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ChIP-seq on ZNF506 overexpression HEK293T to verify ZNF506 binding capacity at PBS-Pro sites.

ABSTRACT: ChIP-seq on ZNF506 overexpression HEK293T to verify ZNF506 binding capacity at PBS-Pro sites.

PROVIDER: PRJNA862539 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20653300_1.fastq.gz	Fastqsanger.gz
	SRR20653300_2.fastq.gz	Fastqsanger.gz
	SRR20653301_1.fastq.gz	Fastqsanger.gz
	SRR20653301_2.fastq.gz	Fastqsanger.gz
	SRR20653302_1.fastq.gz	Fastqsanger.gz

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ChIP-seq on ZNF506 overexpression HEK293T to verify ZNF506 binding capacity at PBS-Pro sites.

Project description:To identify ZNF506 genome-wide target sites, we performed ChIP-seq assay and found that ZNF506 binding sites enriched at PBS-Pro-containing ERV subfamilies (ERVPs) and further motif calling analysis showed that ZNF506 binds to PBS-Pro sequences, promoting formation of H3K9me3 modifications at binding regions. And ChIP-seq assay also indicated that the distinction of H3K9me3 signals closed to ZNF506 peak regions between ZNF506 overexpressing (OE) HEK293T cells and ZNF506 Knockout (KO) HEK293T cells was correlated with the different recruitment of corepressor KAP1. The ChIP-seq experiments using GFP antibodies and H3K9me3 antibodies on ZNF506-GFP OE HEK293T cell lines, and ZNF417-GFP OE HEK293T cell lines were used as controls for H3K9me3 ChIP. Also, the ChIP-seq experiments were performed using H3K9me3 antibodies and KAP1 antibodies on ZNF506 KO HEK293T cells and ZNF506 OE HEK293T cells.

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ChIP-seq on Zfp961 GFP flox/flox mESCs to verify Zfp961 binding capacity at PBS-Lys elements.

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ChIP-seq on Znf417 and Znf587 overexpression 293T to verify Znf417 and Znf587 binding capacity at PBS-Lys elements.

Project description:The ChIP-seq experiments using GFP antibody on ZNF417/ZNF587-GFP overexpressing 293T cells revealed that ZNF417/ZNF587 preferred to bind a PBS-Lys-containing HERVs. Further motif calling analysis showed that both ZNF417 and ZNF587 bind to HERVK PBS-resembled motif.

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ChIP-seq on Zfp961 GFP flox/flox mESCs to verify Zfp961 binding capacity at PBS-Lys elements.

Project description:We performed ChIP-seq assay with anti-GFP antibodies on Zfp961-GFPflox/flox ESCs.We found PBS-Lys-containing endogenous virus K subgroup repeats (ERV-K) were significantly enriched in the strong peak regions (40%, 165 out of 413), compared to their abundance in the mouse genome (~5%), suggesting Zfp961 binding preference towards ERV-K regions. And Zfp961 has a PBS-Lys motif. We performed H3K9me3 ChIP on Zfp961 WT or KO mESCs. We found that Zfp961 recruits H3k9me3 modification at ERVKs, and H3K9me3 level showed a moderate decrease upon Zfp961 deletion.

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ChIP-seq on Zfp961 GFP flox/flox mESCs to verify Zfp961 repression capacity to transcription of ERVKs

Project description:We performed ChIP-seq assay with anti-KAP1 antibodies on Zfp961-GFPflox/flox ESCs.We found KAP1 signal decreased at PBS-Lys sites in Zfp961 KO cells compared to WT, suggesting Zfp961 recruiting KAP1 to ERV-K regions. We performed H3K27ac ChIP on Zfp961 WT or KO mESCs. We found that H3k27ac modification at PBS-Lys sites was elevated upon Zfp961 deletion, indicating Zfp961 serving as a repressive transcription factor.

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