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Expression data of NIH3T3 in G0 and G1 phases

ABSTRACT: NIH3T3 in the middle of G0 to G1 transion consists of the cells which is still staying G0 phase and the cells which enters G1. Monitoring the expressions of p27 and Cdt1 enables to distinguish these two; p27+/Cdt1+ cells as the cells in G0 phase and p27-Cdt1+ cells as G1 phase We sorted p27+Cdt1+ (G0) NIH3T3 cells and p27-Cdt1+ (G1) NIH3T3 cells in the middle of G0-G1 transition, 5 hours after serum addition following the serum addition using mVenus-p27K- and mCherry-hCdt1(30/120) . We compared the expression profiles of these NIH3T3 cells in G0 and G1 phases and identified the genes upregulated in G0 or G1 phases.

ORGANISM(S): Mus musculus

PROVIDER: GSE46511 | GEO | 2014/02/21

SECONDARY ACCESSION(S): PRJNA200707

REPOSITORIES: GEO

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Expression data of NIH3T3 in G0 and G1 phases

Project description:NIH3T3 in the middle of G0 to G1 transion consists of the cells which is still staying G0 phase and the cells which enters G1. Monitoring the expressions of p27 and Cdt1 enables to distinguish these two; p27+/Cdt1+ cells as the cells in G0 phase and p27-Cdt1+ cells as G1 phase We sorted p27+Cdt1+ (G0) NIH3T3 cells and p27-Cdt1+ (G1) NIH3T3 cells in the middle of G0-G1 transition, 5 hours after serum addition following the serum addition using mVenus-p27K- and mCherry-hCdt1(30/120) . We compared the expression profiles of these NIH3T3 cells in G0 and G1 phases and identified the genes upregulated in G0 or G1 phases. The p27+Cdt1+ (G0) NIH3T3 cells and p27-Cdt1+ (G1) NIH3T3 cells were sorted by FACS for RNA extraction and hybridization on Affymetrix microarrays.

2014-02-21 | E-GEOD-46511 | biostudies-arrayexpress

Quantification of membrane protein expression in G0 and G1 cell cycle phase samples in PC3 prostate cancer cells

Project description:Prostate cancer (PCa) has a significant ability to disseminate and survive in the bone marrow (BM). Once there, disseminated tumor cells (DTCs) may lie dormant for years, but often eventually reactivate proliferative pathways, thus largely contributing to bone metastasis, disease progression, and relapse. Unfortunately, quiescent PCa cells are difficult to identify and target with treatment, in part because formerly identified relevant markers are intracellular and regulated by protein stability. We sought to address this problem by identifying a G0 marker that is expressed on the cell surface and therefore amenable to antibody binding for identification and therapeutic targeting. In doing so, we utilized stably transduced fluorescent markers for CDKN1B (p27) and CDT1 protein levels, which separate viable PCa cells into G0, G1, or combined S/G2/M populations (as described in PMID 34957090). We then performed FACS to collect G1 and G0 PC3 PCa cells, isolated membrane proteins, and subsequently used GC-MS proteomics to determine differences in protein abundance between G0 and G1. In total, 3,791 proteins were identified.

2023-03-03 | PXD037378 | Pride

Mus musculus

Project description:Expression data of NIH3T3 in G0 and G1 phases

| PRJNA200707 | ENA

DNA-PK Promotes DNA End Resection at DNA Double Strand Breaks in G0 cells [ChIP-Seq]

Project description:DNA double-strand break (DSB) repair by homologous recombination is confined to the S and G2 phases of the cell cycle partly due to 53BP1 antagonizing DNA end resection in G1 phase and non-cycling quiescent (G0) cells where DSBs must be repaired by non-homologous end joining (NHEJ). Unexpectedly, we uncovered extensive MRE11- and CtIP-dependent DNA end resection at DSBs in G0 mammalian cells. A whole genome CRISPR/Cas9 screen revealed the DNA-dependent kinase (DNA-PK) complex as a key factor in promoting DNA end resection in G0 cells. In agreement, depletion of FBXL12, which promotes ubiquitylation and removal of the KU70/KU80 subunits of DNA-PK from DSBs, promotes even more extensive resection in G0 cells. In contrast, a requirement for DNA-PK in promoting DNA end resection in cycling cells at the G1 or G2 phase cells was not observed. Our findings establish that DNA-PK uniquely promotes DNA end resection in G0, but not in G1 or G2 phase cells, and has important implications for DNA DSB repair in quiescent cells.

