ArticleAmerican journal of cancer research2019
SHEDding light on the role of Pragmin pseudo-kinases in cancer.
Article in American journal of cancer research, 2019. 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.
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.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Current understanding of PEAK family members in regulation of cellular signaling pathways and cancer therapy.Molecular and cellular biochemistry · 2025Review
- Structural mapping of PEAK pseudokinase interactions identifies 14-3-3 as a molecular switch for PEAK3 signaling.Nature communications · 2023Article
- Article
- Recent advances in targeting protein kinases and pseudokinases in cancer biology.Frontiers in cell and developmental biology · 2022Review
- Article
- Src Family Tyrosine Kinases in Intestinal Homeostasis, Regeneration and Tumorigenesis.Cancers · 2020Review
- Collagen Kinase Receptors as Potential Therapeutic Targets in Metastatic Colon Cancer.Frontiers in oncology · 2020Review
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 human kinome comprises more than 50 pseudo-kinases with unclear biological function due to the absence of apparent catalytic activity, and therefore, with presumably little interest for cancer drug discovery. However, it is now acknowledged that several of them, such as Pragmin family members, play roles as important as those of active kinases in human cancer. How these pseudo-kinases promote tumor formation is largely unknown. Recently, independent structural analyses of three Pragmin pseudo-kinases (Pragmin, SGK223, and SGK269/PEAK1) revealed a split helical dimerization (SHED)-based mechanism of action. Additional sequence-structure analysis identified C19orf35 as a new member of the Pragmin family. Based on the results of these molecular studies, we present a unified model on how Pragmin pseudo-kinases may regulate oncogenic signaling, and suggest potential therapeutic strategies to block their tumor activity.
Indexed as
Identifiers
30906642PMC6405979W2991424847What OpenQuestion holds
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.