Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

16 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of human HT-29 WT and SMYD2-KO xenograft implanted into the flanks of Rag1−/− mice

ABSTRACT: Our data suggested that SMYD2 deficiency sensitized cells to apoptosis and necroptosis.To further narrow down the mechanism of cell death induction upon SMYD2 deficiency, RNA-seq analysis was performed on implanted tumor tissues from two clones of SMYD2 deficient and WT HT-29 cells.

INSTRUMENT(S): Illumina HiSeq 1500

ORGANISM(S): Homo sapiens

SUBMITTER: Yuqiang Yu

PROVIDER: E-MTAB-11053 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of mouse heart from mice with a SMYD2 heart-specific deletion

Project description:Effect of Smyd2 cardiac deficiency was analyzed in mouse heart

2010-04-12 | E-MEXP-2542 | biostudies-arrayexpress

The effects of SMYD2 overexpression on ectopic RB in SAOS cells

Project description:Expression analysis of wild-type SAOS cells and SAOS cells transiently transfected with RB, SMYD2, or RB and SMYD2.

2011-01-01 | GSE22842 | GEO

Genome-wide maps of chromatin state of Smyd2 binding in renal epithelial cells

Project description:To identify potential transcriptional targets of Smyd2, we performed ChIP-sequencing (ChIP-seq) analysis in renal epithelial cells with an anti-Smyd2 antibody. We identified 91 potential Smyd2 target genes in Pkd1 wild type MEK cells and 116 potential Smyd2 target genes in Pkd1 null MEK cells. There were 14 genes identified in both Pkd1 wild type and null MEK cells. Thus, the number of potential Smyd2 target genes in Pkd1 null MEK cells are 116 - 14 = 102 genes

2017-08-30 | GSE97708 | GEO

The effects of SMYD2 overexpression on ectopic RB in SAOS cells

Project description:Expression analysis of wild-type SAOS cells and SAOS cells transiently transfected with RB, SMYD2, or RB and SMYD2. Four samples of wild-type, rb1, smyd2 and rb1-smyd2 were analyzed on the Human Genome U133 Plus 2.0 array.

2011-01-01 | E-GEOD-22842 | biostudies-arrayexpress

Chip-chip from MDA-MB-231 cells with SMYD2 and EZH2

Project description:The histone methyl transferase EZH2 and SMYD2 are master epigenetic regulators involved in histone methylation and gene transcription repression. Here, we report that SMYD2 and EZH2 may act as a complex in transcriptional regulation and are involved in the progression of breast cancer. ChIP-on-chip assays were performed to find unique promoters co-targeted by EZH2 and SMYD2 in MDA-MB-231 cells.

2019-11-03 | GSE126055 | GEO

Transcription profiling of human embryonic kidney cells overexpressing SMYD2 to identify which genes are regulated by SMYD2 through its histone lysine methylation activity

Project description:Identification of SMYD2 target genes - The objective of this aim is to identify which genes are regulated by SMYD2 through its histone lysine methylation activity. It is well established that post-translational modification of nucleosomal histones (H2A, H2B, H3 and H4), such as methylation, acetylation and phosphorylation are central to the proper control of gene expression

2008-02-05 | E-MEXP-963 | biostudies-arrayexpress

SMYD2 specificly regulate BIX-01294 induced TP53 target genes revealed by RNA-Seq

Project description:We characterized expression profilings of SMYD2 knockdown and control cells treated by BIX-01294 and Rapamycin. We used siRNAs to knockdown SMYD2 in HCT116 cells, and NC as control. We treated those cell lines with BIX-01294 and Rapamycin, and the expression profilings were perfomed by Illumina high throughput sequencing.

2015-01-01 | E-GEOD-61255 | biostudies-arrayexpress

SMYD2 specificly regulate BIX-01294 induced TP53 target genes revealed by RNA-Seq

Project description:We characterized expression profilings of SMYD2 knockdown and control cells treated by BIX-01294 and Rapamycin.

2015-01-01 | GSE61255 | GEO

RNA-seq of human HT-29 WT and SMYD2-KO xenograft implanted into the flanks of Rag1−/− mice

Project description:RNA-seq of human HT-29 WT and SMYD2-KO xenograft implanted into the flanks of Rag1−/− mice

| PRJEB48141 | ENA

Methylation of the epigenetic regulator KMT2D by SMYD2 contributes to therapeutic response in hormone-dependent breast cancer [KMT2D_ChIP_seq]

Project description:Activating mutations in PIK3CA, the gene encoding PI3Kα, are frequently found in estrogen receptor (ER+) breast cancer and the combination of the PI3K inhibitor alpelisib with the anti-ER agent fulvestrant is approved for therapy. We have uncovered a key role for the chromatin modifier KMT2D in regulating the ER-PI3K crosstalk. PI3Kα effectors, AKT and SGK, negatively regulate KMT2D through S1331 phosphorylation. When PI3K is inhibited, this regulatory event is lost, leading to increased chromatin recruitment of KMT2D and an upregulation of ER-dependent transcription. Here we discovered a previously undescribed methylation site on KMT2D, at K1330 directly adjacent to S1331, catalyzed by the lysine methyltransferase SMYD2. SMYD2 loss attenuates alpelisib-induced KMT2D chromatin binding. Accordingly, loss of SMYD2 abrogates alpelisib-induced changes in gene expression, including ER-dependent transcription. Knockdown or pharmacological inhibition of SMYD2 sensitizes breast cancer cells, patient-derived organoids, and tumors to PI3K/AKT inhibition and endocrine therapy in part through KMT2D K1330 methylation. Methyl dead knock-in clones of KMT2D phenocopy many of the effects of SMYD2 inhibition on cell and tumor growth, drug response, and transcriptional output. Together, our findings uncover a regulatory cross-talk between posttranslational modifications that plays an important role in fine-tuning the functions of KMT2D at the chromatin. This provides a rationale for epigenetic therapy using SMYD2 inhibitors in combination with PI3Kα/AKT inhibitors for the treatment of ER+/PIK3CA mutant breast cancer.

2024-05-04 | GSE255295 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data