ArticlePLoS genetics2010
Dual functions of ASCIZ in the DNA base damage response and pulmonary organogenesis.
Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Linker Length Drives Heterogeneity of Multivalent Complexes of Hub Protein LC8 and Transcription Factor ASCIZ.Biomolecules · 2023Article
- Developing high-affinity decoy receptors to treat multiple myeloma and diffuse large B cell lymphoma.The Journal of experimental 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
- Tumor Hypoxia Drives Genomic Instability.Frontiers in cell and developmental biology · 2021Review
- Genetic Mouse Models and Induced Pluripotent Stem Cells for Studying Tracheal-Esophageal Separation and Esophageal Development.Stem cells and development · 2020Article
- Impact of hypoxia on DNA repair and genome integrity.Mutagenesis · 2020Review
- Atmin modulates Pkhd1 expression and may mediate Autosomal Recessive Polycystic Kidney Disease (ARPKD) through altered non-canonical Wnt/Planar Cell Polarity (PCP) signalling.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- PPARγ Interaction with UBR5/ATMIN Promotes DNA Repair to Maintain Endothelial Homeostasis.Cell reports · 2019Article
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- Dynein light chain regulates adaptive and innate B cell development by distinctive genetic mechanisms.PLoS genetics · 2017Article
- Mechanisms and consequences of ATMIN repression in hypoxic conditions: roles for p53 and HIF-1.Scientific reports · 2016Article
- ATMIN is required for the ATM-mediated signaling and recruitment of 53BP1 to DNA damage sites upon replication stress.DNA repair · 2014Article
- Atmin mediates kidney morphogenesis by modulating Wnt signaling.Human molecular genetics · 2014Article
- ATMIN is a transcriptional regulator of both lung morphogenesis and ciliogenesis.Development (Cambridge, England) · 2014Article
- ATM signalling and cancer.Oncogene · 2014Review
- The novel zinc finger protein dASCIZ regulates mitosis in Drosophila via an essential role in dynein light-chain expression.Genetics · 2014Article
- Essential developmental, genomic stability, and tumour suppressor functions of the mouse orthologue of hSSB1/NABP2.PLoS genetics · 2013Article
- The Zinc-finger protein ASCIZ regulates B cell development via DYNLL1 and Bim.The Journal of experimental medicine · 2012Article
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zn²(+)-finger proteins comprise one of the largest protein superfamilies with diverse biological functions. The ATM substrate Chk2-interacting Zn²(+)-finger protein (ASCIZ; also known as ATMIN and ZNF822) was originally linked to functions in the DNA base damage response and has also been proposed to be an essential cofactor of the ATM kinase. Here we show that absence of ASCIZ leads to p53-independent late-embryonic lethality in mice. Asciz-deficient primary fibroblasts exhibit increased sensitivity to DNA base damaging agents MMS and H2O2, but Asciz deletion knock-down does not affect ATM levels and activation in mouse, chicken, or human cells. Unexpectedly, Asciz-deficient embryos also exhibit severe respiratory tract defects with complete pulmonary agenesis and severe tracheal atresia. Nkx2.1-expressing respiratory precursors are still specified in the absence of ASCIZ, but fail to segregate properly within the ventral foregut, and as a consequence lung buds never form and separation of the trachea from the oesophagus stalls early. Comparison of phenotypes suggests that ASCIZ functions between Wnt2-2b/ß-catenin and FGF10/FGF-receptor 2b signaling pathways in the mesodermal/endodermal crosstalk regulating early respiratory development. We also find that ASCIZ can activate expression of reporter genes via its SQ/TQ-cluster domain in vitro, suggesting that it may exert its developmental functions as a transcription factor. Altogether, the data indicate that, in addition to its role in the DNA base damage response, ASCIZ has separate developmental functions as an essential regulator of respiratory organogenesis.
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Registered trials
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.