Novel PRB material
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA624830 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:multifunction material Raw sequence reads
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Project description:Bacillus thuringiensis strain:PRB-1 Raw sequence reads
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Project description:Progesterone receptor (PR) isoforms, PRA and PRB, both progesterone-independent and dependent modulated the biology of breast cancer cells. The different phenotypes in breast cancer mediated by PRA and PRB could due to the differences of their structures, leading to the distinct protein interacting partners and downstream signaling events of each receptor. Here, we constructed Tet-inducible HA-tagged PRA or HA-tagged PRB in T47DC42 breast cancer cells. We performed affinity purification coupled with SILAC mass spectrometry technique to comprehensively study PRA and PRB interacting partners in both liganded and unliganded conditions. To validate our findings, we applied both forward and reverse SILAC to effectively minimize experimental errors. These datasets will be useful in investigating PRA- and PRB-specific molecular mechanisms and can potentially be used as a database for subsequent experiments to identify novel PRA and PRB interacting proteins that differentially mediated different biological functions in breast cancer cells.
2021-03-08 | PXD023920 | Pride
Project description:Fedbatch culture of human fecal material Raw sequence reads
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Project description:Morus alba L. Raw protein sequence reads and sequence
2024-02-08 | PXD049451 | iProX
Project description:Over the last decade, CDK4/6 inhibitors (palbociclib, ribociclib and abemaciclib) have emerged as promising anticancer drugs. Numerous studies have demonstrated that CDK4/6 inhibitors efficiently block the pRb-E2F pathway and induce cell cycle arrest in pRb-proficient cells. Based on these studies, the inhibitors have been approved by the FDA for treatment of advanced hormonal receptor (HR) positive breast cancers in combination with hormonal therapy. However, some evidence has recently shown unexpected effects of the inhibitors, promoting needs to understand more about the mechanism of inhibitors beyond pRb. Our study demonstrates here for the first time how palbociclib impairs the origin firing in the DNA replication process in pRb-deficient cell lines. Strikingly, despite the absence of pRb, cells treated with palbociclib synthesize less DNA without any induced cell cycle arrest. Furthermore, palbociclib treatment disturbs the temporal program of DNA replication and reduces the density of replication forks. Cells treated with palbociclib show a defect in the loading of proteins of the Pre-initiation complex (Pre-IC) on chromatin, indicating a reduced initiation of DNA replication. Our findings highlight hidden effects of palbociclib on the dynamics of DNA replication and on its cytotoxic consequences on cell viability in the absence of pRb. This study provides a potential therapeutic application of palbociclib to target genomic instability towards pRb deficient patient
2023-07-01 | GSE180530 | GEO
Project description:RBP2 is downstream of pRB pathway We used gene expression profiling experiments to investigate if gene expression changes in cells with RBP2 knockdown significantly overlap with gene expression changes in cells overexpressing pRB, consistent with the data that knockdown of RBP2 phenocopies reintroduction of pRB in SAOS-2 (RB-/-) cells Keywords: epistatic experiment
2008-08-29 | GSE9690 | GEO
Project description:In this study, use of a gene-targeted mouse model that is defective for pRb-condensin II interactions, Rb1L, has revealed instances where condensin II localization in interphase nuclei is dependent on pRb. Condensin II binding overlaps significantly with marks of active chromatin, and is enriched at the promoters of genes, including closely spaced divergent promoters. Interestingly, there are some bidirectional promoters where condensin II binds in an pRb-dependent manner and transcription of only one of the two genes is upregulated in Rb1L/L MEFs, suggesting the pRb-condensin II complex may be acting as a repressor or an insulator at distinct genomic locations to influence transcription. Chromatin conformations at these locations demonstrated that the pRb-condensin II complex may be responsible for maintaining more static, long-range interactions. In addition, pRb also recruits TFIIIC, another condensin II interactor, to many genomic loci. These recently discovered non-canonical transcriptional functions of the pRb-condensin II complex may represent an additional mechanism of pRb-mediated tumor suppression.
2019-11-04 | GSE125139 | GEO
Project description:The specific deletion of Rb gene in epidermis leads to altered proliferation and differentiation, but not to the development of spontaneous tumors. Our previous data have demonstrated the existence of a functional compensation of Rb loss by Rbl1 (p107) in as the phenotypic differences with respect to controls are intensified. However, the possible evolution of this aggravated phenotype, in particular in relationship with tumorigenesis, has not been evaluated due to the premature death of the double deficient mice. We have now investigated whether p107 can also act as a tumor suppressor in pRb-deficient epidermis using different experimental approaches. We found spontaneous tumor development in doubly-deficient skin grafts. Moreover, Rb-deficient keratinocytes are susceptible to Ha-ras-induced transformation, and this susceptibility is enhanced by p107 loss. Further functional analyses, including microarray gene expression profiling, indicated that the loss of p107, in the absence of pRb, produces the reduction of p53-dependent pro-apoptotic signals. Overall, our data demonstrate that p107 behaves as a tumor suppressor in epidermis in the absence of pRb and suggest novel tumor-suppressive roles for p107 in the context of functional p53 and activated Ras Keywords: epidermis, tumorigenesis, pRb, p107, Ras, p53, apoptosis
2007-11-13 | GSE9567 | GEO