Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Maternal DBP exposure promotes synaptic formation in offspring by activiting astrocytes via AKT/NF-κB/IL-6/JAK2/STAT3 signaling pathway

ABSTRACT: Maternal DBP exposure promotes synaptic formation in offspring by activiting astrocytes via AKT/NF-κB/IL-6/JAK2/STAT3 signaling pathway

PROVIDER: PRJNA779982 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16930984_1.fastq.gz	Fastqsanger.gz
	SRR16930984_2.fastq.gz	Fastqsanger.gz
	SRR16930985_1.fastq.gz	Fastqsanger.gz
	SRR16930985_2.fastq.gz	Fastqsanger.gz
	SRR16930986_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Maternal DBP exposure promotes synaptic formation in offspring by activiting astrocytes via AKT/NF-κB/IL-6/JAK2/STAT3 signaling pathway

Project description:In summary, we revealed that maternal DBP exposure activated astrocytes through the AKT/NF-κB/IL-6/JAK2/STAT3 signaling pathway and up-regulated the expression of TSP1, which then affected the density and morphology of dendritic spines and synaptic formation of hippocampal neurons, ultimately leading to decreased autonomy and exploration behavior of offspring.

2023-11-11 | GSE188707 | GEO

Interleukin-17 activates JAK2/STAT3, PI3K/Akt and nuclear factor-κB signaling pathway to promote the tumorigenesis of cervical cancer.

Project description:Interleukin (IL)-17 has been regarded as a significant factor in inflammation. In addition, IL-17 is known to be involved in the progression of cancers; however, the function of IL-17 in cervical cancer remains unclear. In the present study, cell viability was detected by Cell Counting Kit-8 assay. Quantitative PCR and western blotting were performed to detect gene and protein expression levels, respectively, in cancer cells or tissues. Ki-67 staining was used to evaluate cell proliferation. Wound-healing assay was used to detect cell migration. Moreover, Transwell assay was performed to investigate the invasion of cervical cancer cells. The results revealed that IL-17 significantly promoted the proliferation of cervical cancer cells. Additionally, IL-17 notably enhanced the migration and invasion of cervical cancer cells in vitro. IL-17 promoted the progression of cervical cancer via the activation of JAK2/STAT3 and PI3K/Akt/NF-κB signaling. In conclusion, IL-17 was a key regulator during the progression of cervical cancer through the JAK2/STAT3 and PI3K/Akt/nuclear factor-κB signaling pathway, which may serve as a novel target for the treatment of cervical cancer.

| S-EPMC8461522 | biostudies-literature

TEL-JAK2 dependent transcriptome

Project description:TEL-JAK2 is a fusion oncogene resulting from a t(9;12) chromosomal translocation in T-ALL, translated as a constitutively activated TEL-JAK2 tyrosine kinase. Mice carrying a TEL-JAK2 transgene develop T-ALL. Gene deregulated in TEL-JAK2 T-ALL cells as compared to mouse thymocytes were identified Leukemic cells were collected from the thymus of terminally-ill TEL-JAK2 mice; thymocytes were collected from the thymus of 2 months-old mice. All mice on C57B/6 background. RNA was extracted from each sample and processed for hybridization to Affymetrix arrays.

2013-09-28 | E-GEOD-51241 | biostudies-arrayexpress

Transcriptomic profile of reactive astrocytes induced by activation of the JAK2-STAT3 pathway in mouse striatal astrocytes

Project description:We analyzed the transcriptional profile of normal astrocytes and astrocytes made reactive by AAV gene transfer of a contitutive form of JAK2 (JAK2ca). We show that activation of the JAK2-STAT3 pathway by JAK2ca induces significant transcriptional changes in astrocytes, recapitulating several molecular hallmarks of reactivity

