Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data in HeLa cells treated with CENP-E siRNA or Eg5 siRNA in the presence of BubR1 siRNA

ABSTRACT: The molecular mechanism responsible for cell fate after mitotic slippage is unclear. We investigate the postmitotic effects of different mitotic aberrations, misaligned chromosomes produced by CENP-E siRNA (siCENP-E), and monopolar spindles resulting from Eg5 siRNA (siEg5). To determine which signaling pathways contribute to the postmitotic effect of siCENP-E in the presence of siBubR1 (siCENP-E+siBubR1) compared with siEg5+siBubR1, we performed a comprehensive gene expression analysis by microarray comparisons. SUBMITTER_CITATION: Expression data of HeLa cells treated with CENP-E siRNA or Eg5 siRNA in the presence of BubR1 siRNA, Yusuke Nakayama, Akihiro Ohashi, Genomics Data, Volume 6, December 2015, Pages 44-45, doi:10.1016/j.gdata.2015.08.002

ORGANISM(S): Homo sapiens

PROVIDER: GSE67905 | GEO | 2015/06/25

SECONDARY ACCESSION(S): PRJNA281179

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data in HeLa cells treated with CENP-E siRNA or Eg5 siRNA in the presence of BubR1 siRNA

Project description:The molecular mechanism responsible for cell fate after mitotic slippage is unclear. We investigate the postmitotic effects of different mitotic aberrations, misaligned chromosomes produced by CENP-E siRNA (siCENP-E), and monopolar spindles resulting from Eg5 siRNA (siEg5). To determine which signaling pathways contribute to the postmitotic effect of siCENP-E in the presence of siBubR1 (siCENP-E+siBubR1) compared with siEg5+siBubR1, we performed a comprehensive gene expression analysis by microarray comparisons. HeLa cells were treated with siNS (non-silencing) +siBubR1, siCENP-E+siBubR1, or siEg5+siBubR1. The siNS cells were used as a control. Each siRNA treatment was duplicated. Three days after the siRNA treatments, the siRNA-transfected HeLa cells were collected for RNA extraction and hybridization on Affymetrix microarrays.

2015-06-25 | E-GEOD-67905 | biostudies-arrayexpress

Self-priming of Plk1 binding to BubR1 ensures accurate mitotic progression

Project description:Plk1 is a key mitotic kinase that localizes to distinct subcellular structures to promote accurate mitotic progression. Plk1 recruitment depends on direct interaction between polo-box domain (PBD) on Plk1 and PBD binding motif (PBD BM) on the interactors. However, recent study showed that PBD BM alone is not enough for stable binding between CENP-U and Plk1 highlighting the complexity of the interaction which warrants further investigation. An important interactor for Plk1 during mitosis is the checkpoint protein BubR1. Plk1 bound to BubR1 via PBD interaction with pT620 phosphorylates BubR1 S676/T680 to promote BubR1-PP2A/B56 interaction. The BubR1-PP2A/B56 complex counteracts the destablizing effect on kinetochore-microtubule attachments by mitotic kinases to promote mitotic progression. Here we show that Plk1 phosphorylates T600/T608 on BubR1 and the double phosphorylation is critical for BubR1-Plk1 interaction. A similar mechanism for Plk1-Bub1 interaction also exists indicating a general principle for Plk1 kinetochore recruitment through self-priming. Mechanistically preventing BubR1 T600/T608 phosphorylation impairs chromosome congression and checkpoint silencing by reducing Plk1 and PP2A/B56 binding to BubR1. Increasing the binding affinity towards Plk1 and PP2A/B56 in BubR1 through protein engineering bypasses the requirement of T600/T608 phosphorylation for mitotic progression. These results reveal a new layer of regulation for accurate mitotic progression.

