Role of OCT4 as a transcription factor in pluripotent stem cells [ChIP-seq]
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ABSTRACT:
PROVIDER: PRJNA1188605 | ENA |
REPOSITORIES: ENA
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Project description:Pluripotent stem cells (PSCs), known for their unlimited ability to self-renew and differentiate into all three germ layers, have emerged as a promising cell source for regenerative therapies aimed at treating various diseases and injuries.OCT4 is a key pluripotent marker and transcription factor in PSCs, which regulates numerous biological processes of PSCs. This data demonstrates the potential role of OCT4 as a transcription factor.
2025-07-02 | GSE282454 | GEO
Project description:The nucleosome is a fundamental unit of chromatin in eukaryotes, and generally prevents the binding of transcription factors to genomic DNA. Pioneer transcription factors overcome the nucleosome barrier, and bind their target DNA sequences in chromatin. OCT4 is a representative pioneer transcription factor that plays a role in stem cell pluripotency. In the present study, we biochemically analyzed the nucleosome binding by OCT4. Crosslinking mass spectrometry showed that OCT4 binds the nucleosome.
2020-05-13 | PXD019160 | JPOST Repository
Project description:Pluripotency can be induced in murine and human fibroblast by transduction of four transcription factors (Oct4, Sox2, Klf4 and c-Myc). Previously we reported that two factors (Oct4 and Klf4) are sufficient for reprogramming adult mouse neural stem cells (NSCs) to a pluripotent state. However, although NSCs endogenously express the factors Sox2, c-Myc, and Klf4, our previous report does not elucidate why exogenous expression of either Klf4 or c-Myc is still required for reprogramming. Here we report that exogenous expression of Oct4 is sufficient to generate one-factor induced pluripotent stem (1F iPS) cells without any oncogenic factors, such as c-Myc and Klf4, from mouse adult NSCs, which endogenously express Sox2, c-Myc, and Klf4, and also intermediate reprogramming markers alkaline phosphatase (AP), stage-specific embryonic antigen-1 (SSEA-1). These results extend our previous report proposing that somatic cells can be reprogrammed to a pluripotent state with a reducing number of reprogramming factors when the complementing factors are endogenously expressed in the somatic cells. Experiment Overall Design: 10 hybridizations in total. Experiment Overall Design: NSC-derived iPS cells by one-factor (Oct4) in triplicate: Experiment Overall Design: - NSC_1F_iPS_1 Experiment Overall Design: - NSC_1F_iPS_2 Experiment Overall Design: - NSC_1F_iPS_3 Experiment Overall Design: One-factor (Oct4) iPS cell-derived NSC in triplicate: Experiment Overall Design: - 1F_iPS_NSC_1 Experiment Overall Design: - 1F_iPS_NSC_2 Experiment Overall Design: - 1F_iPS_NSC_3 Experiment Overall Design: Neural stem cell (NSC) derived from brain of OG2/Rosa26 mice: Experiment Overall Design: - NSC_1 Experiment Overall Design: - NSC_2 Experiment Overall Design: - NSC_3 Experiment Overall Design: - NSC_4
2009-02-08 | E-GEOD-12499 | biostudies-arrayexpress
Project description:Understanding the molecular underpinnings of pluripotency is a prerequisite for optimal maintenance and application of embryonic stem cells (ESCs). We mapped the protein-protein interactions of OCT4 in naive and primed hESCs, revealing extensive connections to ATP-dependent nucleosome remodeling complexes. In naive hESCs, OCT4 is associated with both BRG1 and BRM, the two mutually exclusive ATPase subunits of the BAF complex. Genome-wide location analyses and genetic deletion studies reveal that these two enzymes exert a functionally redundant role in transcriptional regulation of blastocyst-specific genes. In contrast, OCT4 cooperates with BRG1 and the transcription factor SOX2 to create an open chromatin architecture at neural lineage-associated genes in primed hESCs. This work offers insight into the regulation of human stem cell identity and reveals how a common transcription factor utilizes differential compositions of the BAF complex in controlling distinct transcriptional programs governing naive vs. primed human pluripotent states.
2021-07-01 | GSE147716 | GEO
Project description:Resolution of early molecular events preceding endogenous OCT4 activation is critical to understanding the mechanism of reprogramming somatic cells to induced pluripotent stem cells (iPSCs), yet capturing transient regulators at the onset of reprogramming is difficult in heterogeneous populations of asynchronously reprogramming fibroblasts following four-factor transduction. To address this need, we used a heterokaryon system to identify an early and transiently expressed homeobox transcription factor, NKX3-1. Upon knockdown of NKX3-1, iPSC reprogramming is abrogated. Further, we identify that NKX3-1 functions downstream of the IL6-STAT3 regulatory network to activate endogenous OCT4. Importantly, we show that NKX3-1 can substitute for exogenous OCT4 to reprogram both mouse and human fibroblasts at comparable efficiencies generate fully pluripotent stem cells. Our findings establish an essential role for NKX3-1, previously known as a prostate-specific tumor suppressor, in iPSC reprogramming.
