripotence naïve. Nous avons observé que l'expression de Esrrb, Klf4, Tfcp2l1 et Nanog oscille au cours du cycle cellulaire avec une diminution de l'expression entre la phase G1 précoce et le début de S, puis une ré-augmentation entre le début de S et la phase G2/M. Ces résultats suggèrent que le réseau de pluripotence naïve est déstabilisé transitoirement lors du passage de la phase G1 à la phase S du cycle cellulaire
Mouse 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
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Books on the topic "CCNE2"

1

Inc, Syngress Media, ed. CCNE Cisco certified network associate study guide: (exam 640-407). Berkeley, Calif: Osborne/McGraw-Hill, 1998.

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Fay 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.

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NA. Cnap Networkg Ccna1& Routrs Ccna2& CCNA Commd. Addison Wesley Longman, 2006.

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Clarke. Novell's Ccne Update Netware 6-apdf. Wiley & Sons, Incorporated, John, 2003.

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NA. Cnap Routers Ccna2 Comp& Lab& Sg& Quick Ref Pk. Addison Wesley Longman, 2006.

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NA. Cnap Routrs Ccna2 & Ccna1& 2 Eng Jrnl REV Pk. Addison Wesley Longman, 2006.

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Neville, John. CCNB1, 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.

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Book chapters on the topic "CCNE2"

1

van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CCNA2." In Encyclopedia of Signaling Molecules, 282. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100188.

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Leask, Andrew. "CCN2 in Skin Fibrosis." In 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.

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Luo, Chao, Xiaojie Li, Yucheng Chen, Xi Wu, Jia He, and Jiliu Zhou. "CCNET: Cascading Convolutions for Cardiac Segmentation." In Lecture Notes in Computer Science, 3–11. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24265-7_1.

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Liu, Gang, Jing Ming, Xinyun Wu, and Rifeng Jiang. "CCNet: Unpaired Keypoints for Skull Fracture Detection." In 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.

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Ortega, John E., Iria de-Dios-Flores, José Ramom Pichel, and Pablo Gamallo. "Revisiting CCNet for Quality Measurements in Galician." In Lecture Notes in Computer Science, 407–12. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-98305-5_38.

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Kawata, Kazumi, Satoshi Kubota, and Masaharu Takigawa. "Analysis of Transcytosis of CCN2 by Chondrocytes." In 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.

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Nishida, Takashi, Satoshi Kubota, and Masaharu Takigawa. "Production of Recombinant CCN2 Protein by Mammalian Cells." In 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.

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Aoyama, Eriko, Takako Hattori, Satoshi Kubota, and Masaharu Takigawa. "Production of Recombinant CCN2 Protein in Escherichia coli." In 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.

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Hattori, Takako, Mitsuhiro Hoshijima, and Masaharu Takigawa. "Protein Imaging of CCN2 and CCN3 in Living Cells." In 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.

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Shimo, Tsuyoshi, Hiroaki Takebe, Saki Fujii, and Akihiro Hosoya. "Immunohistochemical Analysis of CCN2 in Experimental Fracture Healing Models." In Methods in Molecular Biology, 335–42. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2744-0_23.

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Conference papers on the topic "CCNE2"

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Lathrop, Scott. "CCNet." In the 1995 ACM/IEEE conference. New York, New York, USA: ACM Press, 1995. http://dx.doi.org/10.1145/224170.285578.

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Huang, Zilong, Xinggang Wang, Lichao Huang, Chang Huang, Yunchao Wei, and Wenyu Liu. "CCNet: Criss-Cross Attention for Semantic Segmentation." In 2019 IEEE/CVF International Conference on Computer Vision (ICCV). IEEE, 2019. http://dx.doi.org/10.1109/iccv.2019.00069.

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Taylor-Harding, Barbie, Hasmik Agadjanian, Paul Joseph Aspuria, Takako Mizuno, Dong-Joo Cheon, Sandra Orsulic, Beth Karlan, Christine Walsh, and Wolf Ruprecht Wiedemeyer. "Abstract B48: Targeting chemo-resistance in CCNE1-amplified ovarian cancer." In 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.

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Martinez-Soria, N., L. McKenzie, S. Nakjang, V. Forster, A. Isa, HJ Blair, and O. Heidenreich. "CCND2 is a RUNX1/ETO target required for leukaemic propagation." In 30. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch-onkologische Forschung. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1602192.

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Bai, Shoumei, and Ronald J. Buckanovich. "Abstract 2060: Therapeutic approaches for CCNE1-amplified HR-proficient ovarian cancer." In 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.

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Doberstein, Kai, Alison Karst, Paul T. Kroeger, Paul Jones, William Hahn, and Ronny Drapkin. "Abstract PR01: Cyclin E: Targeting cell cycle dependencies in CCNE1-amplified tumors." In 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.

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Yue, Taotao, Wenming Yang, and Qingmin Liao. "CCNET: Cross Coordinate Network for Joint Diabetic Retinopathy and Diabetic Macular Edema Grading." In 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.

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Amrish, Amrish, and Shwetank Shwetank. "HRD-GKV-CCNet: A Deep Learning-based Multitask Method for Human Crowd Management." In 2022 2nd International Conference on Emerging Smart Technologies and Applications (eSmarTA). IEEE, 2022. http://dx.doi.org/10.1109/esmarta56775.2022.9935448.

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Jonathan Weber, Lukas, Alice Kirchheim, and Axel Zimmermann. "W&G-Bert: A Concept for a Pre-Trained Automotive Warranty and Goodwill Language Representation Model for Warranty and Goodwill Text Mining." In 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.

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The request for precise text mining applications to extract information of company based automotive warranty and goodwill (W&G) data is steadily increasing. The progress of the analytical competence of text mining methods for information extraction is among others based on the developments and insights of deep learning techniques applied in natural language processing (NLP). Directly applying NLP based architectures to automotive W&G text mining would wage to a significant performance loss due to different word distributions of general domain and W&G specific corpora. Therefore, labelled W&G training datasets are necessary to transform a general-domain language model in a specific-domain one to increase the performance in W&G text mining tasks.
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Cao, Harry, Yu Sun, and Ariel Jiang. "An Application to Provide Translated Subtitles and Pictures for Youth English Learners using Speech-to-Text and Nlp Techniques." In 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.

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Currently, thousands of free K-12 educational videos exist online with the aim of trying to help young students learn outside of the typical scholastic environment. However, most of these videos are in English, so without subtitles it may be difficult for non-native English-speaking students to fully understand them. These students may need to spend time searching for translations and understanding content, which can distract them from grasping the important concepts within the videos. The state-ofthe- art of speech-to-text and NLP techniques might help this group digest the content of instructional videos more effectively. This paper proposes an application that uses speech-to-text, machine translation, and NLP techniques to generate translated subtitles and visual learning aids for viewers of instructional videos. This video application supports more than 20 languages. We applied our application to some popular online educational videos and conducted a qualitative evaluation of its approach and effectiveness. The results demonstrated that the application could successfully translate the English of the videos into the viewers’ native language(s), detect keywords, and display relevant images to further facilitate contextual understanding.
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