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Displaying 17 of 17 results for "CDK11B"
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  1. Expression data from human osteosarcoma cells treated with CDK11 siRNA BioProject

    ID: PRJNA297856

    Keywords: Transcriptome or Gene expression

    Access Type: download

  2. CD11B_RAT UniProt:Swiss-Prot

    ID: P46892

    Description: Cyclin-dependent kinase 11B Protein kinase ATP Calmodul...

  3. Transcription profiling by array of human PMA-activated Jurkat cells ArrayExpress

    ID: E-GEOD-10232

    Description: Cyclin T1-dependent genes in activated Jurkat cells. HIV-1 is dependent upon cellular co-fact...

  4. Transcription profiling of human parental MM6 cell response to lipoloysaccharide and phorbal ester ArrayExpress

    ID: E-GEOD-10739

    Description: ected by the treatments were identified. HIV-1 is dependent upon cellular co-factors to mediate its replication cycle in CD4+ T cells and macrophages, the two major cell types infected by the virus in vivo. One critical co-factor is Cyclin T1, a s...

  5. Transcription profiling by array of human LPS-activated MM6 cells with Cyclin D1 knockdown ArrayExpress

    ID: E-GEOD-10234

    Description: Cyclin T1-dependent genes in LPS-activated MM6 cells. HIV-1 is dependent upon cellular co-fac...

  6. Transcription profiling by array of human non-activated MM6 cells with cyclin T1 knockdown ArrayExpress

    ID: E-GEOD-10738

    Description: Cyclin T1-dependent genes in LPS-activated MM6 cells. HIV-1 is dependent upon cellular co-fa...

  7. Transcription profiling by array of human PMA-activated MM6 cells with cyclin T1 knockdown ArrayExpress

    ID: E-GEOD-10233

    Description: Cyclin T1-dependent genes in PMA-activated MM6 cells. HIV-1 is dependent upon cellular co-fac...

  8. LPS and PMA response in parental MM6 cells BioProject

    ID: PRJNA108869

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: ected by the treatments were identified. HIV-1 is dependent upon cellular co-factors to mediate its replication cycle in CD4+ T cells and macrophages, the two major cell types infected by the virus in vivo. One critical co-factor is Cyclin T1, a s...
  9. CTDG in non-activated MM6 cells BioProject

    ID: PRJNA108867

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: Cyclin T1-dependent genes in LPS-activated MM6 cells. HIV-1 is dependent upon cellular co-fac...
  10. CTDG in PMA-activated Jurkat cells BioProject

    ID: PRJNA108897

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: Cyclin T1-dependent genes in activated Jurkat cells. HIV-1 is dependent upon cellular co-fact...
  11. CTDG in PMA-activated MM6 cells BioProject

    ID: PRJNA108899

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: Cyclin T1-dependent genes in PMA-activated MM6 cells. HIV-1 is dependent upon cellular co-fac...
  12. CTDG in non-activated Jurkat cells BioProject

    ID: PRJNA108865

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: Cyclin T1-dependent genes in non-activated Jurkat cells. HIV-1 is dependent upon cellular co-...
  13. CTDG in LPS-activated MM6 cells BioProject

    ID: PRJNA108901

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: Cyclin T1-dependent genes in LPS-activated MM6 cells. HIV-1 is dependent upon cellular co-fac...
  14. Increased expression of Bcl11b in human transformed T cell lines leads to chemoresistance accompanied by G1 accumulation ArrayExpress

    ID: E-GEOD-21382

    Description: ith upregulation of CDKN1C (p57) and CDKN2C (p18) cyclin dependent kinase inhibitors. Moreover, p27 and p130 proteins accumulated and the SKP2 gene encoding a protein of the ubiquitin-binding complex responsible for their degradation was repressed. Furthermore, the expression of the MYCN oncogene was silenced which resulted in significant depletion of the protein in cells expressing high BCL11B levels. Both cell cycle restriction and resistance to DNA-damage-induced apoptosis coincided and required the histone deacetylase binding N-terminal domain of Bcl11b. The sensitivity to genotoxic stress could be restored by the histone deacetylase inhibitor trichostatine A. Conclusions: The data presented here suggest a potential role of BCL11B in tumor survival and encourage developing Bcl11b-inhibitory approaches as a potential tool to specifically target chemoresistant tumor cells. Using a retroviral-vector-based system in Jurkat cells BCL11B overexpression was compared to controls transfected with the empty vector. Of each group one biological replicate was analyzed on one array....

  15. Expression profiling of MRC5 senescent fibroblasts ArrayExpress

    ID: E-GEOD-15919

    Description: Microarrays analysis identifies WNT16in senescent fibroblasts. To identify genes expressed in replicative senescence, microarray experiments were cond...

  16. Expression profiling of MRC5 senescent fibroblasts BioProject

    ID: PRJNA116923

    Keywords: Transcriptome or Gene expression

    Access Type: download

  17. Increased expression of Bcl11b in human transformed T cell lines leads to chemoresistance accompanied by G1 accumulation. BioProject

    ID: PRJNA126073

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: ith upregulation of CDKN1C (p57) and CDKN2C (p18) cyclin dependent kinase inhibitors. Moreover, p27 and p130 proteins accumulated and the SKP2 gene encoding a protein of the ubiquitin-binding complex responsible for their degradation was repressed. Furthermore, the expression of the MYCN oncogene was silenced which resulted in significant depletion of the protein in cells expressing high BCL11B levels. Both cell cycle restriction and resistance to DNA-damage-induced apoptosis coincided and required the histone deacetylase binding N-terminal domain of Bcl11b. The sensitivity to genotoxic stress could be restored by the histone deacetylase inhibitor trichostatine A. Conclusions: The data presented here suggest a potential role of BCL11B in tumor survival and encourage developing Bcl11b-inhibitory approaches as a potential tool to specifically target chemoresistant tumor cells. Overall design: Using a retroviral-vector-based system in Jurkat cells BCL11B overexpression was compared to controls transfected with the empty vector. Of each group one biological replicate was analyzed on one array....

Displaying 17 of 17 results for "CDK11B"