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Expression profiling in palatal mesenchymal cells stimulated with TGF-beta2 in the presence and absence of TGFbRI and Tak1 kinase inhibitors

ABSTRACT: TGF-beta signaling in neural crest cells is required for normal craniofacial development. This signaling can be transduced via TGF-beta type I receptors (TGFbRI) using Smad-dependent or Smad independent signaling pathways. We used microarrays to identify TGF-beta-responsive genes that are dependent either on TGFbRI kinase, Tak1 kinase or both.

ORGANISM(S): Mus musculus

PROVIDER: GSE45491 | GEO | 2013/03/27

SECONDARY ACCESSION(S): PRJNA194531

REPOSITORIES: GEO

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Expression profiling in palatal mesenchymal cells stimulated with TGF-beta2 in the presence and absence of TGFbRI and Tak1 kinase inhibitors

Project description:TGF-beta signaling in neural crest cells is required for normal craniofacial development. This signaling can be transduced via TGF-beta type I receptors (TGFbRI) using Smad-dependent or Smad independent signaling pathways. We used microarrays to identify TGF-beta-responsive genes that are dependent either on TGFbRI kinase, Tak1 kinase or both. Primary palatal mesenchymal cell cultures were established. Cultured cells were stimulated with TGF-beta2 in the presence or absence of TGFbRI kinase and Tak1 kinase inhibitors. Unstimulated cells were used as controls. Total RNAs were isolated and hybridized on Affymetrix microarrays.

2013-03-27 | E-GEOD-45491 | biostudies-arrayexpress

Pharmacological Inhibition of TAK1 Prevents and Induces Regression of fibrosis

Project description:To evaluate the effects of TAK1 inhibition on TGF-beta regulated fibrosis using a novel small molecule inhibitor of TAK1.

2023-05-17 | GSE232435 | GEO

The innate immunity kinase TAK1 phosphorylates Rab1 on a hotspot for post-translational modifications by host and pathogen

Project description:TGF-β Activated Kinase 1 (TAK1) is a critical signaling hub responsible for translating antigen binding signals to immune receptors for the activation of the AP-1 and NF-κB master transcriptional programs. Despite its importance, known substrates of TAK1 are limited to kinases of the MAPK and IKK families and include no direct effectors of biochemical processes. Here, we identify over 200 novel substrates of TAK1 using a chemical genetic kinase strategy. We validate phosphorylation of the dynamic switch II region of GTPase Rab1 at T75 to be regulated by TAK1 in vivo. TAK1 preferentially phosphorylates the inactive (GDP-bound) state of Rab1. Phosphorylation of Rab1 disrupts interaction with GDP Dissociation Inhibitor 1 (GDI1), but not GEF or GAP proteins, and is exclusive to membrane localized Rab1, suggesting phosphorylation may stimulate Rab1 activation and membrane association. We found phosphorylation of Rab1 at T75 to be necessary for normal Rab1 mediated ER to Golgi vesicular transport. Previous studies established that the pathogen Legionella pneumophila is capable of hijacking Rab1 function through post-translational modifications of the switch II region. Here, we present the first evidence that Rab1 is regulated by the host in a similar fashion; and that the innate immunity kinase TAK1 and Legionella effectors compete directly to regulate Rab1 by switch II modifications during infection.

2016-07-19 | PXD004213 | Pride

Transcriptional Corepressors HIPK1 and HIPK2 Control Angiogenesis via TGF-b-TAK1-depdendent Mechanism

Project description:Transforming growth factor-b (TGF-b) regulates various aspects of vascular development, yet the signaling mechanisms of TGF-b in the control of angiogenesis remain poorly characterized. Here we show that homeodomain interacting protein kinases, HIPK1 and HIPK2, are transcriptional corepressors that regulate TGF-b-depednent angiogenesis during embryonic development. Loss of HIPK1 and HIPK2 leads to marked up-regulations of several potent angiogenic genes, including Vegf and Mmp10, which result in excessive endothelial proliferation and poor adherens junction formation. This robust phenotype can be recapitulated by siRNA knock down of Hipk1 and Hipk2 in human umbilical vein endothelial cells, as well as in endothelial cell-specific TGF-b type II receptor (TbRII) conditional mutants. The effects of HIPK proteins are mediated through its interaction with MEF2C and HDAC7, and this interaction can be further enhanced by TGF-b and TAK1. Remarkably, TGF-b-TAK1 signaling activates HIPK2 by phosphorylating a highly conserved tyrosine residue Y-361 within the kinase domain. Point mutation in this tyrosine completely eliminates the effect of HIPK2 in the transcriptional suppression of target genes. Together, these results reveal a previously unrecognized role of HIPK proteins in connecting TGF-b signaling pathway with the transcriptional programs for angiogenesis in early embryonic development.

