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Links from GEO DataSets

Items: 20

1.

N6-methyladenosine mRNA Modification Is Essential for Human Pancreatic Lineage Specification

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platforms:
GPL20795 GPL24676
44 Samples
Download data: TXT
Series
Accession:
GSE163964
ID:
200163964
2.

N6-methyladenosine mRNA Modification Is Essential for Human Pancreatic Lineage Specification [m6A-Seq]

(Submitter supplied) Recent advances in pancreatic differentiation from human pluripotent stem cells (hPSCs) hold great potentials for disease modeling and regenerative medicine, and more precise control over the dynamic differentiation process is critical. N6-methyladenosine (m6A) is the most prevalent internal messenger RNA (mRNA) modification, while the roles of m6A mark in pancreatic differentiation and development remain elusive. more...
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL20795
24 Samples
Download data: TXT
Series
Accession:
GSE163963
ID:
200163963
3.

N6-methyladenosine mRNA Modification Is Essential for Human Pancreatic Lineage Specification [RNA-Seq]

(Submitter supplied) Recent advances in pancreatic differentiation from human pluripotent stem cells (hPSCs) hold great potentials for disease modeling and regenerative medicine, and more precise control over the dynamic differentiation process is critical. N6-methyladenosine (m6A) is the most prevalent internal messenger RNA (mRNA) modification, while the roles of m6A mark in pancreatic differentiation and development remain elusive. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
20 Samples
Download data: TXT
4.

The role of ALKBH5 in maternal RNA decay during mammalian oocyte meiosis [RNA-seq]

(Submitter supplied) To investigate the function of ALKBH5 in the regulation of maternal RNA decay during mice oocyte meiosis, we established Alkbh5 knockout mice and analyzed the transcriptome changes between control and Alkbh5 knockout oocyte at different meiotic maturation stages
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
12 Samples
Download data: TXT
Series
Accession:
GSE229774
ID:
200229774
5.

The role of ALKBH5 in maternal RNA decay during mammalian oocyte meiosis

(Submitter supplied) To investigate the function of ALKBH5 in the regulation of maternal RNA decay during mice oocyte meiosis, we established Alkbh5 knockout mice and analyzed the m6A level changes between control and Alkbh5 knockout oocyte at GV stage
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: TXT
Series
Accession:
GSE229771
ID:
200229771
6.

TimeLapse-seq reveals that ALKBH5 modulates RNA stability of metabolic transcripts

(Submitter supplied) N6-methyadenosine (m6A) RNA modification controls numerous cellular processes through regulation of RNA stability and translational efficiency. Whether the RNA m6A modification regulates energy metabolism process by posttranscriptional regulation is unknown. We here show that loss of the m6A demethylase ALKBH5 results in instability of oxogluatarate-dehydrogenase (Ogdh) messenger RNA and transcripts of other metabolic enzymes.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
8 Samples
Download data: BEDGRAPH, CSV
Series
Accession:
GSE194148
ID:
200194148
7.

Mapping the targeting transcripts and binding sites of ALKBH5 by individual-nucleotide resolution UV crosslinking and immunoprecipitation-based sequencing (iCLIP-seq)

(Submitter supplied) To investigate whether the ALKBH5-mediated metabolic changes via demethylation of its target mRNA(s) is important in regulating viral response, we mapped the targeting transcripts and binding sites of ALKBH5 in the virus infected cells and uninfected cells by using iCLIP-seq. Biological replicates of iCLIP-seq confirmed that OGDH is the direct targeting transcript of ALKBH5 and the binding capacity of ALKBH5 to OGDH mRNA was decreased upon viral infection. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL17021
4 Samples
Download data: BED
Series
Accession:
GSE134754
ID:
200134754
8.

Next Generation Sequencing Analysis of the Transcriptomes of Wild Type and ALKBH5-/- Peritoneal Macrophages

(Submitter supplied) By performing RNA sequencing (RNA-seq) analysis on the peritoneal macrophages that derived from ALKBH5-/- mice and littermate mice infected with or without vesicular stomatitis virus (VSV), we want to investigate whether deficiency of ALKBH5 controls viral replication through a more general mechanism such as enhancing innate response, and if not, what's the critical downstream target(s) of ALKBH5. RNA-seq analysis showed that mRNA expression of innate genes remained unchanged or not increased in ALKBH5-deficient cells. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
12 Samples
Download data: TXT
Series
Accession:
GSE127739
ID:
200127739
9.

Transcriptome-wide m6A Methylation Profiling of Wild Type and ALKBH5-/- Peritoneal Macrophages by m6A-seq

(Submitter supplied) By performing m6A-seq analysis on the peritoneal macrophages that derived from ALKBH5-/- mice and littermate mice infected with or without vesicular stomatitis virus (VSV), we want to investigate whether ALKBH5 deficiency-mediated m6A RNA methylation contributes to the regulation of its target genes expression. m6A-seq analysis revealed enriched and specific m6A peaks on the transcript of ALKBH5-targeted gene, which were substantially increased in ALKBH5-deficient peritoneal macrophages than that in wild-type cells whatever infected with or without VSV. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
16 Samples
Download data: BED
Series
Accession:
GSE127732
ID:
200127732
10.

