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Displaying 16 of 16 results for "PRDM11"
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  1. Crystal structure of Methyltransferase domain of human PR domain-containing protein 11 PDB

    ID: PDB:3RAY

    Description: PR domain-containing protein 11

  2. Expression data from EμMyc;Prdm11 WT and EμMyc;Prdm11 KO end-stage splenic tumors BioProject

    ID: PRJNA242328

    Keywords: Transcriptome or Gene expression

    Access Type: download

  3. PRDM11 ChIP in U2932 cells BioProject

    ID: PRJNA242327

    Keywords: Epigenomics

    Access Type: download

  4. Expression data from EμMyc;Prdm11 WT and EμMyc;Prdm11 KO end-stage splenic tumors ArrayExpress

    ID: E-GEOD-56063

    Description: The PR-domain family (PRDMs) encodes transcriptional regulators, several of which are deregulated in cancer. We foun...

  5. Effect of PRDM11 depletion in U2932 cells BioProject

    ID: PRJNA242683

    Keywords: Transcriptome or Gene expression

    Access Type: download

  6. PRDM11 ChIP in U2932 cells ArrayExpress

    ID: E-GEOD-56064

    Description: The PR-domain family e(PRDMs) encodes transcriptional regulators, several of which are deregulated in cancer. We fou...

  7. PRDM11 ChIP in U2932 cells OmicsDI

    ID: E-GEOD-56064

    Date Released: 03-04-2016

    Description: The PR-domain family e(PRDMs) encodes transcriptional regulators, several of which are deregulated in cancer. We fou...

  8. Expression data from EμMyc;Prdm11 WT and EμMyc;Prdm11 KO end-stage splenic tumors OmicsDI

    ID: E-GEOD-56063

    Date Released: 03-04-2016

    Description: The PR-domain family (PRDMs) encodes transcriptional regulators, several of which are deregulated in cancer. We foun...

  9. Transcription profiling by high throughput sequencing of PRDM11 depletion in U2932 cells ArrayExpress

    ID: E-GEOD-56235

    Description: The PR-domain family e(PRDMs) encodes transcriptional regulators, several of which are deregulated in cancer. We fou...

  10. Transcription profiling by high throughput sequencing of PRDM11 depletion in U2932 cells OmicsDI

    ID: E-GEOD-56235

    Date Released: 03-04-2016

    Description: The PR-domain family e(PRDMs) encodes transcriptional regulators, several of which are deregulated in cancer. We fou...

  11. Transcriptome analysis of Prdm11 knockout mice after OVA challenge BioProject

    ID: PRJNA215095

    Keywords: Transcriptome or Gene expression

    Access Type: download

  12. Transcriptome analysis of Prdm11 knockout mice after OVA challenge OmicsDI

    ID: E-GEOD-49705

    Date Released: 11-24-2015

    Description: ells several PRDM family members were identified. Prdm11 has and outsider position within the PRDM family due to the lack of zinc-finger domains. However, a zic-finger binding motive i present and likely assue the function of protein-protein interactionl. Prdm11 was described as a candidate for tumor suppresser. However, the function of this gene is still unknown. Our study give evide...

  13. Transcriptome analysis of Prdm11 knockout mice after OVA challenge ArrayExpress

    ID: E-GEOD-49705

    Description: ells several PRDM family members were identified. Prdm11 has and outsider position within the PRDM family due to the lack of zinc-finger domains. However, a zic-finger binding motive i present and likely assue the function of protein-protein interactionl. Prdm11 was described as a candidate for tumor suppresser. However, the function of this gene is still unknown. Our study give evide...

  14. PRDM11: a novel tumor suppressor ArrayExpress

    ID: E-GEOD-56065

    Description: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

  15. PRDM11: a novel tumor suppressor OmicsDI

    ID: E-GEOD-56065

    Date Released: 03-04-2016

    Description: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

  16. 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: ediated by the Fas pathway. Fas is a cell surface protein of the tumor necrosis receptor family that is responsible for the elimination of activated NK and T cells. We hypothesize that drug therapy that induces apoptosis in the leukemic T cells and NK cells or sensitizes these cells to endogenous elimination through the Fas apoptotic pathway may provide effective drug therapy for LGL leukemia Standard therapy for both NK and T-LGL leukemia remains undefined. Treatment indications for LGL leukemia are severe neutropenia or anemia. We have shown that oral low dose methotrexate (MTX) is efficacious in treatment of neutropenia associated with T-LGL leukemia. However, response to MTX is slow requiring several months for the neutrophil count to increase above 500/mm3. Moreover, complete clinical remissions may not be achieved until after one year of MTX therapy or longer. Oral cyclophosphosphamide (Cy) has been the primary drug used for treatment of severe transfusion-dependent anemia associated with T-LGL leukemia. Beneficial clinical effects are seen despite this treatment having no apparent effect on the abnormal LGL clone. Normal hematocrits are maintained after cessation of Cy. These results contrast the effects seen with MTX, in which clinical remissions are often associated with the disappearance of the clone, detected by Southern blot assay. We have found that MTX targets a population of proliferating activated LGL. Most LGL in the peripheral blood are no longer actively proliferating. This data could explain the prolonged time required for a clinical response. We found that Ras inhibitors induced apoptosis when added in vitro to leukemic cells from the peripheral blood and also blocked the proliferation of cycling cells. Therefore, a quicker clinical response would be anticipated than seen with MTX therapy. Correlative laboratory studies will determine if molecular complete responses are associated with minimal residual disease and whether in vitro drug sensitivity correlates with elimination of the leukemic cells. There are no prospective clinical trials to assess the efficacy of drug therapy for NK-LGL leukemia. There is no animal model for LGL leukemia. Data in animal models of other lymphoproliferative diseases may provide insight into the pathogenesis of LGL leukemia. A lymphoproliferative disease that occurs in MLR-lpr/lpr and gld/gld mice can be explained by defects in apoptotic pathways. In one allele of lpr there is defective expression of Fas antigen due to retroviral insertion into the second intron of the Fas antige...

Displaying 16 of 16 results for "PRDM11"