E-MTAB-7451
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-7451 | ExpressionAtlas | 2021-01-19
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Dis3L2 regulates cell proliferation and tissue growth through a conserved mechanism
| PRJEB42162 | ENA
Project description:METTL6 is a tRNA m3C methyltransferase that regulates translation and tumor cell proliferation
2020-12-09 | E-MTAB-8872 | ExpressionAtlas
Project description:Nkx6.1 regulates islet beta-cell proliferation via Nr4a1 and Nr4a3 nuclear receptors
2015-08-04 | E-GEOD-55077 | ExpressionAtlas
Project description:The exosome-independent exoribonuclease DIS3L2 is mutated in Perlman syndrome. Here we used extensive global transcriptomic and targeted biochemical analyses to identify novel DIS3L2 substrates in human cells. We show that DIS3L2 regulates pol II transcripts, comprising selected canonical and histone-coding mRNAs, and a novel FTL_short RNA from the ferritin mRNA 5' UTR. Importantly, DIS3L2 contributes to surveillance of pre-snRNAs during their cytoplasmic maturation. Among pol III transcripts, DIS3L2 particularly targets vault and Y RNAs and an Alu-like element BC200 RNA, but not Alu repeats, which are removed by exosome-associated DIS3. Using 3' RACE-Seq, we demonstrate that all novel DIS3L2 substrates are uridylated in vivo by TUT4/TUT7 poly(U) polymerases. Uridylation-dependent DIS3L2-mediated decay can be recapitulated in vitro, thus reinforcing the tight cooperation between DIS3L2 and TUTases. Together these results indicate that catalytically inactive DIS3L2, characteristic of Perlman syndrome, can lead to deregulation of its target RNAs to disturb transcriptome homeostasis. To investigate DIS3L2 functions genome-wide, total RNA samples were collected from model cell lines producing either WT or mut DIS3L2 three days after induction with doxycycline. The RNA samples were rRNA-depleted before preparation of strand-specific total RNA libraries according to the standard TruSeq (Illumina) protocol. TruSeq library preparation favours RNA molecules longer than 200 nt, and shorter transcripts are suboptimal for sequencing via this protocol. Thus, to obtain information about potential DIS3L2 RNA substrates with lengths between 20 and 220 nt, another RNA-Seq was carried out in parallel (with size selection through gel purification). The stable inducible HEK293 cell lines producing DIS3L2 variants were obtained using âpAL_01â and âpAL_02â plasmid constructs and the Flp-In⢠T-REx⢠system according to the manufacturerâs guidelines. âpAL_01â and âpAL_02â plasmids are vectors for co-expression of recoded C-terminal FLAG-tagged DIS3L2 [wild type (WT) variant or its catalytic mutant counterpart (mut), respectively] and sh-miRNAs directed against endogenous DIS3L2 mRNA.
2016-07-19 | E-GEOD-82336 | biostudies-arrayexpress
Project description:Using conditional knockout mice model, here we report the essential role of DIS3L2 in regulating male germline proliferation, growth and differentiation to ensure male fertility. We document that DIS3L2 is essential for spermatogonial homeostasis. DIS3L2-specific deletion in spermatogonia results in the reduction of the undifferentiated spermatogonial population and the block in transition to the differentiating stage in postnatal testes.
2021-07-15 | GSE160104 | GEO
Project description:Protein Kinase C alpha (PKC) is a critical mediator of cell signaling and cancer growth. We show that PKC inhibitors decrease proliferation in squamous cell carcinoma of the head and neck (SCCHN) cells and abrogate growth of SCCHN tumors in mouse xenografts. Analysis of gene expression arrays reveals that PKC regulates cell cycle genes required for DNA synthesis. In particular, PKC increases cyclin E protein expression, cyclinE/cdk2 complex formation, and transcription of cyclin E and E2F target genes. Consistent with this mechanism, expression of cyclin E rescues the block in DNA synthesis caused by PKC inhibition. In SCCHN tissue, PKC and cyclin E expression increase progressively from normal and dysplastic to malignant human head and neck tissue. Furthermore, PKCÂ expression correlates with poor prognosis in SCCHN. These results demonstrate that PKC regulates growth by stimulating DNA synthesis through cyclin E and E2F and identify PKC as a therapeutic target that is highly expressed in aggressive SCCHN. Experiment Overall Design: 9 samples composed of treated replicates at three time points
2009-03-28 | E-GEOD-10299 | biostudies-arrayexpress
Project description:AtPRMT5 regulates shoot regeneration through modulating multiple genes expression analyzed by RNA-seq
2016-12-15 | E-MTAB-5044 | ExpressionAtlas
Project description:DIS3-like 3'-5' exoribonuclease 2 (DIS3L2) degrades aberrant RNAs, however, its function in tumorigenesis remains largely unexplored.hnRNP U regulates the alternative splicing of pre-mRNA, and our results also showed that RNA promoted the interaction between DIS3L2 and hnRNP U, suggesting that DIS3L2 may be involved in splicing regulation. Thus, we next performed RNA-Seq to investigate whether DIS3L2 regulated pre-mRNA alternative splicing in cancer cells.
2020-01-01 | GSE133759 | GEO
Project description:The exosome-independent exoribonuclease DIS3L2 is mutated in Perlman syndrome. Here we used extensive global transcriptomic and targeted biochemical analyses to identify novel DIS3L2 substrates in human cells. We show that DIS3L2 regulates pol II transcripts, comprising selected canonical and histone-coding mRNAs, and a novel FTL_short RNA from the ferritin mRNA 5' UTR. Importantly, DIS3L2 contributes to surveillance of pre-snRNAs during their cytoplasmic maturation. Among pol III transcripts, DIS3L2 particularly targets vault and Y RNAs and an Alu-like element BC200 RNA, but not Alu repeats, which are removed by exosome-associated DIS3. Using 3' RACE-Seq, we demonstrate that all novel DIS3L2 substrates are uridylated in vivo by TUT4/TUT7 poly(U) polymerases. Uridylation-dependent DIS3L2-mediated decay can be recapitulated in vitro, thus reinforcing the tight cooperation between DIS3L2 and TUTases. Together these results indicate that catalytically inactive DIS3L2, characteristic of Perlman syndrome, can lead to deregulation of its target RNAs to disturb transcriptome homeostasis.
2016-07-19 | GSE82336 | GEO
Project description:Thioredoxin DCC1 regulates shoot regeneration through modulating multiple genes expression by RNA-seq analyses in Arabidopsis
2016-12-15 | E-MTAB-5236 | ExpressionAtlas