Evidence map›Paper›PMID 21490919›Full record

ArticlePloS one2011

CASZ1b, the short isoform of CASZ1 gene, coexpresses with CASZ1a during neurogenesis and suppresses neuroblastoma cell growth.

Zhihui Liu, Arlene Naranjo, Carol J Thiele

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Biomedicines · 2023
    Review
  3. Article
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  7. CASZ1b is a novel transcriptional corepressor of mineralocorticoid receptor.Hypertension research : official journal of the Japanese Society of Hypertension · 2021
    Article
  8. Article
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  14. CASZ1 is a novel promoter of metastasis in ovarian cancer.American journal of cancer research · 2016
    Article
  15. Article
  16. Article
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  19. Article
  20. Differential regulation of CASZ1 protein expression during cardiac and skeletal muscle development.Developmental dynamics : an official publication of the American Association of Anatomists · 2014
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

Zhihui LiuPediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.
Arlene Naranjo
Carol J Thiele
Center for Cancer Research · USNational Cancer Institute · USUniversity of Florida · US

Funding

Regulation of Differentiation of Pediatric Embryonal Tumors- NeuroblastomaZIABC010788 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI THIELE, CAROL J · 2009 to 2025
$29.7M
Intramural NIH HHS
6 · The paper itself

Abstract

In Drosophila, the CASZ1 (castor) gene encodes a zinc finger transcription factor and is a neural fate-determination gene. In mammals, the CASZ1 gene encodes two major isoforms, CASZ1a with 11 zinc fingers and CASZ1b with 5 zinc fingers. CASZ1b is more evolutionally conserved since it is the only homologue found in drosophila and Xenopus. Our previous study showed that full length CASZ1 (CASZ1a) functions to suppress growth in neuroblastoma tumor. However, the function of CASZ1b isoform in mammals is unknown. In this study, realtime PCR analyses indicate that mouse CASZ1b (mCASZ1b) is dynamically expressed during neurogenesis. CASZ1b and CASZ1a co-exist in all the neuronal tissues but exhibit distinct expression patterns spatially and temporally during brain development. CASZ1b and CASZ1a expression is coordinately upregulated by the differentiation agent Retinoic Acid, as well as agents that modify the epigenome in neural crest derived neuroblastoma cell lines. In contrast CASZ1b is down regulated while CASZ1a is upregulated by agents that raise intracellular cAMP levels. CASZ1b and CASZ1a have no synergistic or antagonistic activities on the regulation of their target NGFR gene transcription. Specific restoration of CASZ1b in NB cells suppresses tumor growth in vitro and in vivo. Consistent with its function role, we find that low CASZ1b expression is significantly associated with decreased survival probability of neuroblastoma patients (p<0.02). This study indicates that although their mechanisms of regulation may be distinct, both CASZ1b and CASZ1a have largely redundant but critical roles in suppressing tumor cell growth.

Indexed as

AnimalsBlotting, WesternCell LineCell Line, TumorCell ProliferationDNA-Binding ProteinsFemaleFluorescent Antibody Technique, IndirectHumansMiceMice, SCIDNeuroblastomaNeurogenesisPolymerase Chain ReactionPromoter Regions, GeneticProtein IsoformsCASZ1 protein, humanDNA-Binding ProteinsProtein IsoformsTranscription Factors

Identifiers

PMID21490919
PMCPMC3072398
OpenAlexW1980912623

What OpenQuestion holds

Textmetadata
LicenceCC0
Read underepoch 390

Registered trials

None linked

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.