2024-10-31 | MSV000096264 | MassIVE

Homo sapiens

Project description:Expression data in HeLa cells treated with CENP-E siRNA or Eg5 siRNA in the presence of BubR1 siRNA

| PRJNA281179 | ENA

Mitotic stress is an integral part of the oncogene-induced senescence program that promotes multinucleation and cell cycle arrest

Project description:Oncogene-induced senescence (OIS) is a tumor suppression mechanism that blocks cell proliferation in response to oncogenic signalling. OIS is frequently accompanied by multinucleation; however, the origin of this is unknown. Here we show that multinucleate OIS cells originated mostly from failed mitosis. Prior to senescence, mutant RasV12 activation in primary human fibroblasts compromised mitosis, associated with abnormal expression of mitotic genes that enter M-phase. Simultaneously, RasV12 activation enhanced survival of damaged mitoses, culminating in extended mitotic arrest and aberrant exit from mitosis via mitotic slippage. ERK-dependent transcriptional up-regulation of Mcl1 was responsible for enhanced slippage of cells with mitotic defects and subsequent cell survival. Importantly, mitotic slippage and oncogene signalling synergistically induced senescence and key senescence regulators p21 and p16. We propose that activated Ras induces transcriptional changes that predispose cells undergoing OIS to mitotic stress and multinucleation.

2015-08-13 | GSE70668 | GEO

Mitotic stress is an integral part of the oncogene-induced senescence program that promotes multinucleation and cell cycle arrest

2015-08-13 | E-GEOD-70668 | biostudies-arrayexpress

Expression data from HeLa cells transiently transfected with control siRNA or SON siRNA

2011-04-01 | GSE26888 | GEO

LncRNA OIP5-AS1/cyrano suppresses GAK expression to control mitosis

Project description:Long noncoding RNAs (lncRNAs) have been found to regulate the expression of mRNAs with which they share partial complementarity. We sought to identify the mechanism through which the lncRNA OIP5-AS1, which is abundant in the cytoplasm, suppressed cell proliferation. Silencing of OIP5-AS1 in human cervical carcinoma cells revealed the appearance of many aberrant (monopolar, multipolar, misaligned) mitotic spindles. By biotin-oligomer affinity pulldown, proteomic, and bioinformatic analyses, we identified a subset of human cell cycle regulatory proteins encoded by mRNAs that were capable of interacting with OIP5-AS1. Further investigation revealed that GAK mRNA, which encodes a cyclin G-associated kinase important for mitotic progression, was a prominent target of OIP5-AS1. The interaction between these two transcripts led to a reduction in GAK mRNA stability and GAK protein abundance, as determined in cells in which OIP5-AS1 levels were increased or decreased. Importantly, the aberrant mitotic cell division seen after silencing OIP5-AS1 was partly rescued if GAK was simultaneously silenced. These findings indicate that the abnormal mitoses seen after silencing OIP5-AS1 was caused by an untimely rise in GAK levels and suggest that OIP5-AS1 suppresses cell proliferation at least in part by reducing GAK levels

2017-09-25 | GSE93551 | GEO

Expression data from HeLa cells transiently transfected with control siRNA or SON siRNA

Project description:SON is a large Ser/Arg (SR)-related protein localized in nuclear speckles. SON siRNA causes defects in mitotic progression and genome instability. We used microarrays to detail the pattern of gene expression after SON knockdown. HeLa cells were grown in 100 mm dishes and transfected with negative control siRNA or SON siRNA (400 pmol). Then, cells were harvested after 66 hours and RNAs were isolated. Microarrays were performed using GeneChip Human Genome U133A 2.0 (Affymetrix).

2011-04-01 | E-GEOD-26888 | biostudies-arrayexpress

siRna

Project description:siRna Transcriptome or Gene expression

| PRJNA308857 | ENA

RNA-seq of control siRNA, p150 siRNA and p60 siRNA transfected mES cells

Project description:RNA-seq of control siRNA, p150 siRNA and p60 siRNA transfected mES cells

| PRJEB6962 | ENA