ArticleThe Journal of experimental medicine2012
The Zinc-finger protein ASCIZ regulates B cell development via DYNLL1 and Bim.
Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 40 citations in OpenAlex.
- Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026Review
- Article
- Linker Length Drives Heterogeneity of Multivalent Complexes of Hub Protein LC8 and Transcription Factor ASCIZ.Biomolecules · 2023Article
- A novel zinc metabolism-related gene signature to predict prognosis and immunotherapy response in lung adenocarcinoma.Frontiers in immunology · 2023Article
- Developing high-affinity decoy receptors to treat multiple myeloma and diffuse large B cell lymphoma.The Journal of experimental medicine · 2022Article
- DLEU1 promotes cell survival by preventing DYNLL1 degradation in esophageal squamous cell carcinoma.Journal of translational medicine · 2022Article
- ATMIN enhances invasion by altering PARP1 in MSS colorectal cancer.American journal of cancer research · 2022Article
- ATMIN Suppresses Metastasis by Altering the WNT-Signaling Pathway via PARP1 in MSI-High Colorectal Cancer.Annals of surgical oncology · 2021Article
- The ASCIZ-DYNLL1 Axis Is Essential for TLR4-Mediated Antibody Responses and NF-κB Pathway Activation.Molecular and cellular biology · 2021Article
- Loss of CEP70 function affects acrosome biogenesis and flagella formation during spermiogenesis.Cell death & disease · 2021Article
- The dynein light chain 8 (LC8) binds predominantly "in-register" to a multivalent intrinsically disordered partner.The Journal of biological chemistry · 2020Article
- Dynein light chain binding determines complex formation and posttranslational stability of the Bcl-2 family members Bmf and Bim.Cell death and differentiation · 2020Article
- The ASCIZ-DYNLL1 axis promotes 53BP1-dependent non-homologous end joining and PARP inhibitor sensitivity.Nature communications · 2018Article
- Article
- The established and the predicted roles of dynein light chain in the regulation of mitochondrial apoptosis.Cell cycle (Georgetown, Tex.) · 2018Article
- Proapoptotic BIM Impacts B Lymphoid Homeostasis by Limiting the Survival of Mature B Cells in a Cell-Autonomous Manner.Frontiers in immunology · 2018Article
- Dynein light chain regulates adaptive and innate B cell development by distinctive genetic mechanisms.PLoS genetics · 2017Article
- Dynein light chain 1 induces assembly of large Bim complexes on mitochondria that stabilize Mcl-1 and regulate apoptosis.Genes & development · 2017Article
- Article
- Perturbed hematopoiesis in mice lacking ATMIN.Blood · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Developing B lymphocytes expressing defective or autoreactive pre-B or B cell receptors (BCRs) are eliminated by programmed cell death, but how the balance between death and survival signals is regulated to prevent immunodeficiency and autoimmunity remains incompletely understood. In this study, we show that absence of the essential ATM (ataxia telangiectasia mutated) substrate Chk2-interacting Zn(2+)-finger protein (ASCIZ; also known as ATMIN/ZNF822), a protein with dual functions in the DNA damage response and as a transcription factor, leads to progressive cell loss from the pre-B stage onwards and severely diminished splenic B cell numbers in mice. This lymphopenia cannot be suppressed by deletion of p53 or complementation with a prearranged BCR, indicating that it is not caused by impaired DNA damage responses or defective V(D)J recombination. Instead, ASCIZ-deficient B cell precursors contain highly reduced levels of DYNLL1 (dynein light chain 1; LC8), a recently identified transcriptional target of ASCIZ, and normal B cell development can be restored by ectopic Dynll1 expression. Remarkably, the B cell lymphopenia in the absence of ASCIZ can also be fully suppressed by deletion of the proapoptotic DYNLL1 target Bim. Our findings demonstrate a key role for ASCIZ in regulating the survival of developing B cells by activating DYNLL1 expression, which may then modulate Bim-dependent apoptosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.