Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

37 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional profiling by array of wild-type vs TNIK-/- hippocampi in adult mice

ABSTRACT: Hippocampi from adult TNIK-/- and TNIK+/+ mice were dissected out, the mRNA extracted, and hybridized to arrays. The aim was to determine the extent and nature of differential expression in the mutant, particularly those changes which might be indicative of major physiological changes.

ORGANISM(S): Mus musculus

SUBMITTER: Nathan Skene

PROVIDER: E-MTAB-1202 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

TNiK is required for postsynaptic and nuclear signaling pathways and cognitive function.

Coba Marcelo P MP Komiyama Noboru H NH Nithianantharajah Jess J Kopanitsa Maksym V MV Indersmitten Tim T Skene Nathan G NG Tuck Ellie J EJ Fricker David G DG Elsegood Kathryn A KA Stanford Lianne E LE Afinowi Nurudeen O NO Saksida Lisa M LM Bussey Timothy J TJ O'Dell Thomas J TJ Grant Seth G N SG

The Journal of neuroscience : the official journal of the Society for Neuroscience 20121001 40

Traf2 and NcK interacting kinase (TNiK) contains serine-threonine kinase and scaffold domains and has been implicated in cell proliferation and glutamate receptor regulation in vitro. Here we report its role in vivo using mice carrying a knock-out mutation. TNiK binds protein complexes in the synapse linking it to the NMDA receptor (NMDAR) via AKAP9. NMDAR and metabotropic receptors bidirectionally regulate TNiK phosphorylation and TNiK is required for AMPA expression and synaptic function. TNiK ...[more]

PMID: 23035106

Similar Datasets

Transcriptome analysis of WT and gp91-/- mice infected with Salmonella enteric server Typhimurium

Project description:During an infection, bacteria are exposed to the complex host immune response and has to adapt to the changing environment in order to successfully grow within tissues. In the present sturdy we analysed the transcriptome of both host (mouse) and bacteria (Salmonella Typhimurium) at different time points during the infection to gain a better insight into the attack mounted by the host to repel the bacterial infection and how the bacteria adapts to it. For this, mice were infected intravenously with Salmonella Typhimurium and spleens were collected for RNA isolation at specific time points. Transcription profile of infected mice was compared to uninfected controls.

2018-02-01 | E-MTAB-5494 | biostudies-arrayexpress

Novel players in myogenesis identified by target validation for muscle specific microRNAs in C2C12 myoblasts

Project description:Search of novel miR-206 target genes in C2C12 cells, based on differential expression of transcripts containing putative miR-206 binding sites. miR-206 candidate target genes were hpothesized to be upregulated in AM206 vs Day2 sample and downregulated in siRNA vs Day 1 sample. total RNA extracted from various differentiation stages of C2C12 cells, as well as cells treated with miR-206 mimic or miR-206 inhibitor

2012-07-22 | E-GEOD-34069 | biostudies-arrayexpress

IL-17 downregulates filaggrin and affects epidermal barrier function gene expression; potential role in the pathogenesis of atopic eczema

Project description:Genome-wide analysis of gene expression after stimulation with cytokines to assess the main processes, molecular functions and cellular components affected as well as genes related to skin barrier function. HaCaT cells were exposed to IL-17A (200ng/ml) for 12h. The cells were lysed, total RNA was extracted and microarray study was performed on Illumina HT12 platform.

2012-11-01 | E-GEOD-27533 | biostudies-arrayexpress

ETV4 promotes metastasis in response to combined activation of PI3kinase and RAS signaling in a mouse model of advanced prostate cancer

Project description:Analysis of the transcriptome of mouse models of prostate cancer. NP (Nkx3.1CreERT2/+; Ptenfloxed/floxed) mice develop non-metastatic tumors while NPK (Nkx3.1CreERT2/+; Ptenfloxed/floxed; KrasG12D/+) mice develop metastatic tumors The NPK mice are also analyzed at early and late stages of tumorigenesis (1 vs. 3 months after induction) Total RNA obtained from prostate tumors of different genotypes and at different stages of dissease as indicated

2013-07-23 | E-GEOD-47697 | biostudies-arrayexpress

Cross-species analysis of genome-wide regulatory networks identifies a synergistic dependency between FOXM1 and CENPF that drives prostate cancer malignancy

Project description:Analysis of the transcriptome of mouse models of prostate cancer to assemble a mouse prostate cancer interactome. To assemble the mouse prostate cancer interactome, we collected 13 distinct mice or genetically-engineered mouse models (GEMMs), which together represent the full spectrum of prostate cancer phenotypes including: normal epithelium (i.e., wild-type), low-grade PIN (i.e., Nkx3.1 and APT), high-grade PIN and adenocarcinoma (i.e., APT-P; APC; Myc; NP; Erg-P; and NP53), castration-resistant prostate cancer (i.e., NP-AI), and metastatic prostate cancer (i.e., NPB; NPK; and TRAMP). To further enhance the heterogeneity afforded by this diversity of mouse models, we pharmacologically perturbed each GEMM using 13 different drugs (or appropriate vehicle). The resulting mouse prostate tissue/tumor dataset encompassed 384 expression profiles Total RNA obtained from prostate tumors/tissues of 13 mouse models of prostate cancer treated with 13 different drugs for 5 consecutive days. Prostate tumors/tissues were harvested and processed for RNA isolation and transcriptome analysis.