ALKBH5

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24247 GPL24676
8 Samples
Download data
Series
Accession:
GSE224652
ID:
200224652
11.

Effect of depletion of ALKBH5 on transcriptional landscape in bone marrow neutrophils from septic mice

(Submitter supplied) By performing RNA-seq analysis on bone marrow neutrophils from the Alkbh5-deficient mice and Wild-type littermates undergoing CLP-induced sepsis, we want to investigate the effect of ALKBH5 on transcriptional landscape of mouse bone marrow neutrophils during bacterial infection. Then, we performed gene expression profiling and Gene Ontology enrichment analysis of the significantly differentially expressed genes using data obtained from RNA-seq.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: TXT
Series
Accession:
GSE224651
ID:
200224651
12.

Effect of depletion of ALKBH5 on transcriptional landscape in human neutrophils during bacterial infection

(Submitter supplied) By performing RNA-seq analysis on ALKBH5-deficient (ALKBH5-/-, KO) and Wild-type (WT) dHL-60 human neutrophils infected with Escherichia coli, we want to investigate the effect of ALKBH5 on transcriptional landscape of human neutrophils during bacterial infection. Then, we performed gene expression profiling and Gene Ontology enrichment analysis of the significantly differentially expressed genes using data obtained from RNA-seq.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
4 Samples
Download data: TXT
Series
Accession:
GSE224650
ID:
200224650
13.

Transcriptome-wide m6A Methylation Profiling of dHL-60 human neutrophils by m6A-seq

(Submitter supplied) By performing m6A-seq analysis on dHL-60 human neutrophils infected with Escherichia coli, we want to identify the m6A methylation pattern in neutrophils after bacteria challenge. m6A-seq analysis revealed that the consensus m6A motifs were most significantly enriched within the m6A peaks with typical m6A peak distribution features, and m6A methylation sites were located primarily in the protein coding sequence region and 3′ untranslated region of mRNA transcripts, in neutrophils with bacterial infection. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL24676
4 Samples
Download data: TXT
Series
Accession:
GSE201060
ID:
200201060
14.

ALKBH5 K235 acetylation regulates the RNA m6A profiles

(Submitter supplied) We performed the transcripome-wild m6A-sequencing to compare the m6A profiles of negative control (NC) HeLa cells and ALKBH5 KO HeLa cells stably re-expressing wild type ALKBH5 (WT) or its mutant K235R (K235R)
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: XLSX
15.

ALKBH5-mediated m6A modification of 5-HT3A mRNA in primary sensory neurons promotes neuropathic pain behaviors

(Submitter supplied) trigeminal-mediated nerve injury increases the expression of the m6A demethylase ALKBH5 in the injured TG, which elevates the level of 5-HT3A in TG and induces pain-related behaviors.
Organism:
Rattus norvegicus
Type:
Expression profiling by high throughput sequencing; Other
Platform:
GPL25947
12 Samples
Download data: XLSX
Series
Accession:
GSE226989
ID:
200226989
16.

Chromatin state maintains human myeloid leukemia by regulating m6A demethylase ALKBH5 expression [Slam-seq]

(Submitter supplied) ALKBH5 is the RNA N(6)-methyladenosine (m6A) demethylase. To understhand the function and mechnism of ALKBH5 in human acute myeloid leukemia, we compared the RNA decay rate in wild-type and ALKBH5-knock-down THP1 cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20795
16 Samples
Download data: CSV
Series
Accession:
GSE146874
ID:
200146874
17.

Chromatin state maintains human myeloid leukemia by regulating m6A demethylase ALKBH5 expression [Ribo-seq]

(Submitter supplied) ALKBH5 is the RNA N(6)-methyladenosine (m6A) demethylase. To understhand the function and mechnism of ALKBH5 in human acute myeloid leukemia, we compared the translational efficiency in wild-type and ALKBH5-knock-down THP1 cells.
Organism:
Homo sapiens
Type:
Other
Platform:
GPL20795
8 Samples
Download data: XLSX
Series
Accession:
GSE146849
ID:
200146849
18.

Chromatin state maintains human myeloid leukemia by regulating m6A demethylase ALKBH5 expression [ATAC-seq]

(Submitter supplied) ALKBH5 is the RNA N(6)-methyladenosine (m6A) demethylase. To understhand the function and mechnism of ALKBH5 in human acute myeloid leukemia, we compared the translational efficiency in wild-type and ALKBH5-knock-down MOLM-13 cells.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
2 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE146831
ID:
200146831
19.

Chromatin state maintains human myeloid leukemia by regulating m6A demethylase ALKBH5 expression

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Other
Platforms:
GPL20795 GPL24676
38 Samples
Download data: BIGWIG, BW, NARROWPEAK, TSV
Series
Accession:
GSE128575
ID:
200128575
20.

Chromatin state maintains human myeloid leukemia by regulating m6A demethylase ALKBH5 expression [RNA-Seq]

(Submitter supplied) ALKBH5 is the RNA N(6)-methyladenosine (m6A) demethylase. To under sthand the function and mechnism of ALKBH5 in human acute myeloid leukemia, we compared the m6A profiling in wild-type, ALKBH5-knock-down, and ALKBH5 rescue THP1 cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20795
6 Samples
Download data: TSV
Series
Accession:
GSE128574
ID:
200128574
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