ArticleOncogene2002
Study of the 2719 mutant of the c-H-ras oncogene in a bi-intronic alternative splicing system.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Review
- Alternative-splicing defects in cancer: Splicing regulators and their downstream targets, guiding the way to novel cancer therapeutics.Wiley interdisciplinary reviews. RNA · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C-H-ras proto-oncogene forms part of the signal transduction pathway of numerous external stimuli. This proto-oncogene is regulated by alternative splicing within its intron D due to the presence of the alternative intron D exon (IDX). The alternative splicing produces mRNA which encodes for the putative p19 protein, that lacks transforming potential. Herein, we demonstrated that SR proteins regulate the intron D splicing. Moreover, we studied the 2719 mutation of H-ras which has higher transforming potential than Ile12 and Val12 H-ras mutants and is also known to affect the 5' splice site of the IDX. However, here we show that the 2719 mutant can still be spliced when the upstream 5' splice-site is blocked. During these later studies, additionally, we generated a short 11 nucleotides 5' terminal exon that was fully defined and spliced in a bi-intronic pre-mRNA. The definition of this mini-exon was also addressed in this work.
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Registered trials
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