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Mirc11 role in myeloid differentiation

ABSTRACT: Mirc11 role in myeloid differentiation

PROVIDER: PRJNA672344 | ENA |

REPOSITORIES: ENA

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Gene expression of Mirc11-/- hematopoietic myeloid progenitors

Project description:Compared gene expression between Lin-Sca1-cKit+ myeloid progenitors isolated from the bone marrow of 6-8 week old wildtype and Mirc11-/- mice. Previously observed that overexpression of Mirc11 in hematopoietic progenitors increased myeloid differentiation whereas loss of Mirc11 decreased myeloid differentiation. Performed RNA-seq to identify potential genes involved in myeloid differentiation regulated by Mirc11. Gene expression analysis of Mirc11 deficient myeloid progenitors revealed a decrease in Toll like receptor and interferon signaling. This anti-inflammatory phenotype was further observed in mature cells as Mirc11-/- bone marrow derived macrophages (BMDMs) have an attenuated response to inflammatory lip-opolysaccharide (LPS).

2020-11-18 | GSE160214 | GEO

Gene expression of Mirc11-/- hematopoietic myeloid progenitors

Project description:Gene expression of Mirc11-/- hematopoietic myeloid progenitors

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Mirc11 role in myeloid differentiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-11-18 | GSE160215 | GEO

The dose-dependent role of PU.1 in Myeloid differentiation

Project description:The dose-dependent role of PU.1 in Myeloid differentiation

| PRJNA315126 | ENA

Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: Listeria_challenge)

Project description:Lack of Mirc11 significantly reduces NK cell-mediated cytokine production in vivo Mirc11 cluster targets NF-kB and AP-1-mediated gene transcriptions

2019-08-20 | GSE136013 | GEO

Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: IL-2_expanded_NKG2D_stimulation)

Project description:Lack of Mirc11 significantly reduces NK cell-mediated cytokine production in vivo Mirc11 cluster targets NF-kB and AP-1-mediated gene transcriptions

2019-08-20 | GSE136014 | GEO

SUMOylation disassembles the tetrameric pyruvate kinase M2 to block myeloid differentiation of leukemia cells

Project description:Leukemia arises from blockage of the differentiation/maturation of hematopoietic progenitor cells at different stages with uncontrolled proliferation of leukemic cells. However, the signal pathways that block cell differentiation remain unclear. Herein we found that SUMOylation of the M2 isoform of pyruvate kinase(PKM2), a rate-limiting glycolytic enzyme catalyzing the dephosphorylation of phosphoenolpyruvate to pyruvate, is prevalent in a variety of leukemic cell lines as well as primary samples from patients with leukemia through multiple-reaction monitoring based targeted mass spectrometry analysis. SUMOylation of PKM2 lysine 270(K270) triggered conformation change from tetrameric to dimeric of PKM2, reduced PK activity, and led to nuclear translocation of PKM2. SUMO1 modiﬁcation of PKM2 recruits and promotes degradation of RUNX1 via a SUMO-interacting motif, resulting in blockage of myeloid differentiation of NB4 and U937 leukemia cells. Replacement of wild type PKM2 with a SUMOylation-deﬁcient mutant (K270R) abrogated the interaction with RUNX1 and the blockage of myeloid differentiation in vitro and in xenograft model. Our results establish PKM2 as an essential modulator of leukemia cell differentiation and a potential therapeutic target which may offer synergistic effect with differentiation therapy in the treatment of leukemia.

2020-12-26 | PXD023317 | iProX

Heme-Nrf2 signaling shifts myeloid differentiation

Project description:Heme-Nrf2 signaling shifts myeloid differentiation

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Hematopoietic differentiation is required for initiation of acute myeloid leukemia [ATAC-seq]

Project description:Leukemia initiating cells (LICs) of acute myeloid leukemia (AML) may arise from self-renewing hematopoietic stem cells (HSCs) and from committed progenitors. However, it remains unclear how leukemia-associated oncogenes instruct LIC formation from cells of different origins and if differentiation along the normal hematopoietic hierarchy is involved. Here, using murine models with the driver mutations MLL-AF9 or MOZ-TIF2, we found that regardless of the transformed cell types, myelomonocytic differentiation to the granulocyte macrophage progenitor (GMP) stage is critical for LIC generation. Blocking myeloid differentiation through disrupting the lineage-restricted transcription factor C/EBPa eliminates GMPs, blocks normal granulopoiesis, and prevents AML development. In contrast, restoring myeloid differentiation through inflammatory cytokines “rescues” AML transformation. Our findings identify myeloid differentiation as a critical step in LIC formation and AML development, thus guiding new therapeutic approaches. Examination of chromatin accessibility in Cebpa knock-out and control conditions.

2015-08-04 | E-GEOD-71688 | biostudies-arrayexpress

Secretory MPP3 reinforce myeloid differentiation trajectory and amplify myeloid cell production

Project description:Hematopoietic stem cells (HSC) and downstream lineage-biased multipotent progenitors (MPP) tailor blood production and control myelopoiesis on demand. However, a precise resolution of myeloid differentiation trajectories and cellular heterogeneity in various MPP populations and understanding of their role in controlling myeloid cell production remains largely lacking. Here, we analyze that myeloid-biased MPP3 are functionally and molecularly heterogenous, with a distinct subset of myeloid-primed secretory cells with high endoplasmic reticulum (ER) volume.

2021-08-18 | GSE181902 | GEO

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