2022-06-29 | GSE107486 | GEO

TEL-JAK2 dependent transcriptome

2013-09-28 | GSE51241 | GEO

SPAG9-JAK2 gene expression array in Ba/F3 cells

Project description:SPAG9-JAK2 is a novel fusion gene identified in a pediatric patient with Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL). In this study, we performed functional analysis of the SPAG9-JAK2 fusion to establish molecular targeted therapy. Ba/F3 cells expressing SPAG9-JAK2 generated by retroviral transduction (Ba/F3-SPAG9-JAK2), proliferated in the absence of IL-3, and exhibited constitutive phosphorylation of the tyrosine residues in the JAK2 kinase domain of the fusion protein and STAT3/STAT5. Mutation of tyrosine residues in the JAK2 kinase domain (SPAG9-JAK2 mut) abolished IL-3 independence, but had no influence on STAT3/STAT5 phosphorylation levels. Gene expression analysis revealed that Stat1 was significantly up-regulated in Ba/F3-SPAG9-JAK2 cells. STAT1 was also phosphorylated in Ba/F3-SPAG9-JAK2 but not SPAG9-JAK2 mut cells, suggesting that STAT1 is key for SPAG9-JAK2-mediated cell proliferation. Consistently, STAT1 induced expression of the anti-apoptotic proteins, BCL-2 and MCL-1, as did SPAG9-JAK2, but not SPAG9-JAK2 mut. Ruxolitinib abrogated Ba/F3-SPAG9-JAK2-mediated proliferation in vitro, but was insufficient in vivo. Venetoclax (a BCL-2 inhibitor) or AZD5991 (an MCL-1 inhibitor) enhanced the effects of ruxolitinib on Ba/F3-SPAG9-JAK2 in vitro. These findings suggest that activation of the JAK2-STAT1-BCL-2/MCL-1 axis contributes to SPAG9-JAK2-related aberrant growth promotion. BCL-2 or MCL-1 inhibition is a potential therapeutic option for B-ALL with SPAG9-JAK2 fusion.

2021-05-18 | GSE174578 | GEO

Jak2

Project description:Rattus norvegicus Jak2, Janus kinase 2 [Source:RGD Symbol;Acc:2939], is expressed in 6 baseline experiment(s);

| ENSRNOG00000059968 | ExpressionAtlas

Jak2

Project description:Rattus norvegicus Jak2, Janus kinase 2 [Source:RGD Symbol;Acc:2939], is differentially expressed in 28 experiment(s);

| ENSRNOG00000059968 | ExpressionAtlas

JAK2

Project description:Monodelphis domestica JAK2, Janus kinase 2 [Source:NCBI gene;Acc:100017930], is expressed in 2 baseline experiment(s);

| ENSMODG00000015373 | ExpressionAtlas

Splicing factor Ybx1 maintains persistent Jak2-mutated neoplasms via Mknk1-ERK-signaling

Project description:Janus kinases (Jak) mediate cytokine, hormone and growth factor responses in hematopoietic cells. Jak2 is one of the most frequently mutated genes in the aging hematopoietic system and in hematopoietic cancers. Mutations in Jak constitutively activate downstream signaling and are drivers of myeloproliferative neoplasms (MPN). In clinical use, Jak-inhibitors have incomplete effects on overall disease burden of Jak2 mutated clones, prompting us to investigate the mechanism underlying disease persistence. By in-depth phospho-proteome profiling we here identify proteins involved in mRNA processing as targets of mutant Jak2. Inactivation of the post-translationally modified Jak2-target Ybx1 sensitizes Jak-inhibitor persistent cells to apoptosis and results in RNA mis-splicing, retained intron enrichment and disruption of the transcriptional control of extracellular signal-regulated kinase (ERK) signaling. In combination with pharmacological Jak-inhibition it induces apoptosis in Jak2-dependent murine and primary human cells, leading to in vivo regression of the malignant clones and inducing remission. This identifies and validates a novel cell-intrinsic mechanism how differential protein phosphorylation results in splicing-dependent alterations of Jak2-ERK-signaling and the maintenance of Jak2V617F malignant clones. Therapeutic targeting of Ybx1 dependent ERK-signaling in combination with Jak2-inhibition may eradicate Jak2-mutated cells.

2020-08-20 | PXD006921 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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