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PIP degron-stabilized Dacapo/p21Cip1 and mutations in ago act in an anti- versus pro-proliferative manner, yet both trigger an increase in Cyclin E levels

ABSTRACT: PIP degron-stabilized Dacapo/p21Cip1 and mutations in ago act in an anti- versus pro-proliferative manner, yet both trigger an increase in Cyclin E levels

PROVIDER: PRJNA552625 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9643740.fastq.gz	Fastqsanger.gz
	SRR9643741.fastq.gz	Fastqsanger.gz
	SRR9643742.fastq.gz	Fastqsanger.gz
	SRR9643743.fastq.gz	Fastqsanger.gz
	SRR9643744.fastq.gz	Fastqsanger.gz

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PIP degron-stabilized Dacapo/p21Cip1 and mutations in ago act in an anti- versus pro-proliferative manner, yet both trigger an increase in Cyclin E levels

Project description:During cell cycle progression, the activity of the CycE-Cdk2 complex gates S-phase entry. CycE-Cdk2 is inhibited by CDK inhibitors (CKIs) of the Cip/Kip family, which include the human p21Cip1 and Drosophila Dacapo proteins. Both the CycE and Cip/Kip proteins are under elaborate control via protein degradation, mediated by the Cullin-Ring-Ligase (CRL) family of ubiquitin ligase complexes. The CRL complex SCFFbxw7/Ago targets phosphorylated CycE while p21Cip1 and Dap are targeted by the CRL4Cdt2 complex, binding to the PIP degron. The role of CRL-mediated degradation of CycE and Cip/Kip proteins during CNS development is not well understood. Here, we analyse the role of ago (Fbxw7) mediated CycE degradation and of Dap/p21Cip1 degradation during Drosophila CNS development. We find that ago mutants display over-proliferation, accompanied by elevated CycE expression levels. In contrast, expression of PIP degron mutant Dap/p21Cip1 transgenes inhibit proliferation. However, surprisingly, this is also accompanied by elevated CycE levels. Hence, ago mutation and PIP degron Cip/Kip transgenic expression trigger opposite effects on proliferation, but similar effects on CycE levels.

2019-07-06 | GSE133825 | GEO

CROP-seq + PIP-seq

Project description:We used PIP-seq with a CROP-seq library to evaluate the feability of PIP-seq for large pooled CRISPR screens

2023-01-12 | GSE202915 | GEO

CROP-seq + PIP-seq

Project description:CROP-seq + PIP-seq

| PRJNA923463 | ENA

AGO pathway

Project description:AGO pathway

| PRJNA121635 | ENA

Compound PIP-RBPJ-1 treated human neural stem cells

Project description:The study of the compond PIP-RBPJ-1‘ function on neural stem cell. Synthetic DNA-binding inhibitors capable of gaining precise control over neurogenesis factors could obviate the current clinical barriers associated with small molecule use in regenerative medicine. Here, we show the design and bio-efficacy of a synthetic ligand PIP-RBPJ-1 to cause promoter-specific suppression of neurogenesis-associated HES1, and its downstream genes. Furthermore, PIP-RBPJ-1 alone could alter the neural system-associated notch signaling factors and remarkably induce neurogenesis with an efficiency that is comparable to a conventional approach. Here is one day treatment of the PIP-RBPJ-1 on neural stem cells.

2018-07-19 | GSE109916 | GEO

COMPASS-degron cells

Project description:COMPASS-degron cells

| PRJNA753080 | ENA

A functional and regulatory network associated with PIP expression in human breast cancer

Project description:Background The PIP (prolactin-inducible protein) gene has been shown to be expressed in breast cancers, with contradictory results concerning its implication. As both the physiological role and the molecular pathways in which PIP is involved are poorly understood, we conducted a combined gene expression profiling and network analysis studies on selected breast cancer cell lines presenting distinct PIP expression levels and hormonal receptor status, to explore the functional and regulatory network of PIP co-modulated genes. Results Microarray analysis allowed identification of genes co-modulated with PIP independently of modulations resulting from hormonal treatment or cell line heterogeneity. Relevant clusters of genes that can discriminate between [PIP+] and [PIP-] cells were identified. Functional and regulatory network analyses based on knowledge database revealed a master network of PIP co-modulated genes, including many interconnecting oncogenes and tumor suppressor genes, half of which were detected as differentially expressed through high-precision measurements. The networks identified appear associated with an inhibition of proliferation coupled with an increase of apoptosis and an enhancement of cell adhesion in breast cancer cell lines. Finally, the STAT5 motif was identified in promoters of an important part of genes belonging to the PIP networks. Conclusion Our global exploratory approach was found to be an effective strategy to identify the biological pathways modulated along with the PIP expression, thus supporting good prognostic value of disease-free survival time in breast cancer based on previous reports focusing on PIP’s favorable signature. Moreover, our data allowed us to provide the first insight in its regulatory subnetwork in which STAT5 appears as a potential key regulator.

2009-03-06 | GSE11627 | GEO

SF3B1 Degron knockdown RNA-seq

Project description:Knockdown of mutant and/or wild-type SF3B1 in MEL202 cell line by Degron knock-in, followed by RNA-seq, to identify splicing events governed by mutant SF3B1. Control: parental MEL202 cell line. Experiments: mutant-SF3B1 knockdown; wildtype-SF3B1 knockdown; mutant SF3B1 knockout. Treatments: each of these four conditions plus and minus shld.

2015-03-11 | E-GEOD-66719 | biostudies-arrayexpress

Ago and Fkbp project

Project description:Ago and Fkbp project

| PRJNA744096 | ENA

ago-Transcriptome of the argonaute (ago) mutant

Project description:ra04-02_ago - ago - Identification of the regulation pathways implied in adventitious root formation control in Arabidopsis - Transcription analisys of 2 different AGO1 mutants Keywords: gene knock out

2007-06-20 | GSE7989 | GEO

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