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Gain-of-function Variants in SMAD4 compromise Respiratory Epithelial cells

ABSTRACT: Gain-of-function Variants in SMAD4 compromise Respiratory Epithelial cells

PROVIDER: PRJNA1127656 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29528333_1.fastq.gz	Fastqsanger.gz
	SRR29528333_2.fastq.gz	Fastqsanger.gz
	SRR29528334_1.fastq.gz	Fastqsanger.gz
	SRR29528334_2.fastq.gz	Fastqsanger.gz
	SRR29528335_1.fastq.gz	Fastqsanger.gz

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Gain-of-function Variants in SMAD4 compromise Respiratory Epithelial cells

Project description:To investigate how SMAD4 mutations associated with Myhre syndrome impact SMAD4 protein levels, activation and physiological functions in patient derived nasal epithelial cells. We derived primary nasal basal stem cells from inferior turbinate brushings of healthy subjects and Myhre syndrome patients (SMAD4-Ile500Val, Arg496Cys, Ile500Thr). After ALI differentiation, RNA was collected from healthy nasal basal epithelial cells and Myhre syndrome-epithelial cells to perform mRNA Deep sequencing. We then performed gene expression profiling analysis using data obtained from RNA-seq.

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SMAD4 lossdifferentlyshapespancreatictumorswithdistinct KRASmutations

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Transcriptional profile of Smad4-deficient CTLs is similar to TRM

Project description:Transforming growth factor β (TGFβ) is a morphogenic protein that augments antiviral immunity by altering the functional properties of pathogen-specific memory CD8 T cells. During infection, TGFβ inhibits formation of effector (TEFF) and circulating memory CD8 T cells, while encouraging tissue-resident memory CD8 T cells (TRM) to settle in peripheral tissues. SMAD proteins are signaling intermediates that are used by members of the TGF cytokine family to modify gene expression. Using RNA-sequencing we determined that SMAD4 altered the transcriptional profile of antiviral CTLs during respiratory infection. Our data show that SMAD4 and TGFβ use alternate signaling pathways to cooperatively regulate a collection of genes that determine whether pathogen-specific memory CD8 T cells localize in peripheral or lymphoid tissues. During infection, SMAD4 acts independently of TGF to inhibit TRM development, while inducing genes that support formation of circulating memory CD8 T cells. The genes that are modulated by SMAD4 include several homing receptors (CD103, KLRG1 and CD62L) and transcription factors (Hobit and EOMES) that support memory formation.

2021-12-22 | GSE151637 | GEO

Gene expression analyses of SMAD4 knockdown in pancreatic cell line

Project description:The transforming growth factor ? (TGF-?) signaling protein SMAD4 is lost in 60% of PDAC, and this has been associated with poorer prognosis. We expressed SMAD4 in human PDAC cell lines BxPC3, by selection of stable clones containing an inducible SMAD4 Tet-ON construct. After 24h of SMAD4 expression, TGF-? signaling-dependent G1-arrest was observed in BxPC3 cells with an increase in the G1-phase fraction from 48.9% to 71.5%. Microarray analysis of gene expression at 8h, 24h, and 48h after SMAD4 expression characterized the regulatory impact of SMAD4 expression in a SMAD4-null PDAC cell line and identified novel targets of TGF-? signaling. We used BxPC3 cells infected by pINDCUER-SMAD4-Puro virus. After 24h, 1µg/ml doxycycline was added to experimental wells. We profiled the gene expression after 8hr, 24hr and 48hr treatment with doxycycline as well as control at 8hr.

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Human Germline Heterozygous Gain-of-Function STAT6 Variants Cause Severe Allergic Disease

Project description:Human Germline Heterozygous Gain-of-Function STAT6 Variants Cause Severe Allergic Disease

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Human Germline Heterozygous Gain-of-Function STAT6 Variants Cause Severe Allergic Disease

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Project description:The tumor suppressive effects of TGF-β are classically associated with the activation of the “canonical” SMAD-mediated pathway, whereas its oncogenic effects are largely attributed to its “non-canonical signaling”. We herein provide evidence of an oncogenic effect for SMAD2 and 3 in response to TGF-β in SMAD4-null cancer cells. Using the CRISPR/Cas9 technology, we report that simultaneous knockout of Smad2 and 3 in Smad4-negative pancreatic ductal adenocarcinoma (PDAC) cells compromises TGF-β-driven collective migration mediated by FAK and Rho/Rac signaling. Moreover, RNA-sequencing analyses highlight a TGF-β gene signature related to aggressiveness mediated by SMAD2 and 3 in the absence of SMAD4. Using PDAC patients cohorts, we reveal that SMAD4-negative tumors with high levels of (phospho)-SMAD2 are more aggressive and have a poorer prognosis. Thus, loss of SMAD4 tumor suppressive activity in PDAC is associated with oncogenic gain-of-function of SMAD2 and 3 and the onset of associated deleterious effects.

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2011-04-17 | E-GEOD-15736 | biostudies-arrayexpress

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