ArticleOncotarget2015
Caspase cleavage of iASPP potentiates its ability to inhibit p53 and NF-κB.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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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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
16 citing papers in PubMed, 20 citations in OpenAlex.
- Structural alterations in PPP1R13L, SAE1, ATP5A1 and PCK2 disrupt NF-κB signalling and mitochondrial metabolism in primary dermal fibroblasts in systemic sclerosis.Rheumatology (Oxford, England) · 2026Article
- Comprehensive bioinformatics analysis and clinical validation of PPP1R13L in rectal adenocarcinoma.BMC cancer · 2026Article
- PPP1R13L drives cervical cancer progression by suppressing p63-mediated PTEN transcription.Cellular and molecular life sciences : CMLS · 2025Article
- Cardiocutaneous syndrome is caused by aggregation of iASPP mutants.Cell death discovery · 2024Article
- Mutant Ras and inflammation-driven skin tumorigenesis is suppressed via a JNK-iASPP-AP1 axis.Cell reports · 2022Article
- iASPP is essential for HIF-1α stabilization to promote angiogenesis and glycolysis via attenuating VHL-mediated protein degradation.Oncogene · 2022Article
- Inhibitor of apoptosis-stimulating p53 protein protects against inflammatory bowel disease in mice models by inhibiting the nuclear factor kappa B signaling.Clinical and experimental immunology · 2021Article
- Nuclear iASPP determines cell fate by selectively inhibiting either p53 or NF-κB.Cell death discovery · 2021Article
- P53 vs NF-κB: the role of nuclear factor-kappa B in the regulation of p53 activity and vice versa.Cellular and molecular life sciences : CMLS · 2020Review
- A previously identified apoptosis inhibitor iASPP confers resistance to chemotherapeutic drugs by suppressing senescence in cancer cells.The Journal of biological chemistry · 2020Article
- The anti-apoptotic proteins NAF-1 and iASPP interact to drive apoptosis in cancer cells.Chemical science · 2019Article
- CD44v6 engages in colorectal cancer progression.Cell death & disease · 2019Review
- MicroRNA-150 inhibits the proliferation and metastasis potential of colorectal cancer cells by targeting iASPP.Oncology reports · 2018Article
- Mild Therapeutic Hypothermia Protects the Brain from Ischemia/Reperfusion Injury through Upregulation of iASPP.Aging and disease · 2018Article
- CDK1 interacts with iASPP to regulate colorectal cancer cell proliferation through p53 pathway.Oncotarget · 2017Article
- iASPP overexpression is associated with clinical outcome in spinal chordoma and influences cellular proliferation, invasion, and sensitivity to cisplatinOncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An intriguing biological question relating to cell signaling is how the inflammatory mediator NF-kB and the tumour suppressor protein p53 can be induced by similar triggers, like DNA damage or infection, yet have seemingly opposing or sometimes cooperative biological functions. For example, the NF-κB subunit RelA/p65 has been shown to inhibit apoptosis, whereas p53 induces apoptosis. One potential explanation may be their co-regulation by common cellular factors: inhibitor of Apoptosis Stimulating p53 Protein (iASPP) is one such common regulator of both RelA/p65 and p53. Here we show that iASPP is a novel substrate of caspases in response to apoptotic stimuli. Caspase cleaves the N-terminal region of iASPP at SSLD294 resulting in a prominent 80kDa fragment of iASPP. This caspase cleavage site is conserved in various species from zebrafish to Homo sapiens. The 80kDa fragment of iASPP translocates from the cytoplasm to the nucleus via the RaDAR nuclear import pathway, independent of p53. The 80kDa iASPP fragment can bind and inhibit p53 or RelA/p65 more efficiently than full-length iASPP. Overall, these data reveal a potential novel regulation of p53 and RelA/p65 activities in response to apoptotic stimuli.
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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.