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Impaired repopulating ability of Uhrf2-/- hematopoietic progenitor cells in mice. [CUT & Tag]

ABSTRACT: We generated Uhrf2-/- mice to clarify the role of deletion of UHRF2 in hematopoiesis. In competitive repopulation assay, the proportions of Uhrf2-/- cells were decreased relative to Uhrf2+/+ cells in all lineages.

ORGANISM(S): Mus musculus

PROVIDER: GSE230833 | GEO | 2024/07/01

REPOSITORIES: GEO

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Impaired repopulating ability of Uhrf2-/- hematopoietic progenitor cells in mice. [RNA-Seq]

Project description:We generated Uhrf2-/- mice to clarify the role of deletion of UHRF2 in hematopoiesis. In competitive repopulation assay, the proportions of Uhrf2-/- cells were decreased relative to Uhrf2+/+ cells in all lineages.

2024-07-01 | GSE230415 | GEO

Impaired repopulating ability of Uhrf2-/- hematopoietic progenitor cells in mice. [CUT & Tag]

Project description:Impaired repopulating ability of Uhrf2-/- hematopoietic progenitor cells in mice. [CUT & Tag]

| PRJNA962802 | ENA

Impaired Repopulating Ability of Uhrf2−/− Hematopoietic Progenitor Cells in Mice

Project description:UHRF proteins catalyze the ubiquitination of target proteins and are involved in regulating gene expression. Some studies reported a reduced expression of UHRF2 in acute leukemia cells, but the role of UHRF2 in hematopoiesis remains unknown. Here, we generated Uhrf2−/− mice to clarify the role of UHRF2 deletion in hematopoiesis. Compared to Uhrf2+/+ mice, Uhrf2−/− mice showed no differences in complete blood counts, as well as bone marrow (BM) findings and spleen weights. Proportions of cells in progenitor fractions in BM were comparable between Uhrf2+/+ mice and Uhrf2−/− mice. However, in competitive repopulation assays with BM transplants (BMT), the proportions of Uhrf2−/− cells were decreased relative to Uhrf2+/+ cells in all lineages. After the second BMT, Uhrf2−/− neutrophils were few, while 20–30% of Uhrf2−/− T cells and B cells were still detected. RNA sequencing showed downregulation of some genes associated with stem-cell function in Uhrf2−/− hematopoietic stem/progenitor cells (HSPCs). Interestingly, trimethylated histone H3 lysine 9 was increased in Uhrf2−/− HSPCs in a cleavage under targets and tagmentation assay. While UHRF2 deletion did not cause hematologic malignancy or confer a growth advantage of HSPCs, our results suggest that UHRF2 may play a role in the regulation of hematopoiesis.

| S-EPMC10454722 | biostudies-literature

Impaired repopulating ability of Uhrf2-/- hematopoietic progenitor cells in mice.

Project description:Impaired repopulating ability of Uhrf2-/- hematopoietic progenitor cells in mice.

| PRJNA962800 | ENA

Impaired repopulating ability of Uhrf2-/- hematopoietic progenitor cells in mice. [RNA-Seq]

Project description:Impaired repopulating ability of Uhrf2-/- hematopoietic progenitor cells in mice. [RNA-Seq]

| PRJNA961104 | ENA

Impaired repopulating ability of Uhrf2-/- hematopoietic progenitor cells in mice.

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

2024-07-01 | GSE230834 | GEO

Genome-wide distribution of UHRF2 and ZNF618 in 293T cells.

Project description:We have identified ZNF618 as a novel binding partner of UHRF2. We have found that UHRF2 and ZNF618 co-localize at many genomic loci. Examination of genome-wide distribution of SFB-tagged UHRF2 and ZNF618 in 293T cells using ChIP-seq.

2016-05-31 | E-GEOD-80037 | biostudies-arrayexpress

Gene expression in AML12 cells after Uhrf2 knock-down

Project description:We identified the ubiquitin ligase Uhrf2 as a key regulator of liver regeneration. To determine the underlying mechanisms of action, we performed siRNA-mediated knockdown of Uhrf2 in AML12 cells and analysed the transcriptome of the Uhrf2-deficient cells.

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UHRF2 regulates local 5-methylcytosine and suppresses spontaneous seizures [RNA-seq]

Project description:5-methylcytosine (5mC) regulates multiple cellular processes and is faithfully maintained following DNA replication. Ubiquitin-like PHD and ring finger domain-containing protein 1 (UHRF1) plays an important role in the maintenance of 5mC levels. Interestingly, UHRF1 has a paralog UHRF2 that has similar sequence and domain architecture, but the biological function of UHRF2 is not clear. Here, we have generated Uhrf2 knockout mice and characterized the role of UHRF2 in vivo. Uhrf2 knockout mice are viable, but the adult mice develop frequent spontaneous seizures and display abnormal electrical activities in brain. To explore possible mechanism beyond these phenomenon, we utilized high-throughput sequencing to identify global expression changes in Uhrf2 knockout mice brains. In addition, we explored genome-wide 5mc profiles in these samples to examine if UHRF2 regulates 5mc levels in specific genome loci.

2017-07-21 | GSE98360 | GEO

Genome-wide distribution of UHRF2 and ZNF618 in 293T cells.

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2016-05-31 | GSE80037 | GEO

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