2014-05-12 | E-GEOD-53202 | biostudies-arrayexpress

Predicting drug response in human prostate cancer from preclinical analysis of in vivo mouse models (I)

Project description:Analysis of the transcriptome of mouse models of prostate cancer after treatment with rapamycin and PD0325901 combination therapy or standard of care docetaxel. The Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+ (NPK mice) was used in this study. Two months after tumor induction, mice were randomly assigned to vehicle (Veh) or treatments groups, such as rapamycin and PD0325901 (RAPPD) or docetaxel (Docetaxel). For the treatment groups mice were administered rapamycin (10 mg/kg) and PD0325901 (10 mg/kg) or docetaxel (10 mg/kg) for 5 days (SHORT) or for 1 month (LONG). At the end of the treatment, mice were euthanized, tumors harvested and snap frozen for subsequent molecular analysis. Total RNA obtained from prostate tumors/tissues. Prostate tumors/tissues were harvested and processed for RNA isolation and transcriptome analysis using the MagMAX RNA isolation kit (Ambion). Total RNA was amplified and labelled for subsequent microarrays hybridization using the Illumina TotalPrep RNA Amplification Kit.

2015-09-17 | E-GEOD-69211 | biostudies-arrayexpress

Predicting drug response in human prostate cancer from preclinical analysis of in vivo mouse models (II)

Project description:Analysis of the transcriptome of allografted mouse tumors after treatment with rapamycin and PD0325901. Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+ (NPK mice) were induced and their tumors removed to generate allograft lines by implanting a 1.5 mm3 tumor fragment in the subcutaneous space of athymic nude mice. Allografted NPK tumors were allowed to grow until they reached a volume of 1 cm3, at which moment they were randomly assigned to either vehicle (Veh) or combination therapy using rapamycin and PD0325901 (RAPPD). Allografted mice were administered rapamycin (10 mg/kg) and PD0325901 (10 mg/kg) during five consecutive days (Allo SHORT). Mice were euthanized in the fifth day 6 hours after having received the last treatment and the tumors were harvested and snap frozen for subsequent molecular analysis. Total RNA obtained from prostate tumors/tissues. Prostate tumors/tissues were harvested and processed for RNA isolation and transcriptome analysis using the MagMAX RNA isolation kit (Ambion). Total RNA was amplified and labelled for subsequent microarrays hybridization using the Illumina TotalPrep RNA Amplification Kit.

2015-09-17 | E-GEOD-69213 | biostudies-arrayexpress

Predicting drug response in human prostate cancer from preclinical analysis of in vivo mouse models

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-09-17 | E-GEOD-69214 | biostudies-arrayexpress

The kinase TNIK is an essential activator of Wnt target genes

Project description:Wnt signalling maintains the undifferentiated state of intestinal crypt/progenitor cells through the TCF4/ß-catenin activating transcriptional complex. In colorectal cancer, activating mutations in Wnt pathway components lead to inappropriate activation of the TCF4/ß-catenin transcriptional program and tumourigenesis in the gut epithelium. The mechanisms by which TCF4/ß-catenin activate key target genes are not well understood. Using a proteomics approach, we identified Tnik, a member of the Germinal centre kinase family, as a Tcf4 interactor in the proliferative crypts of mouse small intestine. Tnik is recruited to promoters of Wnt target genes in mouse crypts and in Ls174T colorectal cancer cells in a ß-catenin dependent manner. Depletion of TNIK and expression of TNIK kinase mutants abrogated TCF-LEF transcription, highlighting the essential role of the kinase activity in Wnt target gene activation. siRNA depletion of TNIK followed by expression array analysis demonstrated that TNIK is an essential and exclusive activator of Wnt induced transcriptional program. As an essential component in the TCF4/ß-catenin activator complex, the kinase TNIK may present an attractive candidate for drug targeting in colorectal cancer.

2009-08-13 | GSE17623 | GEO

TNIK signaling imprints CD8+ T memory formation early after priming

Project description:Purpose: The goal of this study is to compare NGS-derived transcriptome profiling (RNA-seq) of naïve/ effector (D6)/ memory (D80) p14 T cell [wild-type (WT) and Tnik-/- (KO)] isolated form spleen of naïve or adoptively transferred and LCMV-WE immunized mice. Methods: Transcriptomic profiles of splenic naïve wild-type (WT) and Tnik-/- (KO) p14 T cells (8-week-old mice) or splenic effector (D6) and memory (D80) p14 T cells (post adoptive transfer and LCMV-WE immunization) were assessed in duplicates or triplicate by deep sequencing, using Illumina HiSeq 2500. qRT–PCR validation was performed using TaqMan and SYBR Green assays. Results: We mapped about 30 million sequence reads per sample to the mouse genome (GRCm38 - mm10) and identified expressed transcripts in splenic WT and Tnik−/− p14 T cells. RNA-seq data confirmed stable expression of known housekeeping genes. Differentially expressed genes between the WT and Tnik−/− p14 T cells from naïve, D6 or D80 were identified with a fold change ≥1.5 and p-value <0.05. Hierarchical clustering and gene ontology analysis of differentially expressed genes uncovered genes that may contribute to regulation of stemness, transcriptional regulation, cell cycle regulation, survival and function of T cells. Conclusions: Our study represents the first detailed transcriptome analysis of WT versus Tnik-/- p14 T cells in the context of acute viral infection, with biologic replicates, generated by RNA-seq technology. Our results show that TNIK regulates T cell fate. Evaluation of mRNA content in effector (D6) and memory (D80) p14 T cells revealed that TNIK-deficiency during T cell activation enhances proliferation, terminal differentiation and glycolysis of effector T cells, while compromising steady-state metabolic activity of memory T cells. We conclude that TNIK imprints memory formation early after CD8+ T cell priming.

2020-02-24 | GSE127734 | 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