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MIZ-1 (c-Myc-interacting Zinc Finger Protein-1, ZBTB17) is required for efficient B cell receptor signaling [RNA-seq]

ABSTRACT: B cell receptor (BCR) signaling is required for the regulation of normal B lymphocyte development. We found that mice expressing a POZ domain-deficient MIZ-1 (MIZ-1ΔPOZ) exhibit impaired BCR signaling. Transcriptomic and ChIP-seq analyses reveal that, in addition to autophagy related genes, MIZ-1 directly regulates genes involved in BCR signaling and actin cytoskeleton dynamics.

ORGANISM(S): Mus musculus

PROVIDER: GSE313263 | GEO | 2026/04/15

REPOSITORIES: GEO

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MIZ-1 (c-Myc-interacting Zinc Finger Protein-1, ZBTB17) is required for efficient B cell receptor signaling [ChIP-seq]

Project description:B cell receptor (BCR) signaling is required for the regulation of normal B lymphocyte development. We found that mice expressing a POZ domain-deficient MIZ-1 (MIZ-1ΔPOZ) exhibit impaired BCR signaling. Transcriptomic and ChIP-seq analyses reveal that, in addition to autophagy related genes, MIZ-1 directly regulates genes involved in BCR signaling and actin cytoskeleton dynamics.

2026-04-15 | GSE313262 | GEO

MIZ-1 (c-Myc-interacting Zinc Finger Protein-1, ZBTB17) is required for efficient B cell receptor signaling [ChIP-seq]

Project description:MIZ-1 (c-Myc-interacting Zinc Finger Protein-1, ZBTB17) is required for efficient B cell receptor signaling [ChIP-seq]

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MIZ-1 (c-Myc-interacting Zinc Finger Protein-1, ZBTB17) is required for efficient B cell receptor signaling [RNA-seq]

Project description:MIZ-1 (c-Myc-interacting Zinc Finger Protein-1, ZBTB17) is required for efficient B cell receptor signaling [RNA-seq]

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Effect of Miz1 POZ domain deletion on expression profiles of B and T leukemia cells

Project description:Acute lymphoblastic leukemia (ALL) is an aggressive blood cancer mainly affecting children. Relapse rates are high and toxic chemotherapies that block DNA replication and induce DNA damage cause health problems later in life, underlining the need for improved therapies. c-Myc is a transcription factor that is hyperactive in a large proportion of cancers including leukemia but is difficult to target in therapy. We show that ablation of the function of the BTB/POZ domain factor Miz-1, an important co-factor of c-Myc, significantly delays T- and B-ALL/lymphoma in mice and interferes with c-Myc oncogenic transcriptional activity. Leukemic cells that still emerge in this system activate DNA replication pathways, which are those targeted by current chemotherapeutic drugs such as cytarabine. We found that the combination of acute ablation of the Miz-1 POZ domain enhances the effect of cytarabine treatment. This combination was effective in both Eµ-Myc and Notch ICN driven leukemia models and prolonged survival of tumor bearing animals by accelerating apoptosis of leukemic cells. These observations suggest that targeting Miz-1 could render current ALL chemotherapies more effective with a better outcome for patients.

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RNA-Seq analysis of T-ALL mouse samples and the effect of Miz1 POZ domain deletions on T-ALL expression profiles

Project description:T cell acute lymphoblastic leukemia (T-ALL) is an aggressive disease mainly affecting children. Relapse rates are high and toxic chemotherapies that block DNA replication and induce DNA damage cause health problems later in life, underlining the need for improved therapies. We show that ablation of the BTB/POZ domain factor Miz-1 significantly delays Notch1-induced T-ALL in mice through induction of p53-dependent cell death. Leukemic cells that still emerge in this system activate DNA replication and strand elongation pathways, which are those targeted by current chemotherapeutic drugs such as cytarabine. Acute Miz-1 ablation enhances the effect of cytarabine treatment and eliminates leukemic cells completely in some cases, suggesting that targeting Miz-1 could render current T-ALL chemotherapies more effective.

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