ArticleOncogene2007
Amyloid-beta precursor-like protein APLP1 is a novel p53 transcriptional target gene that augments neuroblastoma cell death upon genotoxic stress.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
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- APLP1 Interacts with SARM1 and Regulates Axonal Maintenance and Post-Injury Degeneration.Molecular neurobiology · 2025Article
- Dysregulation of extracellular fibronectin and α5-integrin in dermal aging.Molecular biology of the cell · 2025Article
- Transcription factors ASCL1 and OLIG2 drive glioblastoma initiation and co-regulate tumor cell types and migration.Nature communications · 2024Article
- Senescent endothelial cells promote liver metastasis of uveal melanoma in single-cell resolution.Journal of translational medicine · 2024Article
- Ketogenic diet induces p53-dependent cellular senescence in multiple organs.Science advances · 2024Article
- Genomic gain ofScience advances · 2021Article
- DNA methylation and exposure to violence among African American young adult males.Brain, behavior, & immunity - health · 2021Article
- Candesartan Neuroprotection in Rat Primary Neurons Negatively Correlates with Aging and Senescence: a Transcriptomic Analysis.Molecular neurobiology · 2020Article
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- Inhibitors of histone acetyltransferases KAT6A/B induce senescence and arrest tumour growth.Nature · 2018Article
- Amyloid precursor like protein-1 promotes JNK-mediated cell migration in Drosophila.Oncotarget · 2017Article
- Multiple across-strain and within-strain QTLs suggest highly complex genetic architecture for hypoxia tolerance in channel catfish.Molecular genetics and genomics : MGG · 2017Article
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- PIM kinase inhibitor AZD1208 for treatment of MYC-driven prostate cancer.Journal of the National Cancer Institute · 2015Article
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- Genome-wide transcriptional reorganization associated with senescence-to-immortality switch during human hepatocellular carcinogenesis.PloS one · 2013Article
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- Molecular and genomic approach for understanding the gene-environment interaction between Nrf2 deficiency and carcinogenic nickel-induced DNA damage.Oncology reports · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor p53 is a key modulator of the cellular stress response, inducing cell-cycle arrest, apoptosis, senescence and cell differentiation. To evaluate further the molecular mechanism underlying p53 function, the transcriptional profiles of proliferating and senescent WI-38 cells, both wild-type p53 expressers and counterparts with an inactivated p53, were compared by DNA microarray analysis. In particular, the amyloid-beta precursor-like protein 1 (APLP1) is induced in senescent cells in a p53-dependent manner. APLP1 was confirmed to be a novel transcriptional target of p53 by in vivo and in vitro characterization of a p53 responsive element found in the first intron of the APLP1 gene locus. APLP1 knockdown experiments demonstrate that APLP1 is required for the proliferation of fibroblastic and epithelial cells. Moreover, depletion of APLP1 expression diminishes stress-induced apoptosis of neural cells, whereas ectopic APLP1 expression augments apoptosis. Based on these data, a mechanism is proposed whereby p53-dependent induction of APLP1 is involved in neural cell death, and which may exacerbate neuronal cell loss in some acute or chronic neurodegenerative disorders.
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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.