Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression following: RNAi knockdown of grappa, lilliputian, or Suppressor of Triplolethal; induction of Cyclin-dependent kinase 9 dominant negative constructs, or ectopic expression of stand still in Drosophila melanogaster.

ABSTRACT: We report the transcriptional profiling of Drosophila melanogaster gonadectomized adults following RNAi knockdown of grappa (gpp), lilliputian (lilli), or Suppressor of Triplolethal [Su(Tpl)], as well as induction of Dominant Negative (DN) allele of Cyclin-dependent kinase 9 (Cdk9), or ectopic expression of stand still (stil), with a three-component temperature sensitive system. We also included the transcriptional profiling of testes and ovaries of gppRNAi, lilliRNAi, and Su(Tpl)RNAi flies under permissive temperature. All data includes induced and non-induced sham controls.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE77492 | GEO | 2016/09/22

SECONDARY ACCESSION(S): PRJNA310631

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide DNA-binding analysis for Ttk in intestinal progenitor cells and Su(H) in wildtype, seq overexpressed and ttk-RNAi intestinal progenitor cells by DamID

Project description:Purpose: Genome-wide DNA-binding analysis for Ttk in intestinal progenitor cells and comparing Su(H) binding sites between seq overexpressed and ttk-RNAi intestinal progenitor cells in Drosophila midgut by DNA adenine methyltransferase identification(DamID) Methods: Dam(Ctrl) , Ttk-Dam transgenes, Su(H)-Dam, Su(H)-Dam&seq and Su(H)-Dam&ttk-RNAi were expressed in intestinal progenitor cells by esg-Gal4.The guts within 2 days was used for DNA adenine methyltransferase identification (DamID), followed by deep sequencing analysis Results: Ttk suppresses neural specific Notch targets through suppressing Seq in intestinal progenitor cells

2021-02-23 | GSE130941 | GEO

Drosophila melanogaster

Project description:CUT&RUN, Genome-wide DNA binding analysis of Stand still (Stil) in Drosophila melanogaster

| PRJDB11664 | ENA

mTOR signaling pathway and targeting c-myc

Project description:Purpose: To investigate the tumor-promoting role of STIL in bladder cancer. Method: We established the STIL knockout cell line in which the target gene was knocked out by sgRNA. RNA was extracted from cells using trizol reagent(Invitrogen) Result: Through RNA-sequencing analysis of wild-type and STIL-deficient UMUC3 cell lines, the downstream signaling pathways that STIL may be involved in were determined. We found that the PI3K/AKT/mTOR signaling pathway and c-myc were significantly inactivated when STIL was knocked out in bladder cancer. Our RNA-sequencing analysis results showed that the downstream molecules of c-myc (MCM4, HSPD1, EIF2S2, DDX21, DDX18, CBX3, ABCE1) were significantly down-regulated in bladder cancer cells after knockout. Conclusion: STIL enhances the PI3K/AKT/mTOR pathway, which consequently upgraded the expression of c-myc, ultimately promoting the occurrence and progression of bladder cancer C. STIL may suggest potential utility for bladder cancer therapy.

2023-08-01 | GSE211756 | GEO

Transcriptomic analysis of low-density neutrophils (LDNs) in acute generalized pustular psoriasis (GPP)

Project description:Generalized pustular psoriasis (GPP) is a severe disease featured by neutrophilic pustules and enhanced IL-36 inflammatory pathway in skin. Recently, a transcriptomic analysis of PBMCs and neutrophils in MPO-deficient GPP patients has been performed in stable disease state. However, transcriptomic profiling of PBMCs during acute flare of GPP is unclear. Here, we reported a predominant neutrophil signature in GPP PBMC and a marked increase in the CD66+CD16+ low-density neutrophils (LDNs) within the PBMC fraction of acute GPP patients. Transcriptomic and functional analysis of LDNs revealed a hypoinflammatory phenotype yet enhanced release of neutrophil granule proteases, implicating that LDNs might contribute to the IL-36-mediated inflammation in GPP patients.

2022-04-18 | GSE200836 | GEO

A distinct immature low-density neutrophil population characterizes acute generalized pustular psoriasis [PBMC]

2022-04-20 | GSE200977 | GEO

NINJA connects JAZ proteins to the co-repressor TOPLESS

Project description:NINJA (At4g28910) and TOPLESS proteins function as negative regulators of jasmonate responses. Our results point to TPL proteins as general co-repressors that affect multiple signalling pathways through the interaction with specific adaptor proteins. This new insight reveals how stress- and growth-related signalling cascades use common molecular mechanisms to regulate gene expression in plants. Two-condition experiment, Col-0 vs. plants silencing NINJA (RNAi-NINJA) and both Col-0 vs RNAi NINJA treated with coronatine . Biological replicates: 4 control replicates untreated , 4 RNAi NINJA untreated replicates, 4 control treated replicates and 4 RNAi NINJA treated replicates

