scholarly journals Function of the Stem Cell Transcription Factor SALL4 in Hematopoiesis

2018 ◽  
Author(s):  
Jianchang Yang
Keyword(s):  
Transcription Factor ◽  
Stem Cell

scholarly journals Chromatin and transcription factor profiling in rare stem cell populations using CUT&Tag

2021 ◽  
Vol 2 (3) ◽  
pp. 100751
Author(s):  
Yuefeng Li ◽  
Kiran Nakka ◽  
Thomas Olender ◽  
Philippe Gingras-Gelinas ◽  
Matthew Man-Kin Wong ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Stem Cell ◽  
Cell Populations ◽  
Stem Cell Populations

Proteomic analysis of transcription factor interactions in myeloid stem cell development and leukaemia

2002 ◽  
Vol 6 (4) ◽  
pp. 491-495 ◽  
Author(s):  
Gerhard Behre ◽  
Venkateshwar A Reddy ◽  
Daniel G Tenen ◽  
Wolfgang Hiddemann ◽  
Abdul A Peer Zada ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Stem Cell ◽  
Proteomic Analysis ◽  
Cell Development ◽  
Factor Interactions

Abstract 297: Nkx2–5 Transcriptionally Activates C-kit-ligand And Regulates Cardiac Progenitor Cell Populations

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Rebecca L Scotland ◽  
Xiaozhong Shi ◽  
Anwarul Ferdous ◽  
Michael Kyba ◽  
Daniel J Garry
Keyword(s):  
Transcription Factor ◽  
Stem Cell ◽  
Progenitor Cell ◽  
Transcriptional Regulator ◽  
Luciferase Reporter ◽  
Transcriptional Networks ◽  
Cell Populations ◽  
Cardiac Progenitor Cell ◽  
Downstream Target ◽  
Kit Ligand

C-kit-ligand, also known as stem cell factor, is expressed broadly and has a functional role during hematopoesis, gametogenesis, melanogenesis, mast cell growth and differentiation. Although the receptor for c-kit-ligand, c-kit, has been utilized as a marker to identify cardiac stem cell and progenitor cell populations, the transcriptional regulation and biological function of c-kit-ligand during cardiogenesis has not been defined. Here we demonstrate that c-kit-ligand is a novel downstream target of Nkx2–5. The homeodomain transcription factor, Nkx2–5, is one of the earliest markers of the cardiac lineage and mice lacking this transcription factor are nonviable. To identify potential Nkx2–5 downstream target genes, we utilized ES/EBs that were engineered to overexpress Nkx2–5 and undertook transcriptome analysis of embyroid bodies with and without Nkx2–5 induction. We observed a significant increase in c-kit-ligand expression following Nkx2–5 induction suggesting a role for Nkx2–5 in the activation of c-kit-ligand. Furthermore, analysis of the c-kit-ligand promoter revealed three evolutionarily conserved Nkx2–5 response elements, supporting the notion that Nkx2–5 is a transcriptional regulator of gene expression. We undertook transcriptional assays and transfected the c-kit-ligand promoter-luciferase reporter in the absence and presence of increasing amounts of Nkx2–5. We observed that Nkx2–5, in a dose dependent fashion, was a potent transcriptional activator of c-kit-ligand. These studies enhance our understanding of Nkx2–5 mediated transcriptional networks and further emphasize that Nkx2–5 is an important transcriptional regulator of cardiac progenitor cell populations.

scholarly journals Cobalt and Nickel Stabilize Stem Cell Transcription Factor OCT4 through Modulating Its Sumoylation and Ubiquitination

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e86620 ◽  
Author(s):  
Yixin Yao ◽  
Yinghua Lu ◽  
Wen-chi Chen ◽  
Yongping Jiang ◽  
Tao Cheng ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Stem Cell ◽  
Cobalt And Nickel

scholarly journals The Transcription Factor Zfp281 Controls Embryonic Stem Cell Pluripotency by Direct Activation and Repression of Target Genes

Stem Cells ◽  
2008 ◽  
Vol 26 (11) ◽  
pp. 2791-2799 ◽  
Author(s):  
Zheng-Xu Wang ◽  
Christina Hui-Leng Teh ◽  
Caroline Man-Yee Chan ◽  
Ci Chu ◽  
Michael Rossbach ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Stem Cell ◽  
Embryonic Stem Cell ◽  
Target Genes ◽  
Embryonic Stem ◽  
Direct Activation ◽  
Stem Cell Pluripotency ◽  
Embryonic Stem Cell Pluripotency

scholarly journals Mitochondria regulate intestinal stem cell proliferation and epithelial homeostasis through FOXO

