Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Endogenous TBK1-mediated GABARAP-L2 and LC3C phosphorylation site identification

ABSTRACT: In order to identify TBK1-mediated GABARAP-L2 and LC3C phosphorylation sites, cells were treated with TBK1 or control siRNA and TBK1 kinase activity was induced by treatment with CCCP.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell

SUBMITTER: Lina Herhaus

LAB HEAD: Ivan Dikic

PROVIDER: PXD015077 | Pride | 2019-11-06

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Similar Datasets

TBK1-mediated GABARAP-L2 phosphorylation site identification

Project description:In order to identify TBK1-mediated GABARAP-L2 phosphorylation sites, proteins were overexpressed in SILAC labelled cells.

2019-11-06 | PXD015075 | Pride

GABARAP-L2 WT, S87/88D or A interactomes

Project description:TBK1 phosphorylates GABARAP-L2 S87/88. In order to test if this phosphomimetic mutation in GABARAP-L2 changes its binding to other proteins a mass spectrometry based interactome study was performed.

2019-11-06 | PXD015155 | Pride

TBK1-mediated LC3C phosphorylation site identification

Project description:In order to identify TBK1-mediated LC3C phosphorylation sites, proteins were overexpressed in SILAC labelled cells.

2019-11-06 | PXD015076 | Pride

Transcription profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression

Project description:The purpose of the dataset is to analyze expression of genes induced by KRAS and regulated by TBK1; The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF- B anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. Experiment Overall Design: Knock out of TBK1 in the contect of KRAS activation (mutant) and control (WT)

2009-11-15 | E-GEOD-17643 | biostudies-arrayexpress

Analysis of the TBK1 interactors from TBK1-deficient A549 cells reconstituted with moTAP TBK1 or empty vector

Project description:This study aimed at determining the proteins that interact with TBK1.

2018-09-25 | PXD010777 | Pride

Transcription profiling of human lung epithelial cells ollowing oncogenic KRAS expression and TBK1 suppression or infection with oncogenic KRAS (G12V) - SuperSeries

Project description:The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF- B anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. This SuperSeries is composed of the following subset Series:; GSE17643: Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression; GSE17671: Profiling of immortalized human lung epithelial cells following infection with oncogenic KRAS (G12V) Experiment Overall Design: Refer to individual Series

2009-10-31 | E-GEOD-17672 | biostudies-arrayexpress

BMP-2-responsive genes in mouse periodontal ligament-derived PDL-L2 cells with and without endoglin knockdown

Project description:This study was designed to identify endoglin (ENG)-dependent BMP2-responsive genes in the mouse fibroblastic cell line PDL-L2. PDL-L2 cells were treated with an siRNA for endoglin (siENG) or a control siRNA (siCont). After 48hr, the cells were exposed to recombinant human BMP-2 (250 ng/ml) or vehicle and cultured for 12 hr.

2014-01-21 | E-GEOD-54220 | biostudies-arrayexpress

TBK1-mediated phosphorylation sites of ATG8s in vitro

Project description:Identification of LC3 family proteins phoshorylation sites mediated by TBK1

2019-11-06 | PXD015065 | Pride

RNA-seq of whole body L2 females, L2 hermaphrodites, L2 converted females (hermaphrodite-fated larvae induced to develop as females), adult males and mixed stages individuals from the three-sexed nematode Auanema rhodensis

Project description:The nematode Auanema rhodensis is trioecious (co-occurrence of males, females and self-fertile hermaphrodites). To better understand its sex determination system, we have compared the transcriptomic profiles of early (L2) females, hermaphrodites and converted females (hermaphrodite-fated larvae induced to develop as females). Additionally, we sequenced the transcriptome of adult males and individuals from various stages and sexes (mixed stages samples) to compare global gene expression profiles along the assembled draft chromosomes of A. rhodensis (BioProject PRJEB29492). The RNA-seq data was also used to predict genes in the assembled genome. We generated three biological replicates for each RNA-seq condition (L2 females, L2 converted females, L2 hermaphrodites, males and mixed stages). Comparisons of the expression profiles of the L2 conditions was performed to identify genes potentially involved in the sexual differentiation process, using a standard RNA-seq comparison approach. Briefly, the cleaned reads were aligned to the genome using STAR, the abundance and identification of differentially expressed genes were assessed using FeatureCounts and DEseq2 (using as thresholds an absolute log2(Fold Change) >= 2 and an FDR <0.01).

2019-02-11 | E-MTAB-7667 | biostudies-arrayexpress

Arsenic-induced Changes in L2 Cells

Project description:Arsenic is a carcinogen that is known to induce cell transformation and tumor formation. Although studies have been performed to examine the modulation of signaling molecules caused by arsenic exposure, the molecular mechanisms by which arsenic causes cancer are still unclear. We hypothesized that arsenic alters gene expression leading to carcinogenesis in the lung. In this study, we examined global gene expression in response to 0.75 M-BM-5M arsenic treatment for 1-7 days in a rat lung epithelial cell line (L2) using an in-house 10k rat DNA microarray. One hundred thirty one genes were identified using the one-class statistical analysis of microarray (SAM) test. Of them, 33 genes had a fold change of M-bM-^IM-% 2 at least between two time points. These genes were then clustered into 5 groups using K-means cluster analysis based on their expression patterns. Seven selected genes, all associated with cancer, were confirmed by real-time PCR. These genes have functions directly or indirectly related to metabolism, glycolysis, cell proliferation and differentiation, and regulation of transcription, all of which may be involved in neoplastic transformation of cells. Our findings provide important insight for the future studies of arsenic-mediated lung cancer. Keywords: Lung, aresenic, L2, micorarray L2 cells were exposed with 0.75 uM of arsenite for 0, 1, 3, 5, and 7 days (C, D1, D3, D5 and D7). The samples were arranged for hybridization using a loop design. For each paired sample, dye flip and three biological replications were performed for each sample.

2011-12-23 | E-GEOD-9790 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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