ArticleMolecular and cellular biology2003
While K-ras is essential for mouse development, expression of the K-ras 4A splice variant is dispensable.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 105 citations in OpenAlex.
- The impact of RAS on cell differentiation in health and disease.The Biochemical journal · 2025Review
- KRAS4B is required for placental development.Cellular and molecular life sciences : CMLS · 2025Article
- Blocking C-terminal processing of KRAS4b via a direct covalent attack on the CaaX-box cysteine.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Role of RAS in CNS Tumors: A Key Player or an Overlooked Oncogene?International journal of molecular sciences · 2025Review
- "Undruggable KRAS": druggable after all.Genes & development · 2025Review
- The Role of Rab GTPases in the development of genetic and malignant diseases.Molecular and cellular biochemistry · 2024Review
- Splicing alterations in pancreatic ductal adenocarcinoma: a new molecular landscape with translational potential.Journal of experimental & clinical cancer research : CR · 2023Review
- Differential functions of the KRAS splice variants.Biochemical Society transactions · 2023Review
- Article
- Targeting RAS mutants in malignancies: successes, failures, and reasons for hope.Cancer communications (London, England) · 2023Review
- Molecular inhibition of RAS signalling to target ageing and age-related health.Disease models & mechanisms · 2022Review
- Targeting KRAS mutant lung cancer: light at the end of the tunnel.Molecular oncology · 2022Review
- The role of KRAS splice variants in cancer biology.Frontiers in cell and developmental biology · 2022Review
- Past and Future Strategies to Inhibit Membrane Localization of the KRAS Oncogene.International journal of molecular sciences · 2021Review
- Oncogenic KRAS blockade therapy: renewed enthusiasm and persistent challenges.Molecular cancer · 2021Review
- KRAS4A induces metastatic lung adenocarcinomas in vivo in the absence of the KRAS4B isoform.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Targeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells.Nature communications · 2021Article
- Ras Isoforms from Lab Benches to Lives-What Are We Missing and How Far Are We?International journal of molecular sciences · 2021Review
- Review
- K-RAS4A: Lead or Supporting Role in Cancer Biology?Frontiers in molecular biosciences · 2021Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammals, the three classical ras genes encode four highly homologous proteins, N-Ras, H-Ras, and the isoforms K-Ras 4A and 4B. Previous studies have shown that K-ras is essential for mouse development and that while K-ras 4A and 4B are expressed during development, K-ras 4A expression is regulated temporally and spatially and occurs in adult kidney, intestine, stomach, and liver. In the present study, the pattern of K-ras 4A expression was examined in a wide range of wild-type adult mouse tissues, and gene targeting was used to generate K-ras 4A-deficient mice to examine its role in development. It was found that K-ras 4A is also expressed in uterus, lung, pancreas, salivary glands, seminal vesicles, bone marrow cells, and cecum, where it was the major K-Ras isoform expressed. Mating between K-ras(tmDelta4A/+) mice produced viable K-ras(tmDelta4A/tmDelta4A) offspring with the expected Mendelian ratios of inheritance, and these mice expressed the K-ras 4B splice variant only. K-ras(tmDelta4A/tmDelta4A) mice were fertile and showed no histopathological abnormalities on inbred (129/Ola) or crossbred (129/Ola x C57BL/6) genetic backgrounds. The results demonstrate that K-Ras 4A, like H- and N-Ras, is dispensable for normal mouse development, at least in the presence of functional K-Ras 4B.
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Registered trials
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