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Stable knockdown or over expression of the SPOP-substrate ZMYND11 in Y87C SPOP-mutant and control VCaP cells

ABSTRACT: Stable knockdown or over expression of the SPOP-substrate ZMYND11 in Y87C SPOP-mutant and control VCaP cells

PROVIDER: PRJEB28532 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2784290.fastq.gz	Fastqsanger.gz
	ERR2784291.fastq.gz	Fastqsanger.gz
	ERR2784292.fastq.gz	Fastqsanger.gz
	ERR2784293.fastq.gz	Fastqsanger.gz
	ERR2784294.fastq.gz	Fastqsanger.gz

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Similar Datasets

Stable over expression of the SPOP-substrate ZMYND11 in VCaP cells

Project description:SPOP is known to bind to serine/theronine-rich degrons on substrate proteins. We identified two degron sequences within the PWWP and MYND domain of ZMYND11, a novel SPOP substrate, and investigated whether ZMYND11 may contribute to the transcriptional output of mutant SPOP in VCaP cancer cells. Hence, we performed over-expression of degron-deficient ZMYND11 and degron-deficient ZMYND11 with W294A mutation in VCaP cells. While WT ZMYND11 constructs can be robustly over-expressed at the mRNA level, only the degron-deficient variants yielded a robost increase in ZMYND11 protein expression. Degron mutant-induced transcriptional perturbations partially mimicked SPOP mutant-induced gene expression changes, suggesting that ZMYND11 is sufficient to recapitulate certain features of mutant SPOP.

2020-12-16 | E-MTAB-7173 | biostudies-arrayexpress

Identification of ZMYND11 binding sites in VCaP cells with stable overexpression of either mutant (Y87C) or wild-type SPOP.

Project description:SPOP is known to bind to serine/theronine-rich degrons on substrate proteins. We identified two degron sequences within the PWWP and MYND domain of ZMYND11, a novel SPOP substrate, and investigated whether ZMYND11 may contribute to the transcriptional output of mutant SPOP in VCaP cancer cells. We mapped the genomic occupancy of ZMYND11 in VCaP cells over-expressing either wild type SPOP or the recurrent SPOP-Y87C mutant by ChIPseq. Genomic binding sites in the SPOP-Y87C mutant were increased over wild type SPOP, consistent with the increased ZMYND11 expression levels in the former.

2020-12-05 | E-MTAB-7174 | biostudies-arrayexpress

Stable overexpression and knockdown of mutant- or wild type SPOP in VCaP prostate cancer cells

Project description:Purpose: Little is known about the interplay of driver mutations that never co-occur within the same cancer cells. The latter scenario has been identified in prostate cancer where recurrent gene fusions involving the oncogenic ERG transcription factor and point mutations in the ubiquitin ligase adaptor SPOP are strictly mutually exclusive. We show that ERG and mutant SPOP – even though oncogenic on their own – are together synthetic sick. Description: RNA-Seq of lentiviral-transduced VCaP cells with stable knockdown of wild type SPOP (2 x hairpins) or stable overexpression of either wild-type or mutant SPOP (Y87C, F102C, W131G).

2020-12-05 | E-MTAB-7165 | biostudies-arrayexpress

Identification of ZMYND11 binding sites in VCaP cells with stable overexpression of either mutant (Y87C) or wild-type SPOP

Project description:Identification of ZMYND11 binding sites in VCaP cells with stable overexpression of either mutant (Y87C) or wild-type SPOP

| PRJEB28578 | ENA

E3 ligase substrate adaptor SPOP fine tunes the UPR of pancreatic beta cells

Project description:The Cullin 3 E3 ligase adaptor protein, SPOP, targets proteins for ubiquitination and proteasomal degradation. We previously established the β cell transcription factor (TF) and human diabetes gene PDX1 as an SPOP substrate, suggesting a functional role for SPOP in the β cell. Here, we generated a β cell specific Spop deletion mouse strain (SpopβKO) and found that Spop is necessary to prevent aberrant basal insulin secretion and for maintaining glucose- stimulated insulin secretion (GSIS) through impacts on glycolysis and glucose-stimulated calcium flux. Integration of proteomic, TF-regulatory gene network and biochemical analyses identified XBP1 as a functionally important SPOP substrate in pancreatic β cells.Further, loss of SPOP strengthened the IRE1α-XBP1 axis of unfolded protein response (UPR) signaling. ER stress promoted proteasomal degradation of SPOP, supporting a model whereby SPOP fine-tunes XBP1 activation during the UPR. These results position SPOP as a regulatorof β cell function and proper UPR activation.

2024-11-12 | PXD052527 | Pride

Effects of SPOP on gene expression in prostate cancer

Project description:SPOP is a ubiquitin ligase adaptor frequently mutated in prostate cancer. It is involved in ubiquitination and degradation of substrate proteins. We examined the impact of wild-type and mutant SPOP on the transcriptional profile of prostate cancer cells. We cloned several naturally occurring (in human prostate cancer) SPOP mutants and expressed the corresponding constructs in prostate cancer cells. Our experimental conditions were: Human prostate cancer cells (LNCaP-Abl), transfected with control vector, SPOP-wt, and any of the following mutants: SPOP-F102C, SPOP-F133V, SPOP-F133L (2-4 biological replicates each). We analyzed their gene expression profiles for differences induced by SPOP-wt vs SPOP-mutant.

2014-10-10 | E-GEOD-59432 | biostudies-arrayexpress

Stable overexpression and knockdown of mutant- or wild type SPOP in VCaP prostate cancer cells

Project description:Stable overexpression and knockdown of mutant- or wild type SPOP in VCaP prostate cancer cells

| PRJEB28337 | ENA

Gene Expression Profiling of SPOP Knocked Down Cell

Project description:SPOP is one of the most frequent mutated genes in prostate cancer. In the current study, we identified CCNE1 as its substrate. SPOP directly interacts with CCNE1, poly-ubiquitinates CCNE1 in vivo and in vitro, and represses cancer-related phenotypes induced by CCNE1 expression. Thus, we reveal a new mechanism for SPOP in repressing prostate cancer tumorigenesis.

2018-10-03 | GSE100743 | GEO

Effects of SPOP on gene expression in prostate cancer

2014-10-10 | GSE59432 | GEO

Stable overexpression of either mutant- or wild type SPOP in presence/absence of ΔERG in LNCaP prostate cancer cells

Project description:Purpose: Little is known about the interplay of driver mutations that never co-occur within the same cancer cells. The latter scenario has been identified in prostate cancer where recurrent gene fusions involving the oncogenic ERG transcription factor and point mutations in the ubiquitin ligase adaptor SPOP are strictly mutually exclusive. We show that ERG and mutant SPOP – even though oncogenic on their own – are together synthetic sick. Description: LNCaP cells in presence/absence of stable ΔERG overexpression, were infected with lentivirus to overexpress either wild-type or mutant SPOP (Y87C, F102C, W131G, F133S).

2020-12-10 | E-MTAB-7170 | biostudies-arrayexpress

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