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Displaying 18 of 18 results for "PRDM4"
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  1. Crystal structure of methyltransferase domain of human PR domain-containing protein 4 PDB

    ID: PDB:3DB5

    Description: PR domain zinc finger protein 4

  2. Expression analysis of Prdm4 mutant and overexpressing mouse embryonic stem cells BioProject

    ID: PRJNA198721

    Keywords: Transcriptome or Gene expression

    Access Type: download

  3. Zinc knuckle in PRDM4 PDB

    ID: PDB:2L9Z

    Description: PR domain zinc finger protein 4

  4. Expression analysis of Prdm4 mutant and overexpressing mouse embryonic stem cells ArrayExpress

    ID: E-GEOD-46308

    Description: Expression profiling of wild-type, Prdm4 null and Prdm4-EGFP overexpressing mouse embryonic stem cells using Illumina whole genome V2 arrays. The h...

  5. Expression analysis of Prdm4 mutant and overexpressing mouse embryonic stem cells OmicsDI

    ID: E-GEOD-46308

    Date Released: 05-13-2014

    Description: Expression profiling of wild-type, Prdm4 null and Prdm4-EGFP overexpressing mouse embryonic stem cells using Illumina whole genome V2 arrays. The h...

  6. The PR/SET domain Zinc finger protein Prdm4 regulates gene expression in ES cells but plays a non-essential role in the developing mouse embryo. BioProject

    ID: PRJNA209862

    Keywords: Epigenomics

    Access Type: download

  7. The PR/SET domain Zinc finger protein Prdm4 regulates gene expression in ES cells but plays a non-essential role in the developing mouse embryo ArrayExpress

    ID: E-GEOD-48372

    Description: using anti-GFP antibody to map genomic binding of Prdm4-EGFP in stably transfected mouse embryonic stem cells Two independent ChIP-seq replicates for each of two independent Prdm4

  8. The PR/SET domain Zinc finger protein Prdm4 regulates gene expression in ES cells but plays a non-essential role in the developing mouse embryo. OmicsDI

    ID: E-GEOD-48372

    Date Released: 05-04-2014

    Description: using anti-GFP antibody to map genomic binding of Prdm4-EGFP in stably transfected mouse embryonic stem cells Two independent ChIP-seq replicates for each of two independent Prdm4

  9. PRDM4_PONAB UniProt:Swiss-Prot

    ID: Q5R5M1

    Description: PR domain zinc finger protein 4 SET C2H2-type 1; atypical C2H2-type 2 C2H2-type 3 C2H2-type <...

  10. PRDM4_RAT UniProt:Swiss-Prot

    ID: Q9QZP2

    Description: PR domain zinc finger protein 4 SET C2H2-type 1 C2H2-type 2 C2H2-type 3 C2H2-type

  11. PRDM14 drives OCT3/4 recruitment via active demethylation in the transition from primed to naïve pluripotency BioProject

    ID: PRJNA311046

    Keywords: Transcriptome or Gene expression

    Access Type: download

  12. DNA Methylation in PRDM8 is a Biomarker for Dyskeratosis Congenita BioProject

    ID: PRJNA303165

    Keywords: Epigenomics

    Access Type: download

    dataset.description: rved significant hypermethylation in the gene for PR domain containing 8 (PRDM8). Notably, the same genomic region revealed hypermethylation in aplastic anemia (AA), and Down syndrome (DS), indicating that there might be an association with premature aging syndromes. Site-specific analysis of DNAm level in PRDM8 with pyrosequencing and MassArray validated aberrant hypermethylation in 14 DKC patients and 27 AA patients. Notably, telomere length was not directly correlated with DNAm in PRDM8, indicating that the two methods are complementary. In conclu...
  13. Translocations Activating IRF4 Identify a Subtype of Germinal-Center-Derived B-cell Lymphoma Affecting Predominantly Children and Young Adults ArrayExpress

    ID: E-GEOD-22470

    Description: of DLBCL and a classifier for IG/IRF4 positivity containing 27 genes allowed prediction of 3 additional MMML IG/IRF4-positive cases subsequently proven by FISH. IG/IRF4-positivity was associated with a favorable outcome likely due to significant enrichment of IG/IRF4-positive lymphomas in childhood and young adulthood. Conclusions: Our results suggest IRF4 translocations to be primary genetic alterations in a novel molecularly defined subset of GC-derived lymphomas predominantly affecting children. 271 diffuse large B-Cell lymphoma samples were hybridized to HGU133A Affymetrix GeneChips....

