ArticleOncogene2017
Identification of CASZ1 NES reveals potential mechanisms for loss of CASZ1 tumor suppressor activity in neuroblastoma.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting SWI/SNF ATPases reduces neuroblastoma cell plasticity.The EMBO journal · 2024Article
- Role of the CASZ1 transcription factor in tissue development and disease.European journal of medical research · 2023Review
- Multidimensional quantitative phenotypic and molecular analysis reveals neomorphic behaviors of p53 missense mutants.NPJ breast cancer · 2023Article
- Review
- Zinc finger transcription factor CASZ1b is involved in the DNA damage response in live cells.Biochemical and biophysical research communications · 2023Article
- HAND2 Assists MYCN Enhancer Invasion to Regulate a Noradrenergic Neuroblastoma Phenotype.Cancer research · 2023Article
- Transcription factor CASZ1 increases an oncogenic transcriptional process in tumorigenesis and progression of glioma cells.MedComm · 2022Article
- Loss of CASZ1 tumor suppressor linked to oncogenic subversion of neuroblastoma core regulatory circuitry.Cell death & disease · 2022Article
- Mutations of 1p genes do not consistently abrogate tumor suppressor functions in 1p-intact neuroblastoma.BMC cancer · 2022Article
- Exome sequencing in multiplex families with left-sided cardiac defects has high yield for disease gene discovery.PLoS genetics · 2022Article
- CASZ1b is a novel transcriptional corepressor of mineralocorticoid receptor.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- CASZ1 induces skeletal muscle and rhabdomyosarcoma differentiation through a feed-forward loop with MYOD and MYOG.Nature communications · 2020Article
- The Prognostic Significance of Protein Expression of CASZ1 in Clear Cell Renal Cell Carcinoma.Disease markers · 2019Article
- Casz1 controls higher-order nuclear organization in rod photoreceptors.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
As a transcription factor, localization to the nucleus and the recruitment of cofactors to regulate gene transcription is essential. Nuclear localization and nucleosome remodeling and histone deacetylase (NuRD) complex binding are required for the zinc-finger transcription factor CASZ1 to function as a neuroblastoma (NB) tumor suppressor. However, the critical amino acids (AAs) that are required for CASZ1 interaction with NuRD complex and the regulation of CASZ1 subcellular localization have not been characterized. Through alanine scanning, immunofluorescence cell staining and co-immunoprecipitation, we define a critical region at the CASZ1 N terminus (AAs 23-40) that mediates the CASZ1b nuclear localization and NuRD interaction. Furthermore, we identified a nuclear export signal (NES) at the N terminus (AAs 176-192) that contributes to CASZ1 nuclear-cytoplasmic shuttling in a chromosomal maintenance 1-dependent manner. An analysis of CASZ1 protein expression in a primary NB tissue microarray shows that high nuclear CASZ1 staining is detected in tumor samples from NB patients with good prognosis. In contrast, cytoplasmic-restricted CASZ1 staining or low nuclear CASZ1 staining is found in tumor samples from patients with poor prognosis. These findings provide insight into mechanisms by which CASZ1 regulates transcription, and suggests that regulation of CASZ1 subcellular localization may impact its function in normal development and pathologic conditions such as NB tumorigenesis.
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