ArticleOncogene2000
Rit, a non-lipid-modified Ras-related protein, transforms NIH3T3 cells without activating the ERK, JNK, p38 MAPK or PI3K/Akt pathways.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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
32 citing papers in PubMed, 51 citations in OpenAlex.
- Updated ACMG/AMP specifications for variant interpretation and gene curations from the ClinGen RASopathy expert panels.Genetics in medicine open · 2025Article
- RIT1 Promotes the Proliferation of Gliomas Through the Regulation of the PI3K/AKT/c-Myc Signalling Pathway.Journal of cellular and molecular medicine · 2025Article
- Multiomic characterization of oncogenic signaling mediated by wild-type and mutant RIT1.Science signaling · 2021Article
- LZTR1: A promising adaptor of the CUL3 family.Oncology letters · 2021Review
- The molecular functions of RIT1 and its contribution to human disease.The Biochemical journal · 2020Review
- FOXP1-induced lncRNA CLRN1-AS1 acts as a tumor suppressor in pituitary prolactinoma by repressing the autophagy via inactivating Wnt/β-catenin signaling pathway.Cell death & disease · 2019Article
- RIT1 suppresses esophageal squamous cell carcinoma growth and metastasis and predicts good prognosis.Cell death & disease · 2018Article
- RIT1 controls actin dynamics via complex formation with RAC1/CDC42 and PAK1.PLoS genetics · 2018Article
- RIT1 GTPase Regulates Sox2 Transcriptional Activity and Hippocampal Neurogenesis.The Journal of biological chemistry · 2017Article
- Expansion of the RASopathies.Current genetic medicine reports · 2016Article
- Mutations in RIT1 cause Noonan syndrome with possible juvenile myelomonocytic leukemia but are not involved in acute lymphoblastic leukemia.European journal of human genetics : EJHG · 2016Article
- Biochemical Classification of Disease-associated Mutants of RAS-like Protein Expressed in Many Tissues (RIT1).The Journal of biological chemistry · 2016Article
- Spectrum of mutations and genotype-phenotype analysis in Noonan syndrome patients with RIT1 mutations.Human genetics · 2016Article
- Recent advances in RASopathies.Journal of human genetics · 2016Review
- Article
- Elevated expression of RIT1 correlates with poor prognosis in endometrial cancer.International journal of clinical and experimental pathology · 2015Article
- Oncogenic RIT1 mutations in lung adenocarcinoma.Oncogene · 2014Article
- Separate cyclic AMP sensors for neuritogenesis, growth arrest, and survival of neuroendocrine cells.The Journal of biological chemistry · 2014Article
- Article
- Rit subfamily small GTPases: regulators in neuronal differentiation and survival.Cellular signalling · 2013Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The biological functions of Rit (Ras-like protein in tissues) and Rin (Ras-like protein in neurons), members of a novel branch of Ras-related GTP-binding proteins that are approximately 50% identical to Ras, have not been characterized. Therefore, we assessed their activity in growth control, transformation and signaling. NIH cells stably expressing a constitutively activated mutant of Rit [Rit(79L)] (analogous to the oncogenic mutant H-Ras(61L)) demonstrated strong growth transformation, proliferating rapidly in low serum and forming colonies in soft agar and tumors in nude mice. Although Rit(79L) alone did not promote morphologically transformed foci, it cooperated with both Raf and Rho A to form Rac/Rho-like foci. Rin [Rin(78L)] cooperated only with Raf. Rit(79L) but not Rin(78L) stimulated transcription from luciferase reporter constructs regulated by SRF, NF-kappaB, Elk-1 and Jun. However, neither activated ERK, JNK or p38, or PI3-K/Akt kinases in immune complex kinase assays. Interestingly, although Rit lacks any known recognition signal for C-terminal lipidation, Rit-transformed cell growth and survival in low serum is dependent on a farnesylated protein, as treatment with farnesyltransferase inhibitors caused apoptosis. Rin cooperated with Raf in focus assays but did not otherwise function in these assays, perhaps due to a lack of appropriate effector pathways in NIH3T3 fibroblasts for this neural-specific Ras family member. In summary, although Rit shares most core effector domain residues with Ras, our results suggest that Rit uses novel effector pathways to regulate proliferation and transformation.
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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.