  14. A Phase 2 Study of Tipifarnib in Large Granular Lymphocyte (LGL) Leukemia dbGaP

    ID: phs000594.v1.p1

    Description: LGL leukemia can be divided into three subsets including the following: αβ or γδT-LGL and NK-LGL leukemia. All three subtypes will...

    study.schedulesActivity: due to a point mutation in the signal transducing domain. In gld/gld mice there is a point mutation in the Fas ligand gene, causing an inability of Fas ligand to bind to its receptor. Both MLR-lpr/lpr and gld/gld mice develop an autoimmune disease characterized by hypergammaglobulinemia, rheumatoid factor, circulating immune complexes, and expansions of CD4/CD8- double-negative T cells. These autoimmune features are similar to those observed in LGL leukemia. Moreover, lpr/lpr and gld/gld cells have many biologic properties characteristic of leukemic LGL which include 1) decreased or absent IL-2 production, 2) CD8+ origin, 3) expression of activation markers, and 4) rapid triggering of cytotoxic activity by anti-/CD3 Mab. We hypothesize that leukemic LGL accumulate in the peripheral blood due to a failure in normal lymphocyte regulatory pathways. 2.2 Study Agent Tipifarnib is a methyl-quinolinone with a molecular formula of C27H22Cl2N4O. Tipifarnib is a potent and selective nonpeptidomimetic inhibitor of farnesyl tranferase protein (FTP) both in vitro and in vivo. Tipifarnib is supplied by the DCTD, NCI as 100 mg (white, in boxes of 126 tablets each) circular film-coated tablets. Tablets should be stored at room temperature (15-250C, 59-770F). Tablets should be protected from moisture. Tablets are stable for at least 36 months at room temperature (15-250C, 59-770F). Farnesyltransferase is the enzyme that catalyses the transfer of a 15-carbon isoprenyl farnesyl moiety to the carboxy terminus of proteins containing the peptide target sequence "CAAX, often referred to as a CAAX-box". A related enzyme, geranylgeranyl transferase type I (GGT-1) catalyzes the addition of a 20-carbon geranylgeranyl group to CAAX-containing proteins. The "X" residue determines the specificity of these two enzymes. Prenylation catalyzed by geranylgeranyltransferase type 1 is not sensitive to inhibition by tipifarnib. The mechanism of action is cell type dependent and includes angiogenesis inhibition, induction of apoptosis, and antiproliferative effects. 2.3 Rationale To better understand the mechanism of lymphocytosis and resistance to apoptosis, we identified specific anti-apoptotic signaling pathways that were constitutively activated in the leukemic LGL. Blocking these anti-apoptotic pathways could lead to specific elimination of the leukemic LGLs. MAPK/ERK proteins are members of a family of dual specificity kinases that regulate growth and differentiation in response to growth factors.5,6 The signaling pathway that is commonly invoked upon growth factor receptor activation involves the recruitment of Grb-2/SOS to the receptor that leads to the association of Ras.7,8 Ras is a small farneslyated GTPase that becomes recruited to the plasma membrane and leads to the activation of Raf and ERK kinase 1 (MEK-1), which subsequently phosphorylates the TEY motif of ERK1 and ERK2.9 From previous studies in the laboratory, we found that NK and T cells in patients with LGL leukemia express an activated Ras/ERK survival pathway. Our data also showed that this pathway protects from Fas apoptosis. Inhibition of both Ras and MEK led to increased apoptosis of patient leukemic LGL cells and increased sensitivity to Fas-mediated apoptosis. We hypothesize that targeted disruption of Ras with tipifarnib in NK- and T-leukemic LGLs may be a useful new treatment for anemia, neutropenia and arthritis associated with this disease. Tipfarnib may represent a novel approach for targeted drug therapy for the treatment of LGL leukemia. Eight patients with LGL leukemia were to be treated previously with four cycles of therapy at a dose of 300 mg twice daily for 21 days out of a 28- day intermittent cycle. Patient entry criteria and monitoring followed the same rules described in the current protocol with bone marrow biopsies were performed on all patients prior to therapy and then repeated only when worsening cytopenias occurred. As defined in the current protocol, growth factor support with G-CSF was allowed during the 7 days off when the ANC was < 500 cells/µl. Five males and two female participants had T-LGL leukemia received tipifarnib and one female patient had NK-LGL leukemia. Four of the T-LGL leukemia patients failed to complete the study due to toxicity. Three patients were removed from study due to grade 3-4 bone marrow toxicity and/or infections requiring hospitalization and a tipifarnib-unrelated death occurred in one patient. Therefore, three patients completed four cycles and were evaluated for response with a dose reduction for bone marrow toxicity required in one of these evaluable patients. Leukemic LGL cells from the three evaluable patients displayed a dose-dependent increase in apoptosis in vitro and treatment was associated with reduced ALCs in two cases. None of the patients met the pre-determined criteria for response. However, one patient, shown to be growth factor unresponsive prior to therapy, had an unsustained increase in ANC from 0 at baseline to 8,620 cells/µl while receiving G-CSF on week 16. Furthermore, the number of bone marrow colonies increased in this patient after therapy. ...
  15. Translocations Activating IRF4 Identify a Subtype of Germinal-Center-Derived B-cell Lymphoma Affecting Predominantly Children and Young Adults BioProject

