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Effect of Zbtb24-depletion on gene expressions during the activation of peritoneal B1 cells

ABSTRACT: Effect of Zbtb24-depletion on gene expressions during the activation of peritoneal B1 cells

PROVIDER: PRJNA1009804 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26125036_1.fastq.gz	Fastqsanger.gz
	SRR26125036_2.fastq.gz	Fastqsanger.gz
	SRR26125037_1.fastq.gz	Fastqsanger.gz
	SRR26125037_2.fastq.gz	Fastqsanger.gz
	SRR26125038_1.fastq.gz	Fastqsanger.gz

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Effect of Zbtb24-depletion on gene expressions during the activation of peritoneal B1 cells

Project description:ZBTB24-null ICF2 patients suffer from recurrent infections associated with antibody defects, implying a pivitol role of ZBTB24 in B cell biology. We thus generated B-cell specific Zbtb24 knockout mice and investigated its intrinsic role in B cell development and function both in vitro and in vivo. In accordance with findings obtained in ICF2 patients, Zbtb24 is dispensable for B cell developent and maintenance in mice. Strikingly, lack of Zbtb24 does not significantly compromise the primary & secondary antibody responses against TD-Ags, but reduced TID-Ags-elicited antibodies in vivo. At the cellular level, we discovered that Zbtb24-depletion specifically impaires the plasma cell (PC) differentiation of B1, but not the conventional B2 cells comprising follicular and marginal zone B cells, without impacting their survival and proliferation. Mechanistically, ablation of Zbtb24 suppresses the biosynthesis o heme in B1 cells, and supplementation of hemin largely abrogates the differentiation defects of zbtb24-null B1 cells in vitro. Our study not only provides a plausible explanation for the recurrent respiratory and gastrointestinal infections in ICF2 patients, but is also relevant for other B1 cell-mediated barrier defenses and immune regulations.

2024-09-11 | GSE241747 | GEO

Effect of Zbtb24-depletion on gene expressions during the activation of total splenic B cells

2024-09-11 | GSE241746 | GEO

Transcriptome analysis in Jurkat cell with sufficient and deficient ZBTB24 expressions

Project description:We knocked down ZBTB24 expressions in Jurkat cells by lentiviral infections. Four-five days later, virus infected cells (GFP+) were FACS purified for RNA extraction with the Total RNA Kit II (OMEGA). Library construction and sequencing was performed on a BGISEQ-500 by Beijing Genomics Institution (BGI) in Wuhan, China.

2019-05-05 | GSE122191 | GEO

Effect of Zbtb24-depletion on gene expressions during the activation of total splenic B cells

Project description:Effect of Zbtb24-depletion on gene expressions during the activation of total splenic B cells

| PRJNA1009805 | ENA

Gene expression profile of human peritoneal mesothelial cells (HPMC) treated with TGF-b1

Project description:Long-term peritoneal dialysis is associated with progressive fibrosis of the peritoneum. Epithelial-mesenchymal transition (EMT) of mesothelial cells is an important mechanism involved in peritoneal fibrosis, and TGF-b1 is considered central in this process. We conducted network-based integrated analysis of transcriptomic data to systemically characterize the molecular signature of TGF-b1-stimulated human peritoneal mesothelial cells (HPMCs).

2018-10-18 | GSE121372 | GEO

Transcriptome analysis in Jurkat cell with sufficient and deficient ZBTB24 expressions

Project description:Transcriptome analysis in Jurkat cell with sufficient and deficient ZBTB24 expressions

| PRJNA503897 | ENA

Comparison of C57BL/6 and Dkk3-/- purified B1 and B2 cells

Project description:B2 cells were purified from spleen by CD19 Microbeads. B1 cells were purified from peritoneal cavity lavage by CD19 microbeads, followed by a depletion of CD23+ cells. RNA was prepared and differential gene expression analysis performed.

2014-08-19 | E-MTAB-2850 | biostudies-arrayexpress

RNA-seq of B2, B1 and B2toB1 cells

Project description:RNA-seq of splenic follicular B2 cells, peritoneal 5C5 B1 cells and peritoneal B2toB1 cells 30 days post transfer

2019-02-15 | GSE124827 | GEO

Single cell RNA-seq and BCR-seq of peritoneal B cells

Project description:B1 cells account for the majority of B cell population in the peritoneal cavity, and are essential for the innate immune responses and maintaining the homeostasis. The origin of the B1 cells and how to form the B1 cells pool in the postnatal life remain unknown. And the heterogeneity of B1 cells can largely affect the functions of B1 cells. Until now, nobody has performed the single cell RNA-seq of peritoneal B cells. In order to reveal the characteristics of peritoneal B cells, we have performed the scRNA-seq and scBCR-seq of the peritoneal B cells of mouse from different stages.

2022-05-21 | E-MTAB-10081 | biostudies-arrayexpress

Structural basis of specific DNA binding by the transcription factor ZBTB24

Project description:ZBTB24, encoding a protein of the ZBTB family of transcriptional regulators, is one of four known genes – the other three being DNMT3B, CDCA7 and HELLS – that are mutated in immunodeficiency, centromeric instability, and facial anomalies (ICF) syndrome, a genetic disorder characterized by DNA hypomethylation and antibody deficiency. The molecular mechanisms by which ZBTB24 regulates gene expression and the biological functions of ZBTB24 are poorly understood. Here we identified a 12-bp consensus sequence [CT(G/T)CCAGGACCT] occupied by ZBTB24 in the mouse genome. The sequence is present at multiple loci, including the Cdca7 promoter region, and ZBTB24 binding is mostly associated with gene activation. Crystallography and DNA-binding data revealed that the last four of the eight zinc fingers (ZFs) (i.e. ZF5-8) in ZBTB24 confer specificity of DNA binding. Two ICF missense mutations have been identified in the ZBTB24 ZF domain that alter zinc-binding cysteine residues. We demonstrated that the corresponding C382Y and C407G mutations in mouse ZBTB24 abolish specific DNA binding and fail to induce Cdca7 expression. Our analyses indicate, and suggest a structural basis for, the sequence specific recognition by a transcription factor centrally important for the pathogenesis of ICF syndrome.

2019-06-11 | GSE120969 | GEO

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