2013-06-01 | GSE39253 | GEO

Transcriptional Corepressors HIPK1 and HIPK2 Control Angiogenesis via TGF-b-TAK1-depdendent Mechanism

2013-06-01 | E-GEOD-39253 | biostudies-arrayexpress

Time course analysis of gene expression in BCR-stimulated splenic wild type and TAK1-/- B cell

Project description:The activation signaling of transcription factor nuclear factor-kB (NF-kB) plays central role for immune system. One of key kinase mediating this pathway is TAK1 in adaptive and innate immunity. However, role of TAK1 in B cell receptor signaling is still unclear. To know effects of TAK1-deletion on the gene expression induced by anti-IgM, we performed the time course analysis in comparison of wild type with TAK1-deleted splenic B cells.

2013-03-31 | GSE41176 | GEO

Gene expression data from MGHU3 bladder cancer cells (FGFR3-Y375C) treated with TAK1 siRNA and/or PD173074

Project description:The NFκB transcription factor is constitutively active in a number of hematologic and solid tumors, and many signaling pathways implicated in cancer are likely connected to NFκB activation. A critical mediator of NFκB activity is TGFβ-activated kinase 1 (TAK1). Here, we identify TAK1 as a novel interacting protein and direct target of fibroblast growth factor receptor 3 (FGFR3) tyrosine kinase activity. We further demonstrate that activating mutations in FGFR3 associated with both multiple myeloma and bladder cancer can modulate expression of genes which regulate NFκB signaling, and promote both NFκB transcriptional activity and cell adhesion in a manner dependent on TAK1 expression in both cancer cell types. Our findings suggest TAK1 as a potential therapeutic target for FGFR3-associated cancers, and other malignancies in which TAK1 contributes to constitutive NFκB activation.

2013-11-19 | GSE52452 | GEO

Gene expression data from MGHU3 bladder cancer cells (FGFR3-Y375C) treated with TAK1 siRNA and/or PD173074

Project description:The NFM-NM-:B transcription factor is constitutively active in a number of hematologic and solid tumors, and many signaling pathways implicated in cancer are likely connected to NFM-NM-:B activation. A critical mediator of NFM-NM-:B activity is TGFM-NM-2-activated kinase 1 (TAK1). Here, we identify TAK1 as a novel interacting protein and direct target of fibroblast growth factor receptor 3 (FGFR3) tyrosine kinase activity. We further demonstrate that activating mutations in FGFR3 associated with both multiple myeloma and bladder cancer can modulate expression of genes which regulate NFM-NM-:B signaling, and promote both NFM-NM-:B transcriptional activity and cell adhesion in a manner dependent on TAK1 expression in both cancer cell types. Our findings suggest TAK1 as a potential therapeutic target for FGFR3-associated cancers, and other malignancies in which TAK1 contributes to constitutive NFM-NM-:B activation. A total of 12 samples of MGHU3 (Y375C) mutant FGFR3 bladder cancer cells (a kind gift from Dr. Margaret Knowles (University of Leeds, Leeds, UK)) were used for array-based gene expression analysis. 3 replicates of each condition: Control siRNA, Control siRNA + PD173074, TAK1 siRNA, and TAK1 siRNA + PD173074.

2013-11-19 | E-GEOD-52452 | biostudies-arrayexpress

Analysis of gene expression in Ig-lambda/kappa positive bone marrow wild type/TAK1-/- B cell

Project description:The activation signaling of transcription factor nuclear factor-kB (NF-kB) plays central role for immune system. One of key kinase mediating this pathway is TAK1 in adaptive and innate immunity. However, role of TAK1 in bone marrow B cell is still unclear. To know effects of TAK1-deletion, the gene expression of Ig-lambda/kappa positive cells were analyzed in comparison of wild type with TAK1-deficient bone marrow B cells.

2015-10-22 | GSE74248 | GEO

Deubiquitinase USP29 Ameliorates Pathological Cardiac Hypertrophy Through Inhibiting TAK1

Project description:The identification of key factors involved in pathological cardiac hypertrophy is crucial to exploring novel treatments for heart failure. In this study, we elucidated the role of Ubiquitin-specific protease 29 (USP29), a deubiquitinase, in pressure overload-induced cardiac hypertrophy. Genetic knockout of USP29 in mice significantly exacerbated TAC-induced heart hypertrophy, dysfunction, and fibrosis; whereas overexpression of USP29 in cardiomyocytes attenuated the hypertrophic response. Similarly, USP29 markedly alleviated PE-induced hypertrophy of primary neonatal rat cardiomyocytes. Mechanistically, the cardio-protective effects mediated by USP29 were attributed to its suppression of transforming growth factor β-activated kinase 1 (TAK1)-JNK/P38 signaling pathway activation. Collectively, our study suggests that targeting either USP29 or its interaction with TAK1 could represent an innovative therapeutic strategy for treating heart failure and cardiac hypertrophy.

2024-04-20 | GSE263965 | GEO

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