    ID: PRJNA128585

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: of DLBCL and a classifier for IG/IRF4 positivity containing 27 genes allowed prediction of 3 additional MMML IG/IRF4-positive cases subsequently proven by FISH. IG/IRF4-positivity was associated with a favorable outcome likely due to significant enrichment of IG/IRF4-positive lymphomas in childhood and young adulthood. Conclusions: Our results suggest IRF4 translocations to be primary genetic alterations in a novel molecularly defined subset of GC-derived lymphomas predominantly affecting children. Overall design: 271 diffuse large B-Cell lymphoma samples were hybridized to HGU133A Affymetrix GeneChips....
  16. Transcription profiling of human diffuse large B-cell lymphoma (DLBCL) patients ArrayExpress

    ID: E-GEOD-9429

    Description: Those patients with less than a Partial Response (PR) or progressive disease after IFE were removed from the study. Experiment Overall Design: Diagnoses were revised by a panel of pathologists, following the World Health Organization (WHO)9 criteria. Only primary DLBCLs were included in this analysis. T-cell/histiocyte-rich large B-cell lymphomas (T/HRLBCLs) and mediastinal DLBCLs were excluded. Experiment Overall Design: Patients included in this biological analysis were consecutive, selected only on the basis of the availability of formalin-fixed paraffin-embedded or frozen tissue representative of the tumour at diagnosis. The final number of cases analysed was 50. Frozen diagnostic tissue was available from a subset of ten of these patients. Experiment Overall Design: Informed consent was obtained from the patients included in the trial under the supervision of the Local Ethical Committees. Experiment Overall Design: Identifying biological function surrogate markers for clinical prediction Experiment Overall Design: The expression profile was initially analysed in the ten samples from which frozen tissue was available. These included four patients who had died after treatment failure and six who were alive, with complete remission, and free of disease. Experiment Overall Design: All frozen tissue corresponded to a representative area of the tumour with more than 60% of viable tumoral cells present. Experiment Overall Design: We used a multistep gene-set-enrichment approach to identify functional pathways deregulated in DLBCLs resistant to the treatment strategy. Experiment Overall Design: The design of the analysis was as follows (details on the procedure are included as Supplementary information on material and Methods) : Experiment Overall Design: 1. Microarray analysis, using both cDNA and oligonucleotide microarrays in a set of 10 frozen diagnostic samples. Experiment Overall Design: 2. Identification of biological function representative of differentially expressed genes, using the Gene Ontology database () Experiment Overall Design: 3. Selection of surrogate immunohistochemical markers (representative of the biological function identified) Experiment Overall Design: 4. Immunohistochemical study on Tissue Microarrays containing diagnostic initial biopsy tissue in a set of 50 patients Experiment Overall Design: a. Semiquantitative scoring Experiment Overall Design: b. Quantification of the most relevant markers Experiment Overall Design: Identification of biological markers predicting treatment response Experiment Overall Design: The relations between the semiquantitative measurement of the 60 proteins evaluated and the clinical outcome were analysed. The clinical end-points were: a) CR after 3 MegaCHOP, b) CR after IFE and, c) absence of progression after consolidation with HDT/ ASCT. Experiment Overall Design: The chi-square statistic was used to assess associations between the protein-expression levels and the intermediate step of treatment. Significant relationships (p<0.05) and non-significant trends (p<0.1) were identified. Experiment Overall Design: Failure was defined as progression or death attributable to the tumour. Failure-free survival (FFS) curves were plotted using the Kaplan-Meier method. Statistical significance of associations between individual variables and FFS was determined using the log-rank test. Significant relationships (p<0.05) and non-significant trends (p<0.1) were identified. Experiment Overall Design: Genes were clustered on the basis of their biological similarities. Experiment Overall Design: The accumulations or alternations of marker alterations were analysed by the chi-square and Spearman correlation tests. Only significant relati...

