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SMAD4 impedes conversion of NK cells into ILC1-like cells by curtailing non-canonical TGFb signaling

ABSTRACT: SMAD4 impedes conversion of NK cells into ILC1-like cells by curtailing non-canonical TGFb signaling

PROVIDER: PRJNA391153 | ENA |

REPOSITORIES: ENA

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SMAD4 impedes conversion of NK cells into ILC1-like cells by curtailing non-canonical TGFb signaling (human data sets)

Project description:Among the features that distinguish type 1 innate lymphoid cells (ILC1s) from NK cells is a gene signature indicative of TGFb-family cytokine imprinting. To assess the impact of TGFb family cytokines on ILC1 differentation, we examined SMAD4- a transcription factor that facilitates the signaling pathway common to all TGFb family cytokines-was specifically ablated in ILCs and NK cells. While SMAD4 deficiency did not affect ILC1 differentation, NK cells paradoxically aquired an ILC1-like gene signature and were incapable of controlling tumor metastasis and viral infection. We used microarray to compare the transcriptional differences between human blood NK cells. NK cells from a patient with a deleterious SMAD4 mutation or control NK cells were cultured overnight with either IL-2 alone or TGFb1 and IL-2.

2017-07-31 | GSE100246 | GEO

SMAD4 impedes conversion of NK cells into ILC1-like cells by curtailing non-canonical TGFb signaling (mouse data sets)

Project description:Among the features that distinguish type 1 innate lymphoid cells (ILC1s) from NK cells is a gene signature indicative of TGFb-family cytokine imprinting. To assess the impact of TGFb family cytokines on ILC1 differentation, we examined SMAD4- a transcription factor that facilitates the signaling pathway common to all TGFb family cytokines-was specifically ablated in ILCs and NK cells. While SMAD4 deficiency did not affect ILC1 differentation, NK cells paradoxically aquired an ILC1-like gene signature and were incapable of controlling tumor metastasis and viral infection. We used microarray to define the transcriptional differences between splenic NK cells from WT and SMAD4F/F x Ncr1-Cre mice.

2017-07-31 | GSE100247 | GEO

SMAD4 impedes conversion of NK cells into ILC1-like cells by curtailing non-canonical TGFb signaling

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-07-31 | GSE100248 | GEO

SMAD4 impedes the conversion of NK cells into ILC1-like cells by curtailing non-canonical TGF-? signaling.

Project description:Among the features that distinguish type 1 innate lymphoid cells (ILC1s) from natural killer (NK) cells is a gene signature indicative of 'imprinting' by cytokines of the TGF-? family. We studied mice in which ILC1s and NK cells lacked SMAD4, a signal transducer that facilitates the canonical signaling pathway common to all cytokines of the TGF-? family. While SMAD4 deficiency did not affect ILC1 differentiation, NK cells unexpectedly acquired an ILC1-like gene signature and were unable to control tumor metastasis or viral infection. Mechanistically, SMAD4 restrained non-canonical TGF-? signaling mediated by the cytokine receptor TGF?R1 in NK cells. NK cells from a SMAD4-deficient person affected by polyposis were also hyper-responsive to TGF-?. These results identify SMAD4 as a previously unknown regulator that restricts non-canonical TGF-? signaling in NK cells.

| S-EPMC5712491 | biostudies-literature

CUT&RUN LoV-U for SMAD4 in human melanoma cells

Project description:CUT&RUN LoV-U was performed against SMAD4 using two different antibodies in M170117 human melanoma cells under 4 conditions: Control (DMSO), TGFb, MEKi and TGFb + MEKi (Both).

2024-04-22 | E-MTAB-13951 | biostudies-arrayexpress

siRNA screen for modifiers of Smad4 nuclear translocation

Project description:The TGFb signaling pathway is a critical regulator of developmental processes and disease. We developed a system to measure TGFb signaling dynamics by monitoring the localization of Smad4. We performed an unbiased genome-wide RNAi screen to identify genes involved in ligand-dependent Smad4 nuclear translocation

2015-07-15 | GSE70924 | GEO

Altered transcriptional profile of Smad4-deficient CTLs during infection with Listeria

Project description:TGFb is a pleiotropic cytokine which can exert its regulatory effects on differentiation of cytotoxic T lymphocytes (CTLs) and alter their cell fate. Canonical TGFb signaling inhibits the formation of KLRG1+ effector cells and circulating memory cells while inducing the formation of resident memory cells. However, SMAD4 functions contradictory to TGFb where it is required for the formation of KLRG1+ effector cells and circulating memroy cells and actively inhibit the formation of resident memory cells. Using, RNA-Sequencing we identified that Smad4 alters the gene expression profile of pathogen-specific CTLs after intranasal infection with Listeria monocytogenes expressing chicken ovalbumin.

2022-10-04 | GSE214599 | GEO

TGFb/Smad4 targets promter in IOSE cells

Project description:Unlike ovarian cancer, normal ovarian epithelium response to TGFb1 induced growth inhibition. This study tried to idenify promoters that showed Smad4 binding after additionof TGFb1 in immortalized ovarian surface epithelial cells (IOSE) which is derived from normal ovarian epithelial cells Keywords: ChIP-chip

2007-01-13 | GSE6727 | GEO

Gene expression analysis of CD4+ and CD4- ILC1 subsets by RNAseq

Project description:Innate lymphoid cell (ILC) subsets that mirror helper T cells in their effector cytokine profiles have recently emerged as central players in both homeostatic and inflammatory conditions. Like their Th1, Th2 and Th17/Th22 helper T cell counterparts, ILC subsets are categorized based on their expression of specific transcription factors and effector cytokines: group 1 ILC (ILC1) express T-bet and IFN-Î³; group 2 ILC (ILC2) express GATA-3 and type 2 effector cytokines such as IL-13 and IL-5; and group 3 ILC (ILC3) express RORgt and the cytokines IL-22 and/or IL-17. Under this nomenclature, natural killer (NK) cells and lymphoid tissue inducers (LTi) are considered ILC1 and ILC3, respectively. ILC1 contain both CD4+ and CD4- populations, but whether this phenotypic characteristic reflects functional differences between these two populations is unknown. These studies examine the gene expression profiles of CD4+ vs CD4- ILC1 in a cohort of healthy control subjects. ILC subsets were isolated from the peripheral blood of healthy control subjects. cDNA was isolated and amplified from sorted populations, and gene expression was analyzed by RNAseq

2015-12-31 | E-GEOD-69596 | biostudies-arrayexpress

Homo sapiens

Project description:SMAD4 impedes conversion of NK cells into ILC1-like cells by curtailing non-canonical TGFb signaling (human data sets)

| PRJNA391161 | ENA