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Modifications of the mitochondrial fission protein DRP1 (Dynamin-related protein 1) by TBK1 (TANK Binding Kinase 1)

ABSTRACT: This project is a overexpression experiment to check the modifications of DRP1 by TBK1 in HEK293 cell.

ORGANISM(S): Homo Sapiens

SUBMITTER: Pinglong Xu

PROVIDER: PXD021572 | iProX | Fri Sep 18 00:00:00 BST 2020

REPOSITORIES: iProX

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Modifications of TBK1 (TANK Binding Kinase 1) by the main kinase of cellular energy sensing AMPK (Adenosine 5‘-monophosphate (AMP)-activated protein kinase)

Project description:This project is a overexpression experiment to check the modifications of TBK1 by AMPK in HEK293 cells.

2022-05-16 | PXD033926 |

TBK1 protein complex by BioID method

Project description:HEK293 cells were transduced with pCLXSN(GFP)-Myc-BioID-TBK1 or the control vector pCLXSN-Myc-BioID. The cells were cultured in biotin-supplemented medium for 12 h and then subjected to BioID screening.

2019-10-25 | MSV000084505 | MassIVE

Transcription profiling of mouse wild-type, TBK1, IKKi(Ikbke), or TBK1 IKKi doubly deficient embryonic fibroblats to elucidate how TBK1 and/or IKKi mediates B-DNA-mediated innate immune responses

Project description:B-DNA-induced gene expression profile in wild-type, TBK1, IKKi(Ikbke), or TBK1 IKKi doubly deficient embryonic fibroblats; to elucidate how TBK1 and/or IKKi mediates B-DNA-mediated innate immune responses. Experiment Overall Design: Total RNA was extracted from embryonic fibroblats transfected for 4 h with or without poly(dA-dT)-poly(dT-dA), after which cRNA was synthesized. Preparation of cRNA, hybridization and scanning of the microarray were done according to the manufacturer's instructions (Affymetrix). A microarray (MG U74A version 2; Affymetrix) was used with Microarray Suite software (version 5.0; Affymetrix) and GeneSpring software (Silicon Genetics).

2007-12-07 | E-GEOD-4171 | biostudies-arrayexpress

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

Next Generation Sequencing analysis using splenic DCs freshly isolated from Wild Type and TBK1-DKO mice

Project description:In this experiment, we analyzed the gene expression profile of WT and TBK1-deficient splenic DCs by RNA sequencing based on three independent samples. The results revealed significant alterations in the expression of a number of genes, most notably the enhanced expression of a large subset of IFN-responsive genes in the TBK1-deficient DCs.

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TBK1 enhances antifungal immunity by forming a SRC-TBK1 positive feedback loop in phagosomes of macrophages

Project description:TBK1 is a serine/threonine kinase known for its role in antiviral immunity. Here, we identify TBK1 as a key amplifier of antifungal immune responses. Using a mouse model of Candida albicans infection, we show that TBK1 is recruited to phagosomes via SRC-SHP2 signaling and phosphorylates SRC to establish a positive feedback loop. This enhances downstream cytokine production, including IL-6 and TNF-α, and promotes fungal clearance. Bone marrow-derived macrophages (BMDMs) from TBK1fl/fl and TBK1fl/fl Lyz2-Cre mice were stimulated with various fungal components, and RNA-seq was performed to assess transcriptional changes. Our findings define a new role for TBK1 in antifungal host defense and suggest TBK1 as a potential therapeutic target.

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The Loss of TBK1 Kinase Activity in Motor Neurons or in All Cell Types Differentially Impacts ALS Disease Progression in SOD1 Mice

Project description:DNA sequence variants in the TBK1 gene associate with or cause sporadic or familial amyotrophic lateral sclerosis (ALS). Here we show that mice bearing human ALS-associated TBK1 missense loss-of-function mutations, or mice in which the Tbk1 gene is selectively deleted in motor neurons, do not display a neurodegenerative disease phenotype. However, loss of TBK1 function in motor neurons of the SOD1G93A mouse model of ALS impairs autophagy, increases SOD1 aggregation, and accelerates early disease onset without affecting lifespan. By contrast, point mutations that decrease TBK1 kinase activity in all cells also accelerate disease onset but extend the lifespan of SOD1 mice. This difference correlates with the failure to activate high levels of expression of interferon-inducible genes in glia. We conclude that loss of TBK1 kinase activity impacts ALS disease progression through distinct pathways in different spinal cord cell types and further implicate the importance of glia in neurodegeneration.

2020-04-13 | GSE146141 | GEO

TBK1 Regulates Regeneration of Pancreatic b-cells

Project description:b-cell proliferation induction is one of the most tangible therapeutic strategies to restore b-cell mass. However, this approach has proven challenging due to a remarkable resistance of adult human b-cells to proliferation. Here we aim to unravel the role of a non-canonical IkB kinase TBK1 (TANK-binding kinase 1), which is predominantly expressed in b-cells in mammalian islets, in regulating cell cycle progression. Genetic silencing of TBK1 in INS-1 832/13 rat b-cell line promoted proliferation of b-cells. Proteomic and transcriptome analyses further revealed changes of proteins and genes critical for cell growth and proliferation, including upregulation of ribosomal proteins and cell cycle regulators, upon depletion of TBK1. TBK1 overexpression decreased sensitivity of b-cells to the elevation of cAMP levels and reduced proliferation of b-cells in a manner dependent on the activity of phosphodiesterase 3 (PDE3). Importantly, pharmacological inhibition of TBK1 using (E)3-(3-phenylbenzo[c]isoxazol-5-yl) acrylic acid (PIAA) augmented proliferation and function of rat and human embryonic stem cell (hESC)-derived insulin-producing b-cells under basal conditions. Diabetogenic insults further induced TBK1 expression and accordingly, PIAA protected b-cells against cytokine- and streptozotocin-induced diabetogenic challenges and promoted b-cell replication. Furthermore, PIAA increased proliferation of β-cells in normal and type 2 diabetic human islets with elevation in insulin secretion. Altogether, these data unveil novel and essential function of TBK1 as a key cell-autonomous negative regulator of b-cell replication and presenting PIAA as a valid therapeutic strategy for augmenting proliferation and function of b-cells.

2020-02-29 | GSE136670 | GEO

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

In vitro responses of fibroblasts from patients with TBK1 deficiency after TLR3 dependent and independent stimuli

Project description:We report here two unrelated HSE patients carrying different heterozygous mutations (D50A and G159A) in TBK1, the gene encoding TANK-binding kinase 1, a kinase at the crossroads of multiple IFN-inducing signaling pathways. Both mutant TBK1 alleles are loss-of-function, but through different mechanisms: protein instability (D50A) or a loss of kinase activity (G159A). Both are also associated with an autosomal dominant (AD) trait, but by different mechanisms: haplotype-insufficiency (D50A) or negative dominance (G159A). A defect in poly(I:C)-induced TLR3 responses can be detected in fibroblasts heterozygous for G159A, but not for D50A TBK1. Skin fibroblast cell lines were derived from healthy controls (n=3), patients with deficiencies for TBK1 (n=2), TLR3 (n=2), STAT1 (n=1) and cultured for 2 or 8 hours in the presence of IFNa (105 IU/ml), IL1b (20ng/ml), or poly I:C (25ug/ml) or left unstimulated for the same length of time.

2012-07-29 | E-GEOD-38652 | biostudies-arrayexpress

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