Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA361469 | ENA |
REPOSITORIES: ENA
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Project description:Iron metabolism has emerged as a critical factor in cell viability, both in normal and pathological contexts. However, the intricate relationship between iron metabolism and the maintenance of adult stem cells and cancer stem cells remains incompletely understood. The ferritin complex, responsible for intracellular iron storage and buffering, plays a pivotal role in this process. Our research provides insights into the regulatory role of ferritin-mediated iron homeostasis in hematopoietic stem cells (HSCs).
2024-04-17 | GSE240742 | GEO
Project description:Critical Role of Ferritin-Mediated Iron Homeostasis in the Maintenance of Hematopoietic Stem Cells and Leukemia Stem Cells
| PRJNA1005185 | ENA
Project description:Ligase4 is essential for hematopoietic stem cell maintenance
| PRJNA273382 | ENA
Project description:The Saccharomyces cerevisiae transcription factor Aft1 is activated in iron-deficient cells to induce the expression of iron regulon genes, which coordinate the increase of iron uptake and remodel cellular metabolism to survive low iron conditions. In addition, Aft1 has been implicated in numerous cellular processes including cell cycle progression and chromosome stability; however it is unclear if all cellular effects of Aft1 are mediated through iron homeostasis. To further investigate the cellular processes impacted by Aft1 using genome-wide synthetic lethal and synthetic dosage lethal screens, we identified greater than 70 deletion mutants that are sensitive to perturbations in AFT1 levels. Our genetic network reveals that Aft1 impacts a diverse range of cellular processes, including the RIM101 pH pathway, cell wall stability, DNA damage, protein transport, chromosome stability and mitochondrial function. Surprisingly, only a subset of mutants identified are sensitive to iron fluctuations or display genetic interactions with mutants of iron regulon genes AFT2 or FET3. We demonstrate that Aft1 works in parallel with the RIM101 pH pathway and the role of Aft1 in cell wall structure and DNA damage repair is mediated by iron. In contrast, we show that the role of Aft1 in chromosome maintenance is independent of its iron regulatory role and that alterations in iron levels do not impact chromosome loss rates. Our study clearly demonstrates a novel iron-independent role for Aft1. For this experiment 4 samples (2 reference and 2 test samples), consisting of 3 biological reps were hybridized. Cy3 one-color labelling was used for each sample.
2010-05-01 | E-GEOD-20531 | biostudies-arrayexpress
Project description:Hematopoietic stem cells (HSCs) are maintained in the hypoxic niche so as to limit oxidative stress. Although iron is a major factor to evoke oxidative stress, the importance of cellular iron homeostasis in HSCs has been unrecognized. We now demonstrate that iron regulation mediated by FBXL5 is required for the self-renewal capability of HSCs. Conditional ablation of Fbxl5 gene in mouse HSCs resulted in cellular iron overload, leading to the reduction in the number of HSCs. Bone-marrow transplantation experiments revealed that FBXL5-deficient HSCs were unable to reconstitute the hematopoietic system as a result of stem cell exhaustion. Transcriptomic analysis showed abnormal activation of oxidative stress response as well as cell cycle in HSCs. Suppression of IRP2 activity in FBXL5-deficient HSCs restored the stem cell function, suggesting that IRP2 is potentially a novel therapeutic target of stem cell diseases such as myelodysplastic syndrome, which is associated with FBXL5 downregulation in humans.
2017-04-29 | GSE93649 | GEO
Project description:FoxM1 is essential for quiescence and maintenance of hematopoietic stem cell
| PRJNA263909 | ENA
Project description:Myh9 plays essential role in hematopoietic stem/progenitor cells survival and maintenance
| PRJNA813848 | ENA
Project description:Maintenance of hematopoietic stem cell (HSC) function in the niche is an orchestrated event. Osteomacs (OM), are key cellular components of the niche. Previously, we documented that osteoblasts, OM, and megakaryocytes interact to promote hematopoiesis. Here, we further characterize OM and identify megakaryocyte-induced mediators that augment the role of OM in the niche. Single cell mRNAseq, mass spectrometry, and CyTOF examination of megakaryocyte-stimulated OM suggested that upregulation of CD166 and Embigin on OM augment their hematopoiesis maintenance function. CD166 knockout OM or shRNA-Embigin knockdown OM, confirmed that loss of these molecules significantly reduced OM ability to augment the osteoblast-mediated hematopoietic enhancing activity. Recombinant CD166 and Embigin partially substituted for OM function, characterizing both proteins as critical mediators of OM hematopoietic function. Our data identify Embigin and CD166 as OM-regulated critical components of HSC function in the niche and potential participants in various in vitro manipulations of stem cells.
2024-01-11 | MSV000093840 | MassIVE
Project description:Lipid metabolism is recognized as a key process for stem cell maintenance and differentiation but genetic factors that instruct stem cell function by influencing lipid metabolism remain to be delineated. Here we identify Tnfaip2 as an inhibitor of reprogramming of mouse fibroblasts into induced pluripotent stem cells. Tnfaip2 knockout embryonic stem cells (ESCs) exhibit differentiation failure and knockdown of the planarian orthologue, Smed-exoc3, abrogates in vivo differentiation of somatic stem cells, tissue homeostasis, and regeneration. Tnfaip2 deficient ESCs fail to induce synthesis of cellular triacylglycerol (TAG) and lipid droplets (LD) coinciding with reduced expression of Vimentin (Vim) – a known inducer of LD formation. Knockdown of Vim and Tnfaip2 act epistatically in enhancing cellular reprogramming of mouse fibroblasts. Similarly, planarians devoid of Smed-exoc3 displayed acute loss of TAGs. Supplementation of palmitic acid (PA) and palmitoyl-L-carnitine (a mitochondrial carrier of PA) restores the differentiation capacity of Tnfaip2 deficient ESCs as well as stem cell differentiation and organ maintenance in Smed-exoc3-depleted planarians. Together, these results identify a novel pathway, which is essential for stem cell differentiation and organ maintenance by instructing lipid metabolism.
2020-11-16 | GSE134301 | GEO
Project description:Lipid metabolism is recognized as a key process for stem cell maintenance and differentiation but genetic factors that instruct stem cell function by influencing lipid metabolism remain to be delineated. Here we identify Tnfaip2 as an inhibitor of reprogramming of mouse fibroblasts into induced pluripotent stem cells. Tnfaip2 knockout embryonic stem cells (ESCs) exhibit differentiation failure and knockdown of the planarian orthologue, Smed-exoc3, abrogates in vivo differentiation of somatic stem cells, tissue homeostasis, and regeneration. Tnfaip2 deficient ESCs fail to induce synthesis of cellular triacylglycerol (TAG) and lipid droplets (LD) coinciding with reduced expression of Vimentin (Vim) – a known inducer of LD formation. Knockdown of Vim and Tnfaip2 act epistatically in enhancing cellular reprogramming of mouse fibroblasts. Similarly, planarians devoid of Smed-exoc3 displayed acute loss of TAGs. Supplementation of palmitic acid (PA) and palmitoyl-L-carnitine (a mitochondrial carrier of PA) restores the differentiation capacity of Tnfaip2 deficient ESCs as well as stem cell differentiation and organ maintenance in Smed-exoc3-depleted planarians. Together, these results identify a novel pathway, which is essential for stem cell differentiation and organ maintenance by instructing lipid metabolism.
2020-11-16 | GSE148758 | GEO