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Comparison_col0vsskp2-Functional analysis of the SKP2 and CUL4 proteins

ABSTRACT: rs04-04_skp2_cul4 - comparison_col0vsskp2 - Antisense and mutants of the SKP2 and CUL4 genes are compared to the Wt in order to identify the genes controlled by those SCF proteins. - Comparison Col0 versus skp2

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE36651 | GEO | 2012/03/27

SECONDARY ACCESSION(S): PRJNA156935

REPOSITORIES: GEO

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comparison_col0vsskp2-Functional analysis of the SKP2 and CUL4 proteins

Project description:rs04-04_skp2_cul4 - comparison_col0vsskp2 - Antisense and mutants of the SKP2 and CUL4 genes are compared to the Wt in order to identify the genes controlled by those SCF proteins. - Comparison Col0 versus skp2 2 dye-swap - wt vs mutant comparison

2012-03-26 | E-GEOD-36651 | biostudies-arrayexpress

comparison_cul4_as_light-Functional analysis of the SKP2 and CUL4 proteins

Project description:rs04-04_skp2_cul4 - comparison_cul4_as_light - Antisense and mutants of the SKP2 and CUL4 genes are compared to the Wt in order to identify the genes controlled by those SCF proteins. - The seeds have been sown every two days on MS 255 (Duschefa) without 1% sugar. These plates stayed 6 days in the dark at 4 Â°C. Then they were transfered to the light for 6 more days. 4 dye-swap - gene knock out, normal vs antisense mutant comparison

2012-03-26 | E-GEOD-36655 | biostudies-arrayexpress

comparison_cul4_as_light-Functional analysis of the SKP2 and CUL4 proteins

Project description:rs04-04_skp2_cul4 - comparison_cul4_as_light - Antisense and mutants of the SKP2 and CUL4 genes are compared to the Wt in order to identify the genes controlled by those SCF proteins. - The seeds have been sown every two days on MS 255 (Duschefa) without 1% sugar. These plates stayed 6 days in the dark at 4 °C. Then they were transfered to the light for 6 more days.

2012-03-27 | GSE36655 | GEO

comparison_cul4_as_dark_light-Functional analysis of the SKP2 and CUL4 proteins

Project description:rs04-04_skp2_cul4 - comparison_cul4_as_dark_light - Antisense and mutants of the SKP2 and CUL4 genes are compared to the Wt in order to identify the genes controlled by those SCF proteins. - The seeds have been sown every two days on MS 255 (Duschefa) without adding sugar. These plates stayed 2 days in the dark at 4Â°C. Then they got a 8 hours light induction (light induction of germination) and then back to the dark for 5 more days. 4 dye-swap - gene knock out,normal vs antisense mutant comparison

2012-03-26 | E-GEOD-36652 | biostudies-arrayexpress

comparison_cul4_as_dark_light-Functional analysis of the SKP2 and CUL4 proteins

Project description:rs04-04_skp2_cul4 - comparison_cul4_as_dark_light - Antisense and mutants of the SKP2 and CUL4 genes are compared to the Wt in order to identify the genes controlled by those SCF proteins. - The seeds have been sown every two days on MS 255 (Duschefa) without adding sugar. These plates stayed 2 days in the dark at 4°C. Then they got a 8 hours light induction (light induction of germination) and then back to the dark for 5 more days.

2012-03-27 | GSE36652 | GEO

The Replication-initiation determinant protein (RepID) modulates replication by recruiting CUL4 to chromatin

Project description:Cell cycle progression in mammals is modulated by two ubiquitin ligase complexes, CRL4 and SCF, which facilitate degradation of chromatin substrates involved in the regulation of DNA replication. One member of the CRL4 complex, RepID (DCAF14/PHIP), is a WD40-containing protein that selectively binds and activates a group of replication origins. We found that RepID recruits the CRL4 complex to chromatin prior to DNA synthesis, thus playing a crucial architectural role in the proper licensing of chromosomes for replication. In the absence of RepID, cells rely on the alternative ubiquitin ligase, SKP2-containing SCF, to progress through the cell cycle. RepID depletion markedly increases cellular sensitivity to SKP2 inhibitors, which triggered massive genome re-replication. Both RepID and SKP2 interact with distinct, non-overlapping groups of replication origins, suggesting that selective interactions of replication origins with specific CRL components execute the DNA replication program and maintain genomic stability by preventing re-initiation of DNA replication.

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MDAMB231 transcriptome response to SKP2 knockdown

Project description:The SKP2 was knockdown by siRNAs in MDA-MB231 cells and RNA-Seq was used to define the transcriptome response to SKP2

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Comprehensive single cell transcriptomics analysis of murine osteosarcoma uncovers Skp2 function in metastasis, genomic instability and immune activation and reveals additional target pathways

Project description:Osteosarcoma (OS) is the most common primary pediatric bone malignancy. One promising new therapeutic target is SKP2, encoding a substrate recognition factor of the SCF E3 ubiquitin ligase responsible for ubiquitination and proteasome degradation of substrate p27, thus driving cellular proliferation. We have shown previously that knockout of Skp2 in an immunocompetent transgenic mouse model of OS improved survival, drove apoptosis, and induced tumor inflammation. Here, we applied single-cell RNA-sequencing (scRNA-seq) to study primary OS tumors derived from Osx-Cre driven conditional knockout of Rb1 and Trp53. We showed that murine OS models recapitulate the tumor heterogeneity and microenvironment complexity observed in patient tumors. We further compared this model with OS models with functional disruption of Skp2: one with Skp2 knockout and the other with the Skp2-p27 interaction disrupted (resulting in p27 overexpression). We found reduction of T cell exhaustion and upregulation of interferon activation, along with evidence of replicative and endoplasmic reticulum-related stress in the Skp2 disruption models, and showed that interferon induction was correlated with improved survival in OS patients. Additionally, our scRNA-seq analysis uncovered decreased activities of metastasis-related gene signatures in the Skp2-modulated OS, which we validated by observation of a strong reduction in lung metastasis in the Skp2 knockout mice. Finally, we report several potential mechanisms of escape from targeting Skp2 in OS, including upregulation of Myc targets, DNA copy number amplification and overexpression of alternative E3 ligase genes, and potential alternative lineage activation. These mechanistic insights into OS tumor biology and Skp2 function suggest novel targets for new, synergistic therapies, while the data and our comprehensive analysis may serve as a public resource for further big data-driven OS research.

2024-06-28 | GSE262743 | GEO

nt-kis-CKI role in plant development

Project description:rs04-08_ntkis - nt-kis - Transcription profiling of NtKIS overexpressing lines - 35S NtKIS (CDK inhibitor) versus Col0 Keywords: gene knock in (transgenic)

2007-08-09 | GSE8697 | GEO

CKI role in plant development

Project description:rs04-08_ntkis - nt-kis - Transcription profiling of NtKIS overexpressing lines - 35S NtKIS (CDK inhibitor) versus Col0 Keywords: gene knock in (transgenic)

2007-05-31 | GSE7939 | GEO

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