2010-04-05 | E-GEOD-19455 | biostudies-arrayexpress

Comparison of healthy, plaque psoriasis and pustular psoriasis FFPE skin biopsies

Project description:Generalized pustular psoriasis (GPP) is a rare, debilitating, and often life-threatening inflammatory disease characterized by episodic infiltration of neutrophils into the skin, pustule development, and systemic inflammation, which can manifest in the presence or absence of chronic plaque psoriasis (PV). Current treatments are unsatisfactory thus a better understanding the pathogenesis of GPP is warranted. To assess the pathophysiological differences between GPP and PV we performed a gene expression study on formalin-fixed paraffin-embedded biopsies of GPP (n=30) and PV (n=12) lesions and healthy control (n=20) skin. Compared with healthy skin, GPP lesions yielded 365 and PV 898 differentially expressed genes respectively, with 190 upregulated in both diseases. We detected higher expression of IL-1 and IL-36 cytokines in GPP lesions compared with PV, and this occurred proximal to neutrophils. We show both activated neutrophils and isolated neutrophil proteases can activate IL-36. Diverging from the Th1/Th17 pathophysiology of PV, significantly fewer IL23A, IL17A, IFNG, CXCL9, CXCL10 and MX1 transcripts were detected in GPP lesions. Our data indicate a level of sustained activation of IL-1 and IL-36 in GPP, inducing neutrophil chemokine expression, infiltration and pustule formation, suggesting that the IL-1 and IL-36 inflammatory axes are the main drivers of disease pathology in GPP.

2017-01-27 | GSE79704 | GEO

MEK-dependent and -independent signaling events downstream of Tpl-2

Project description:Comparison of Tpl-2 small molecule inhibitor (SMI) versus MEK SMI activities in LPS-treated human monocytes will reveal a subset of genes that require Tpl-2 but are independent of MEK. Tpl-2 is a highly conserved (94% human versus mouse) serine-threonine kinase expressed in cells important to the inflammatory response, including monocytes, macrophages, dendritic cells, and B/T cells. The role of Tpl-2 in monocytes and macrophages has been especially well-studied. It has been shown in these cells that Tpl-2 is required for the expression of cytokines in response to Toll-like receptor ligands, including LPS. In resting cells, Tpl-2 forms a complex with p105 and ABIN-2. Upon stimulation, this complex dissociates. Dissociated p105 is processed to p50, which impacts transcription. Dissociated Tpl-2 phosphorylates MEK, which, in turn, phosphorylates ERK. ERK activates the transcription factor AP-1 and its downstream gene targets. An open question in the field is whether Tpl-2 acts solely through MEK to drive gene expression, or does Tpl-2 have any MEK-independent targets. Answering this question is important both for understanding basic Tpl-2 biology as well as its role in disease. Based on published data, Tpl-2 is important for inflammatory cytokine production, and in animal models where these cytokines contribute to disease (septic shock, IBD), blocking Tpl-2 ameliorates disease symptoms. We have a highly selective SMI of Tpl-2 that effectively blocks cytokine production in purified human monocytes. This SMI can block production of the same cytokines that a MEK inhibitor blocks, which is expected given that Tpl-2 lies upstream of MEK. However, the MEK SMI only partially inhibits certain cytokines, while the Tpl-2 SMI fully blocks them, suggesting there are additional factors downstream of Tpl-2 that are not MEK-dependent.

2019-07-01 | GSE84161 | GEO

Tpl-2 small molecule project

Project description:Tpl-2 is a serine/threonine kinase that has been studied extensively in monocytes. Tpl-2 is believed to phosphorylate MEK1/2, which is upstream of ERK1/2, and regulates inflammatory gene expression in response to TLR and IL-1b receptor signaling. In the course of performing proof-of-concept studies using a small molecule inhibitor (SMI) of Tpl-2, we were surprised to see the inhibitor affect cytokine production in human neutrophils. Unlike human monocytes, which respond at least some degree to both Tpl-2 and MEK inhibitors, neutrophils showed a disconnect between Tpl-2 and MEK. A panel of genes in this cell type can be fully blocked by a Tpl-2 SMI, and yet show no response to a MEK SMI, suggesting Tpl-2 mediates its effect through substrates other than MEK.

2019-07-01 | GSE84153 | GEO

Adipose tissue of gonadectomized mice injected with dihydrotestosterone

Project description:Comparison of retroperitoneal adipose tissue of intact male mice and gonadectomized C57BL6 male mice. Gonadectomized mice were untreated or injected with dihydrotestosterone (DHT) and sacrificed 3 or 24 hours after injection. Keywords: other

2004-04-24 | GSE1091 | GEO

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