Astrammina rara strain:n/a
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ABSTRACT:
PROVIDER: PRJNA47149 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Haloarcula rara strain:SHR3 Genome sequencing
| PRJNA942486 | ENA
Project description:Astrammina rara Genome sequencing and assembly
| PRJNA521081 | ENA
Project description:PML/RARa is of crucial importance in acute promyelocytic leukemia (APL) both pathologically and therapeutically. Using a genome-wide approach, we identified in vivo PML/RARa binding sites in ZnSO4 treated PR9 cells. A total of 2,979 high quality binding sites were identified, representing 1,981 unique RefSeq genes. The supplementary bed file contains all 2,979 high quality PML-RARa binding sites reported in the paper.
2009-11-26 | GSE19202 | GEO
Project description:While acute promyelocytic leukemia (APL) is always driven by fusions involving one of the three retinoic acid receptors, why PML and RARA are the preferred fusion partners has remained largely unsettled. Here we demonstrate that corepressor (NCoR) binding onto the RARA moiety of PML::RARA is required for hematopoietic progenitor immortalization. We establishthat PML-mediated tethering of the UBC9 SUMO conjugating enzyme onto PML::RARA enforces SUMO2 conjugation of multiple RARA partner proteins, notably the NCoR complex, boosting its repressive power. PML mutants that fail to recruit UBC9 yield PML::RARA fusions that neither promote NCoR sumoylation nor transformation. Conversely, direct UBC9/RARA fusion drivesboth efficient NCoR sumoylation and immortalization. Sumoylation inhibitors re-activate retinoic acid target genes in PML::RARA-, but not in RARA-, expressing progenitors and trigger APL differentiation. Thus, fusion of PML to RARA entails an unexpected gain of functionthat boosts RARA-mediated transcriptional repression through sumoylation of PML::RARA-bound proteins, explaining the recurrent implication of PML and RARA in APL pathogenesis.
2026-08-04 | PXD078941 | Pride
Project description:The experimental design was to determine the regulon of the transcriptional activator RarA. This was done by comparing the transcriptome profiles between a rarA overexpressor and the baseline control. RarA overexpression was achieved by plasmid mediated overexpression of the rarA gene and the baseline control was a vector only strain.
2013-03-21 | E-MEXP-3742 | biostudies-arrayexpress
Project description:Analysis of mHSPCs infected with PML/RARa(WT) or PML/RARa(2KR: K227R and K360R in RARa moiety). We used RNA-sequencing to detail the global programme of gene expression in PML/RARa(2KR)-overexpressing mHSPCs. Results provide insight into the reduced clonogenicity caused by PML/RARa(2KR)
2022-02-18 | GSE165046 | GEO
Project description:RARA haploinsufficiency is an invariable consequence of t(15;17) reciprocal translocations in acute promyelocytic leukemia (APL). Furthermore, retinoids and RARA activity have been implicated in hematopoietic self-renewal, lineage commitment and neutrophil maturation. We and others therefore predicted that RARA haploinsufficiency would contribute to APL pathogenesis. To test this hypothesis we crossed RARA+/- mice with mice expressing PML-RARA from the Cathepsin G locus (mCG-PR). We found that RARA haploinsufficiency cooperated with PML-RARA, only modestly influencing the pre-leukemic and leukemic phenotype. Bone marrow from mCG-PR+/- x RARA+/- mice had decreased numbers of mature myeloid cells, increased ex vivo myeloid cell proliferation and an increased competitive advantage following transplantation. RARA haploinsufficiency did not alter mCG-PR dependent leukemic latency or penetrance, but did influence the distribution of leukemic cells; mCG-PR+/- x RARA+/- mice presented more commonly with low to normal white blood cell counts and with myeloid infiltration of lymph nodes. APL arising in these mice was responsive to ATRA, and had virtually no differences in expression profiling compared to tumors arising in mCG-PR+/- x RARA+/+ mice. These phenotypes were dependent on PML-RARA activity, since they were not detected in RARA+/- mice in the absence of the mCG-PR transgene. These data show that RARA haploinsufficiency (like PML haploinsufficiency and RARA-PML) can cooperate with PML-RARA to influence the pathogenesis and phenotype of APL in mice, but that PML-RARA is the driver of t(15;17) APL.
2010-07-29 | GSE23291 | GEO
Project description:Transcriptional profiling of murine cells expressing PML/RARA at the early promyelocyte stage (4 weeks old, preleukemic) and in full blown PML/RARA leukemia generated by transducing PML/RARA bone marrow with a Flt3-ITD retroviral vector
2015-07-15 | GSE59431 | GEO