2019-05-13 | GSE103535 | GEO
Project description:Resolution of early molecular events preceding endogenous OCT4 activation is critical to understanding the mechanism of reprogramming somatic cells to induced pluripotent stem cells (iPSCs), yet capturing transient regulators at the onset of reprogramming is difficult in heterogeneous populations of asynchronously reprogramming fibroblasts following four-factor transduction. To address this need, we used a heterokaryon system to identify an early and transiently expressed homeobox transcription factor, NKX3-1. Upon knockdown of NKX3-1, iPSC reprogramming is abrogated. Further, we identify that NKX3-1 functions downstream of the IL6-STAT3 regulatory network to activate endogenous OCT4. Importantly, we show that NKX3-1 can substitute for exogenous OCT4 to reprogram both mouse and human fibroblasts at comparable efficiencies generate fully pluripotent stem cells. Our findings establish an essential role for NKX3-1, previously known as a prostate-specific tumor suppressor, in iPSC reprogramming.
2019-05-13 | GSE103509 | GEO
Project description:The study investigates the sex-specific effects of the pluripotency factor OCT4 deficiency in endothelial cells (ECs) on angiogenesis. OCT4 is known for its role in embryonic stem cells, but we recently found that it plays a protective role in ECs during atherosclerosis. Herein, we utilized cultured mouse aortic ECs (MAECs) and several in vivo models, including skin wounding, melanoma tumor implantation, and hindlimb ischemia, to explore the role of OCT4 in angiogenesis in both male and female mice. Our findings show significant sexual dimorphism in angiogenic responses to OCT4 deficiency. Male mice with endothelial Oct4 knockout had faster skin wound healing, increased vascularization, and quicker blood flow recovery after hindlimb ischemia than wild-type mice. In contrast, female mice with endothelial Oct4 knockout experienced delayed wound healing, no significant change in blood flow recovery after hindlimb ischemia, and increased tumor growth. Mechanistically, MCP1, a key angiogenic chemokine, was differentially regulated in male and female Oct4 knockout compared to wild-type MAECs, suggesting OCT4-dependent regulation of MCP1 as a critical mechanism for sex differences in angiogenic responses. RNA sequencing (RNAseq) analysis revealed distinct gene expression profiles in male and female MAECs upon OCT4 deficiency, with female ECs showing upregulation of pro-inflammatory genes and male ECs exhibiting increased cell cycle and angiogenesis-related gene expression. Overall, the research provides novel insights into the sex-specific functional role of OCT4 in ECs during angiogenesis and emphasizes the need for developing sex-specific EC-targeting therapeutic strategies for cardiovascular diseases and cancer.
2025-11-19 | GSE309987 | GEO
Project description:Sex-Specific Angiogenic Responses in Endothelial Cells – Role of the Pluripotency Factor OCT4
| PRJNA1364873 | ENA
Project description:The pluripotency factor Oct4 is essential for the maintenance of naïve pluripotent stem cells in vitro and in vivo. However, the specific role of Oct4 in this process remains unknown. Here, we developed a rapid protein-level Oct4 depletion system that demonstrates that the immediate downstream response to loss of Oct4 is reduced expression of key pluripotency factors. Our data show a requirement for Oct4 for the efficient transcription of several key pluripotency factors, and suggest that expression of trophectoderm markers is a subsequent event. Additionally, we find that Nanog is competent to bind to the genome in the absence of Oct4, and this binding is in fact enhanced. Globally, however, active enhancer associated histone mark H3K27ac is depleted. Our work establishes that while Oct4 is required for the maintenance of the naïve transcription factor network, at a normal ESC level it antagonises this network through inhibition of Nanog binding
2021-06-17 | GSE168575 | GEO
Project description:The pluripotency factor Oct4 is essential for the maintenance of naïve pluripotent stem cells in vitro and in vivo. However, the specific role of Oct4 in this process remains unknown. Here, we developed a rapid protein-level Oct4 depletion system that demonstrates that the immediate downstream response to loss of Oct4 is reduced expression of key pluripotency factors. Our data show a requirement for Oct4 for the efficient transcription of several key pluripotency factors, and suggest that expression of trophectoderm markers is a subsequent event. Additionally, we find that Nanog is competent to bind to the genome in the absence of Oct4, and this binding is in fact enhanced. Globally, however, active enhancer associated histone mark H3K27ac is depleted. Our work establishes that while Oct4 is required for the maintenance of the naïve transcription factor network, at a normal ESC level it antagonises this network through inhibition of Nanog binding
2021-06-17 | GSE168576 | GEO