ArticlePurinergic signalling2021
ENTPD5: identification of splicing variants and their impact on cancer survival.
Article in Purinergic signalling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 7 citations in OpenAlex.
- Purinergic signal transduction and metabolic regulation by ENTPD5 and ENTPD6.Frontiers in endocrinology · 2026Review
- Multiple association studies identify 3 novel candidate genes for teat number trait in Danish Landrace and Large White pigs: BRINP3, LIN52, and UBE3B.Journal of animal science · 2025Article
- Integrated machine learning based on cuproptosis and RNA methylation regulators to explore the molecular model of prostate cancer and provide novel insights to immunotherapy.Journal of Cancer · 2025Article
- Developing prognostic models for cholesterol-related genes linked with immune infiltration in prostate cancer.Frontiers in genetics · 2025Article
- Knockdown of ENTPD5 inhibits tumor metastasis and growth via regulating the GRP78/p-eIF-2α/CHOP pathway in serous ovarian cancer.Journal of ovarian research · 2022Article
- The broad range di- and tri-nucleotide exchanger SLC35B1 displays asymmetrical affinities for ATP transport across the ER membrane.The Journal of biological chemistry · 2022Article
- ENTPD5 splice variants: novel players in cancer?Purinergic signalling · 2021Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
NTPDase5 is a nucleotidase of the endoplasmic reticulum that plays an important role in proteostasis as a regulator of protein N-glycosylation. This enzyme was first identified in hamster as a proto-oncogene activated upon a single nucleotide deletion that causes a frameshift leading to a truncated protein. Truncated NTPDase5 proteins were detected in human samples, but an oncogene was never identified. Searching for transcript variants in the GenBank database and using TCGA data, we discovered that splice variants could originate truncated human NTPDase5 proteins. We identified three main splicing events in the ENTPD5 gene: alternative acceptors, exon skipping, and alternative terminators. The analysis of impact of splicing events in cancers showed that skipping of exon 11-the event that leads to truncated proteins similar in size to the hamster oncogene-does not affect the hazard ratio of most tumors and was, in fact, a protective factor in the only two cancer studies where it was significant. We also identified four main patterns of impact of ENTPD5 in cancer and a potential variant-specific regulation by miR-215. Our findings shed light on a two-decade uncertainty about the origin of truncated NTPDase5 and contribute to the characterization of its impacts in cancer.
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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.