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P63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling

ABSTRACT: p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling

PROVIDER: PRJNA606576 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11080412.fastq.gz	Fastqsanger.gz
	SRR11080413.fastq.gz	Fastqsanger.gz
	SRR11080414.fastq.gz	Fastqsanger.gz
	SRR11080415.fastq.gz	Fastqsanger.gz
	SRR11080416.fastq.gz	Fastqsanger.gz

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p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [RNA-seq]

Project description:p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [RNA-seq]

| PRJNA606573 | ENA

p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [scRNA-seq]

Project description:p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [scRNA-seq]

| PRJNA606579 | ENA

p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [ChIP-seq]

Project description:p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [ChIP-seq]

| PRJNA606548 | ENA

p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [RNA-seq]

Project description:Np63+ve cells are multipotent and maintain all epithelial cell lineages of the embryonic and adult salivary gland (SG). However, the molecular mechanisms by which Np63 regulates stem/progenitor (SP) cell populations in the SG remains elusive. To better understand Np63 s role in directing cell fate choices, here we have utilized Np63-null adult mice and primary salivary cell cultures to probe alterations in SP cell differentiation and function. Specifically, we have generated bulk RNA-seq and scRNA-seq data from Np63-null adult mice and p63 and H3K27Ac ChIP-seq data from primary salivary cell cultures. These genomic and epigenomic data sets were leveraged to interrogate altered SG cellular identities and differentiation states resulting from the loss of Np63. Our studies reveal that ablation of Np63 results in a loss of the SP cell population and skewed SG differentiation that is modulated by dysregulated TGF- /Activin signaling. Our findings offer new molecular revelations into the SP cell gene regulatory networks that are likely to be relevant for normal or diseased SG states.

2020-09-23 | GSE145266 | GEO

p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [ChIP-seq]

2020-09-23 | GSE145264 | GEO

p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [scRNA-seq]

2020-09-23 | GSE145267 | GEO

p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling

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

2020-09-23 | GSE145268 | GEO

Changes in follistatin levels by BRCA1 may serve as a regulator of ovarian carcinogenesis

Project description:Follistatin is a folliculogenesis regulating protein that has been found in relatively high concentration in the female ovarian tissues. Follistatin acts as an antagonist to the function of Activin, which is often found elevated in ovarian carcinogenesis and thus presents a possibility for therapeutic intervention in controlling ovarian cancer. Most of the ovarian cancer occurs in its ovarian surface epithelium (OSE) cells. Although breast cancer susceptibility gene 1 (BRCA1) is a known tumor suppressor for breast cancer but its role in ovarian cancer is beginning to unfold. We have shown that in ovarian carcinoma cells (SKOV3), stable overexpression of BRCA1 stimulates Follistatin secretion and simultaneously downregulates Activin expression. Moreover, knock down of BRCA1 in immortalized OSE (IOSE) cells from human ovarian tissue demonstrates downregulation of Follistatin secretion with simultaneous up regulation of Activin expression. IOSE cells generated from an ovarian cancer patient with BRCA1 mutation failed to secrete Follistatin in the medium. Our results indicate a novel function for BRCA1 in the form of regulation of the expression of Follistatin in the ovarian cells. 3 treatments vs 3 controls

2011-07-02 | E-GEOD-30296 | biostudies-arrayexpress

Changes in follistatin levels by BRCA1 may serve as a regulator of ovarian carcinogenesis

2011-07-02 | GSE30296 | GEO

p63 and Its Target Follistatin Maintain Salivary Gland Stem/Progenitor Cell Function through TGF-β/Activin Signaling.

Project description:Multipotent ΔNp63-positive cells maintain all epithelial cell lineages of the embryonic and adult salivary gland (SG). However, the molecular mechanisms by which ΔNp63 regulates stem/progenitor (SP) cell populations in the SG remains elusive. To understand the role of ΔNp63 in directing cell fate choices in this gland, we have generated ΔNp63-deleted adult mice and primary salivary cell cultures to probe alterations in SP cell differentiation and function. In parallel, we have leveraged RNA-seq and ChIP-seq-based characterization of the ΔNp63-driven cistrome and scRNA-seq analysis to molecularly interrogate altered SG cellular identities and differentiation states dependent on ΔNp63. Our studies reveal that ablation of ΔNp63 results in a loss of the SP cell population and skewed differentiation that is mediated by Follistatin-dependent dysregulated TGF-β/Activin signaling. These findings offer new revelations into the SP cell gene regulatory networks that are likely to be relevant for normal or diseased SG states.

| S-EPMC7498843 | biostudies-literature

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