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Identification of Smad2 and Smad3 specific binding sites in a breast cancer cell line model

ABSTRACT: Identification of Smad2 and Smad3 specific binding sites in a breast cancer cell line model

PROVIDER: PRJNA786492 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17139519.fastq.gz	Fastqsanger.gz
	SRR17139520.fastq.gz	Fastqsanger.gz
	SRR17139521.fastq.gz	Fastqsanger.gz
	SRR17139522.fastq.gz	Fastqsanger.gz

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Identification of Smad2 and Smad3 specific binding sites in a breast cancer cell line model

Project description:We identify Smad2 and Smad3 specific binding site in a breast cancer breast cell model MDA-MB-231 using LAP-tag GFP fusion proteins under the control of endogenous regulatory elements. Stable cell lines were generated via transfection with a BAC followed by antibiotics selection. We show that LAP-fused SMad2/3 can be used to recapitulate native TGFB signaling. Smad2/Smad3 specific binding sites were identified by ChIP-seq against GFP before and after TGFB treatment. Genomic DNA was sequenced via single end sequencing on Illumina HiSeq

2021-12-08 | GSE190237 | GEO

Smad2 and Smad3 binding sites in H345-TbRII cells

Project description:Transforming growth factor (TGF)-beta induces apoptosis of many types of cancer cells and acts as a tumor suppressor. We found lower expression of TGF-beta type II receptor (TbRII) in most of SCLC cells and tissues than in normal lung epithelial cells and normal lung tissues, respectively. In vitro cell growth and in vivo tumor formation were suppressed by TGF-beta-mediated apoptosis when the wild-type TbRII was overexpressed in SCLC cells. We therefore determined Smad2 and Smad3 (Smad2/3) binding sites in a SCLC cell line H345 stably expressing exogenous TbRII (H345-TbRII) to identify target genes of TGF-beta. Smad2 and Smad3 binding sites in H345-TbRII cells were determined by ChIP-seq (one sample analysis, without replicates).

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Smad2 and Smad3 binding sites in H345-TbRII cells

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TGF-beta-induced gene expression data and Smad2/3 binding sites of HaCaT keratinocytes

Project description:Smad2/3 are transcription factors that engage in TGF-beta-induced transcription. Here we analyzed the effect of identified Smad2/3 binding sites to transcription. We used expression microarrays to compare the Smad2/3 binding sites identified by ChIP-chip to TGF-beta-induced gene expressions. Keywords: time course We also examined the effect of either ETS1/TFAP2A/SMAD2/SMAD3 siRNAs on TGF-beta-induced gene expression change.

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Smad2 and Smad3 have differential sensitivity in relaying TGF b signaling and inversely regulate early lineage specification

Project description:The transforming growth factor beta (TGFÎ²) related signaling is one of the most important signaling pathways regulating early developmental events. Smad2 and Smad3 are structurally similar and it is mostly considered that they are equally important in mediating TGFÎ² signals. Here, we show that Smad3 is an insensitive TGFÎ² transducer as compared with Smad2. Smad3 preferentially localizes within the nucleus and is thus sequestered from membrane signaling. The ability of Smad3 in oligomerization with Smad4 upon agonist stimulation is also impaired given its unique linker region. Smad2 mediated TGFÎ² signaling plays a crucial role in epiblast development and patterning of three germ layers. However, signaling unrelated nuclear localized Smad3 is dispensable for TGFÎ² signaling-mediated epiblast specification, but important for early neural development, an event blocked by TGFÎ²/Smad2 signaling. Both Smad2 and Smad3 bind to the conserved Smads binding element (SBE), but they show nonoverlapped target gene binding specificity. We conclude that Smad2 and Smad3 possess differential sensitivities in relaying TGFÎ² signaling and have distinct roles in regulating early developmental events. GFP, GFP-Smad2 and GFP-Smad3 constitutively expressed Smad3-/- mouse ESCs were differentiated to day6 neuroepithelia and collected for Chip-Seq with an anti-GFP antibody.

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SMAD2/3 binding pattern in triple-negative breast cancer cell lines, Hs578T and BT549 [ChIP-seq]

Project description:SMAD2 and SMAD3 have diverse binding profiles in triple-negative breast cancer cell lines.

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