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Transcriptome analysis of A549 cells expressing a SUMOylation-deficient TRIM28 mutant in the context of influenza A virus infection

ABSTRACT: Transcriptome analysis of A549 cells expressing a SUMOylation-deficient TRIM28 mutant in the context of influenza A virus infection

PROVIDER: PRJNA551131 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9602260.fastq.gz	Fastqsanger.gz
	SRR9602261.fastq.gz	Fastqsanger.gz
	SRR9602262.fastq.gz	Fastqsanger.gz
	SRR9602253.fastq.gz	Fastqsanger.gz
	SRR9602263.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcriptome analysis of A549 cells expressing a SUMOylation-deficient TRIM28 mutant in the context of influenza A virus infection

Project description:Aim: Identify differentially expressed genes in human lung epithelial cells expressing a SUMOylation-deficient TRIM28 mutant (TRIM28 6KR) compared to TRIM28 wt.

2019-08-05 | GSE133329 | GEO

TRIM28-dependent SUMOylation protects the adult ovary from the male pathway (ChIP-Seq 2)

Project description:We study the role of the protein Trim28 in the maintenance of sexual identity of the adult ovary. With the help of conditional knock out (cKO) of Trim28 using the Nr5a1:Cre, we observed that deletion of the Trim28 gene in granulosa cells of the adult ovary induces their transdifferentiation into Sertoli cells, the supporting cell lineage of the testicular seminiferous tubules. FOXL2 expression has disappeared and follicles were completely remodeled into tubular structures with cells that expressed the Sertoli cell markers SOX8, SOX9 and DMRT1. Histological analysis confirmed the progressive reorganization of ovarian follicles into tubular structures and the and the transdifferentiation of granulosa cells by cells with a Sertoli cell morphology. TRIM28 acts as a SUMO-E3 ligase by interacting with the SUMO-E2 conjugating enzyme UBC9 (encoded by the Ube2i gene) via the Plant homeodomain (PHD), and can self-SUMOylate. To study in vivo the role of TRIM28-dependent SUMOylation, we generated a point mutation in exon 13 of mouse Trim28 within the PHD domain of the TRIM28 protein (C651F) that abrogates its SUMO-E3 ligase activity. We generated Trim28Phd/cKO mice (termed PHD mutant). Like in cKO ovaries, FOXL2 expression was undetectable, whereas we observed expression of the Sertoli cell markers SOX9, SOX8 and DMRT1 within structures organized in pseudo-tubules in PHD ovaries. Our results indicate that maintenance of the female pathway in the adult ovary depends on the E3-SUMO ligase activity of TRIM28.

2022-05-24 | GSE166384 | GEO

TRIM28-dependent SUMOylation protects the adult ovary from the male pathway

Project description:TRIM28-dependent SUMOylation protects the adult ovary from the male pathway

| PRJNA700643 | ENA

TRIM28-dependent SUMOylation protects the adult ovary from the male pathway (RNA-Seq)

Project description:TRIM28-dependent SUMOylation protects the adult ovary from the male pathway (RNA-Seq)

| PRJNA700646 | ENA

Immune response of TRIM28 KO cells infected with H1N1 IAV

Project description:RNAseq analysis of A549-TRIM28 KO cells that were infected with low pathogenic laboratory strain PR8 (H1N1) Differentially expressed genes in infected vs. non-infected cells Project: A549_TRIM28_KO

2022-08-31 | GSE206188 | GEO

TRIM28-dependent SUMOylation protects the adult ovary from the male pathway (RNA-Seq)

2022-05-24 | GSE166382 | GEO

TRIM28-dependent SUMOylation protects the adult ovary from the male pathway (ChIP-Seq 2)

Project description:TRIM28-dependent SUMOylation protects the adult ovary from the male pathway (ChIP-Seq 2)

| PRJNA700645 | ENA

TRIM28-dependent SUMOylation protects the adult ovary from the male pathway (ChIP-Seq 1)

Project description:TRIM28-dependent SUMOylation protects the adult ovary from the male pathway (ChIP-Seq 1)

| PRJNA700648 | ENA

TRIM28-dependent SUMOylation protects the adult ovary from the male pathway (ChIP-Seq 1)

2022-05-24 | GSE166383 | GEO

TRIM28 is essential for erythroblast differentiation in the mouse

Project description:We discovered that Trim28 genetic loss in the adult mouse leads to defective immature erythropoiesis in the bone marrow and consequently to anemia.We further found that TRIM28 controls erythropoiesis in a cell-autonomous manner by inducibly deleting Trim28 exclusively in hematopoietic cells. Finally, in the absence of TRIM28 we observed increased apoptosis as well as diminished expression of multiple erythroid transcription factors and heme biosynthetic enzymes in immature erythroid cells. Thus, TRIM28 is essential for the cell-autonomous development of immature erythroblasts in the bone marrow. To induce Cre recombinase from the Mx1Cre transgene, poly(I:C) was injected 5 times every other day. Mice were analyzed two weeks after completion of poly(I:C) administration. TRIM28 mutant mice generate two distinct types of immature erythroid cells; KOa, with 5-8% of the Trim28 gene remaining undeleted (still bearing 26% of residual mRNA), and KOb, with 1-4% of the gene remaining undeleted (and with 18% of mRNA remaining).

2013-10-04 | E-GEOD-49843 | biostudies-arrayexpress

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