2020 ◽  
Vol 31 (14) ◽  
pp. 1538-1549
Author(s):  
Fan Zhang ◽  
Mehdi Pirooznia ◽  
Hong Xu
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Transcription Factor ◽  
Stem Cell ◽  
Electron Transport Chain ◽  
Intestinal Stem Cell ◽  
Stem Cell Proliferation ◽  
Epithelial Homeostasis ◽  
Chain Complexes ◽  
Transport Chain

Deficiencies in electron transport chain complexes increase the activity of FOXO transcription factor in Drosophila midgut stem cells, which impairs stem cell proliferation and enterocyte specification.

scholarly journals Dissecting Hes-centered transcriptional networks in neural stem cell maintenance and tumorigenesis in Drosophila

2020 ◽  
Author(s):  
Srivathsa S. Magadi ◽  
Chrysanthi Voutyraki ◽  
Gerasimos Anagnostopoulos ◽  
Evanthia Zacharioudaki ◽  
Ioanna K. Poutakidou ◽  
...  
Keyword(s):  
Stem Cells ◽  
Nervous System ◽  
Transcription Factor ◽  
Stem Cell ◽  
Neural Stem Cells ◽  
Cell Fate ◽  
Asymmetric Cell Division ◽  
Transcriptional Networks ◽  
Malignant Tumours ◽  
Stem Cell Maintenance

ABSTRACTNeural stem cells divide during embryogenesis and post embryonic development to generate the entire complement of neurons and glia in the nervous system of vertebrates and invertebrates. Studies of the mechanisms controlling the fine balance between neural stem cells and more differentiated progenitors have shown that in every asymmetric cell division progenitors send a Delta-Notch signal back to their sibling stem cells. Here we show that excessive activation of Notch or overexpression of its direct targets of the Hes family causes stem-cell hyperplasias in the Drosophila larval central nervous system, which can progress to malignant tumours after allografting to adult hosts. We combined transcriptomic data from these hyperplasias with chromatin occupancy data for Dpn, a Hes transcription factor, to identify genes regulated by Hes factors in this process. We show that the Notch/Hes axis represses a cohort of transcription factor genes. These are excluded from the stem cells and promote early differentiation steps, most likely by preventing the reversion of immature progenitors to a stem-cell fate. Our results suggest that Notch signalling sets up a network of mutually repressing stemness and anti-stemness transcription factors, which include Hes proteins and Zfh1, respectively. This mutual repression ensures robust transition to neuronal and glial differentiation and its perturbation can lead to malignant transformation.

scholarly journals NF1 regulates mesenchymal glioblastoma plasticity and aggressiveness through the AP-1 transcription factor FOSL1

2019 ◽  
Author(s):  
Carolina Marques ◽  
Thomas Unterkircher ◽  
Paula Kroon ◽  
Annalisa Izzo ◽  
Yuliia Dramaretska ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Stem Cell ◽  
Mapk Pathway ◽  
Neurofibromatosis Type ◽  
Gene Signature ◽  
Negative Regulator ◽  
Tumor Stem Cell ◽  
Stem Cell Lines ◽  
Mesenchymal Transformation

AbstractThe molecular basis underlying Glioblastoma (GBM) heterogeneity and plasticity are not fully understood. Using transcriptomic data of patient-derived brain tumor stem cell lines (BTSCs), classified based on GBM-intrinsic signatures, we identify the AP-1 transcription factor FOSL1 as a key regulator of the mesenchymal (MES) subtype. We provide a mechanistic basis to the role of the Neurofibromatosis type 1 gene (NF1), a negative regulator of the RAS/MAPK pathway, in GBM mesenchymal transformation through the modulation of FOSL1 expression. Depletion of FOSL1 in NF1-mutant human BTSCs and Kras-mutant mouse neural stem cells results in loss of the mesenchymal gene signature, reduction in stem cell properties and in vivo tumorigenic potential. Our data demonstrate that FOSL1 controls GBM plasticity and aggressiveness in response to NF1 alterations.

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