  17. Deletion of chromosome 11q predicts response to anthracycline-based chemotherapy in early breast cancer BioProject

    ID: PRJNA98645

    Keywords: Variation

    Access Type: download

    dataset.description: in 185 patients with NNBC using assembled arrays containing 2,460 BAC clones for scanning the genome for DNA copy number changes. After surgery, 90 patients received anthracycline-based chemotherapy whereas ninety-five did not. Tamoxifen was administered to patients with hormone-receptor positive tumors. Association of genomic and clinico-pathological data and outcome was computed using Cox proportional hazard models and multiple testing adjustment procedures. Analysis of NNBC genomes revealed a common genomic signature. Specific DNA copy num...
  18. Identification of biological markers of sensitivity to high-clinical-risk-adapted therapy for DLBCL patients BioProject

    ID: PRJNA103175

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: Those patients with less than a Partial Response (PR) or progressive disease after IFE were removed from the study. Diagnoses were revised by a panel of pathologists, following the World Health Organization (WHO)9 criteria. Only primary DLBCLs were included in this analysis. T-cell/histiocyte-rich large B-cell lymphomas (T/HRLBCLs) and mediastinal DLBCLs were excluded. Patients included in this biological analysis were consecutive, selected only on the basis of the availability of formalin-fixed paraffin-embedded or frozen tissue representative of the tumour at diagnosis. The final number of cases analysed was 50. Frozen diagnostic tissue was available from a subset of ten of these patients. Informed consent was obtained from the patients included in the trial under the supervision of the Local Ethical Committees. Identifying biological function surrogate markers for clinical prediction The expression profile was initially analysed in the ten samples from which frozen tissue was available. These included four patients who had died after treatment failure and six who were alive, with complete remission, and free of disease. All frozen tissue corresponded to a representative area of the tumour with more than 60% of viable tumoral cells present. We used a multistep gene-set-enrichment approach to identify functional pathways deregulated in DLBCLs resistant to the treatment strategy. The design of the analysis was as follows (details on the procedure are included as Supplementary information on material and Methods) : 1. Microarray analysis, using both cDNA and oligonucleotide microarrays in a set of 10 frozen diagnostic samples. 2. Identification of biological function representative of differentially expressed genes, using the Gene Ontology database (http://bioinformatics.weizmann.ac.il/cards) 3. Selection of surrogate immunohistochemical markers (representative of the biological function identified) 4. Immunohistochemical study on Tissue Microarrays containing diagnostic initial biopsy tissue in a set of 50 patients a. Semiquantitative scoring b. Quantification of the most relevant markers Identification of biological markers predicting treatment response The relations between the semiquantitative measurement of the 60 proteins evaluated and the clinical outcome were analysed. The clinical end-points were: a) CR after 3 MegaCHOP, b) CR after IFE and, c) absence of progression after consolidation with HDT/ ASCT. The chi-square statistic was used to assess associations between the protein-expression levels and the intermediate step of treatment. Significant relationships (p<0.05) and non-significant trends (p<0.1) were identified. Failure was defined as progression or death attributable to the tumour. Failure-free survival (FFS) curves were plotted using the Kaplan-Meier method. Statistical significance of associations between individual variables and FFS was determined using the log-rank test. Significant relationships (p<0.05) and non-significant trends (p<0.1) were identified. Genes were clustered on the basis of their biological similarities. The accumulations or alternations of marker alterations were analysed by the chi-square and Spearman correlation tests. Only significant relationships (p<0.05) were considered further. One surrogate marker for each altered main cellular function was selected. These markers were considered in order to develop a multivariate logistic regression model predicting failure of treatment. Proteins found to be potentially informative in this analysis were automatically scored. Various multivariate models were fitted using step-up (forward) and step-down (backwards) variable selection and other heuristic procedures. By comparing the fits of t...

Displaying 18 of 18 results for "PRDM4"