2022-05-16 | GSE186086 | GEO

DNA-PK Promotes DNA End Resection at DNA Double Strand Breaks in G0 cells [END-seq]

2022-05-16 | GSE186085 | GEO

LncRNA LIMp27 regulates the DNA damage response through p27 in p53-defective cancer cells

Project description:P53 inactivation occurs in about 50% of human cancers, where p53-driven p21 activity is devoid and p27 becomes essential for the establishment of the G1/S checkpoint upon DNA damage. Here, we show that the E2F1-responsive lncRNA LIMp27 selectively represses p27 expression and contributes to proliferation, tumorigenicity, and treatment resistance in p53-defective colon adenocarcinoma (COAD) cells. LIMp27 competes with p27 mRNA for binding to cytoplasmically localized hnRNA0, which otherwise stabilizes p27 mRNA leading to cell cycle arrest at the G0/G1 phase. In response to DNA damage, LIMp27 is upregulated in both wild-type and p53-mutant COAD cells, whereas cytoplasmic hnRNPA0 is only increased in p53-mutant COAD cells due to translocation from the nucleus. Moreover, high LIMp27 expression is associated with poor survival of p53-mutant but not wild-type p53 COAD patients. These results uncover a lncRNA mechanism that promotes p53-defective cancer pathogenesis and suggest that LIMp27 may constitute a target for the treatment of such cancers.

| MSV000090292 | MassIVE

Cell cycle-dependent resolution of DNA double-strand breaks repair

Project description:Damage to genomic DNA, especially as DNA double strand breaks (DSB), elicits prompt activation of DNA damage response (DDR) which arrest cell-cycle either G1/S or G2/M to avoid entering S and M phase with DNA damage. In mammalian organs cells are in both proliferating and quiescent states. Quiescent cells are already arrested in G0, therefore there may be fundamental difference in DDR between proliferating and quiescent cells. To address these differences we studied recruitment of DSB repair factors and resolution of DNA lesions induced at site-specific DSBs occurring at different cell cycle phases, i.e. in asynchronously proliferating, G0, and G1 arrested cells. Strikingly, DSBs occurring in G0 quiescent cells are irreparable with a sustained activation of p53-pathway. Conversely, reentry of G0-damaged cells into cell cycle progression, show a delayed clearance of recruited DNA repair factors bound at DSBs, indicating an inefficient repair when compared to DSBs induced in asynchronously proliferating or G1 cells. Moreover, we found that initial recognition of DSBs and assembly of DSB factors is largely similar at different cell cycle phases. Our study thereby demonstrates the crucial role of cell cycle phases in repair and resolution of DSBs.

2015-12-30 | GSE71447 | GEO

LncRNA LIMp27 regulates the DNA damage response through p27 in p53-defective cancer cells

Project description:P53 inactivation occurs in about 50% human cancers, where p53-driven p21 activity is devoid and p27 becomes essential for the establishment of the G1/S checkpoint upon DNA damage. Here, we show that the E2F1-responsive lncRNA LIMp27 selectively represses p27 expression and contributes to proliferation, tumorigenicity, and treatment resistance in p53-defective colon adenocarcinoma (COAD) cells. LIMp27 competes with p27 mRNA for binding to cytoplasm-localized hnRNA0, which otherwise stabilizes p27 mRNA leading to cell cycle arrest at G0/G1 phase. In response to DNA-damage, LIMp27 is upregulated in both wild-type and p53-muant COAD cells, whereas cytoplasmic hnRNPA0 is only increased due to translocation from the nucleus in p53-mutant COAD cells. High LIMp27 expression is associated with poor survival of p53-mutant but not wide-type p53 COAD patients. These results uncover a lncRNA mechanism that promotes p53-defective cancer pathogenesis and suggest that LIMp27 may constitute a target for the treatment of such cancers.

2022-12-31 | GSE208711 | GEO

Gene expression analysis of Human CD34+ cells derived from bone marrow, mobilized peripheral blood, umbillial cord blood using Agilent Whole Human Genome Oligo Microarrays (one-color)

Project description:In order to identify genes associated with the engraftment potential of human hematopoietic stem cells, we have employed whole genome microarray expression profiling of G0 and G1 phase CD34+ cells derived from bone marrow, mobilized peripheral blood, and umbilical cord blood. Samples were collected from healthy adult volunteers after obtaining informed consent according to the guidelines of the Investigational Review Board of Indiana University School of Medicine. CD34+ cells were selected and fractionated into G0 and G1 phases of cell cycle on a flow cytometer. Purity of sorted cells was further confirmed by qRT-PCR by measuring the relative expression of Ki67. Sorted cells were subjeccted to microarray analysis.

2010-09-20 | GSE24231 | GEO

cdt1-Characterization of the AtCDT1a and AtCDT1b by RNAi

Project description:rs04-06_cdt1 - cdt1 - CDT1 is a protein of the pre-replication complex, and accumulates during the G1-S transition, thus play a major role in S-phase entry - Comparison of 3 independant RNAi lines Keywords: normal vs rnai mutant comparaison

2007-06-20 | GSE7997 | GEO

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