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Orthotopic KI tumors treated with vehicle or IRAK4 inhibitor CA-4948 for two weeks

ABSTRACT: We treated FVBN/J mice bearing orthotopic KI tumors with vehicle or CA-4948 for two weeks and performed bulk RNASeq to assess transcriptomic changes in the tumor

ORGANISM(S): Mus musculus

PROVIDER: GSE197328 | GEO | 2022/12/31

REPOSITORIES: GEO

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scRNAseq of the PDAC tumors from autochtonous KPC mice treated with vehicle or IRAK4 inhibitor CA-4948

Project description:We treated 6 week-old KPC mice with vehicle or CA-4948 and perform scRNASeq to assess transcriptomic changes in CAFs and immune cells

2022-12-31 | GSE197329 | GEO

Murine colonic epithelial cells: Trabid(Zranb1) C443S hetero knock-in mouse (KI/+) vs. homo knock-in mouse (KI/KI)

Project description:Transcriptional profiling of colonic epithelial cells comparing control Trabid KI/+ with KI/KI

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Ki-67 organises heterochromatin during cell proliferation

Project description:Antigen Ki-67 is a nuclear protein expressed in proliferating mammalian cells. It is widely used in cancer histopathology but its functions remain unclear. Here, we show that Ki-67 controls heterochromatin organisation. Altering Ki-67 expression levels did not significantly affect cell proliferation in vivo. Ki-67 mutant mice developed normally and cells lacking Ki-67 proliferated efficiently. Conversely, upregulation of Ki-67 expression in differentiated tissues did not inhibit cell cycle arrest. Ki-67 interactors included proteins involved in nucleolar processes and chromatin regulators. Ki-67 depletion disrupted nucleologenesis but did not inhibit pre-rRNA processing. In contrast, it altered gene expression. Ki-67 silencing also had wide-ranging effects on chromatin organisation, disrupting heterochromatin compaction and long-range genomic interactions. Trimethylation of histone H3K9 and H4K20 at heterochromatin was strongly reduced. Overexpression of human or Xenopus Ki-67 induced ectopic heterochromatin formation. Altogether, our results suggest that Ki-67 expression in proliferating cells spatially organises heterochromatin, thereby controlling gene expression.

2018-10-26 | PXD003551 | Pride

Gene expression analysis in lung fibroblasts from p38+/+ (wt) and p38ki/ki (ki) mice

Project description:To assess differently expressed genes beween wt and ki fibroblasts Total RNA was purified from fibroblasts of 3 different mice for wt and 3 different mice for ki

2016-06-01 | E-GEOD-80825 | biostudies-arrayexpress

Glioblastoma Orthotopic Xenograft Transcriptome

Project description:Transcriptional profiling of glioblastoma orthotopic xenografts Descriptive experiment, comparison of 39 glioblastoma tumors as orthotopic xenografts

2012-07-10 | E-GEOD-38814 | biostudies-arrayexpress

Azotobacter vinelandii CA strain:CA

Project description:Azotobacter vinelandii CA strain:CA Genome sequencing

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Gene expression analysis in lung fibroblasts from p38+/+ (wt) and p38ki/ki (ki) mice

Project description:To assess differently expressed genes beween wt and ki fibroblasts

2016-06-01 | GSE80825 | GEO

Gene regulation in ki-ras transfected murine fibroblasts

Project description:Ki-ras gene mutations are involved in the carcinogenesis of acute myeloid leukemia, melanoma and different carcinomas. In order to define potential mutation-specific therapeutic targets, expression profiling analyses were performed using stable transfected NIH3T3 cells carrying different ki-ras gene mutations. Maybe, this analysis allows the discorvery of ras-associated cellular mechanisms, which might lead to the identification of physiological targets for pharmacological interventions of the treatment of Ki-ras-associated human tumors. Keywords: cDNA microarray, murine fibroblast, ki-ras mutations, carcinogenesis

2008-08-01 | GSE8372 | GEO

Gene regulation in ki-ras transfected murine fibroblasts

2010-05-25 | E-GEOD-8372 | biostudies-arrayexpress

Ki-67 is necessary during DNA replication for forks protection and genome stability

Project description:Ki-67 molecular functions and properties have remained quite obscure for a long time, despite its importance as a major proliferation marker in clinic. Only recently it has been shown that Ki-67 has a major role in the formation of the mitotic chromosome periphery compartment, and it is a protein phosphatase 1 (PP1) binding protein. Understanding Ki-67 functions at different stages of the cell cycle has been so far hindered by the fact that the different phenotypes observed in cells upon Ki-67 depletion could be the outcome of secondary effects. Here, by using Auxin-inducible-degron (AID) system, we show that Ki-67 degradation at the G1/S boundary causes the disassembly of the replication machinery and leads to DNA damage. This triggers the interferon response and causes replication delay. Our results support the model whereby Ki-67 contributes to replication forks protection, and it is important for timely DNA replication and genome maintenance.

2024-04-13 | PXD037513 | Pride

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