ReviewThe Biochemical journal2020
The molecular functions of RIT1 and its contribution to human disease.
Review in The Biochemical journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Revisiting RAS family GTPase signaling: effector selectivity and oncogenic bypass.The Biochemical journal · 2026Review
- Continuous multi-omics pathway enrichment analysis resolves hidden functional heterogeneity.Briefings in bioinformatics · 2026Article
- Transcriptional profiling of circulating extracellular vesicles from prebiopsy prostate cancer patients.Molecular oncology · 2026Article
- Neonatal Noonan syndrome with acute kidney injury and systemic capillary leak syndrome caused by aFrontiers in pediatrics · 2026Article
- Phenotypic Analysis of Embryos in a Noonan Syndrome Model Mouse With the Rit1 A57G Mutation.Molecular genetics & genomic medicine · 2025Article
- Mutant RIT1 cooperates with YAP to drive an EMT-like lung cancer state.Cell reports · 2025Article
- RIT1 Drives Oncogenic Transformation and Is an Actionable Target in Lung Adenocarcinoma.Cancer research · 2025Article
- Modulating PAK1: Accessory Proteins as Promising Therapeutic Targets.Biomolecules · 2025Review
- Oncogenic RIT1 mutations confer ferroptosis vulnerability in lung adenocarcinoma.Biology direct · 2025Article
- "Undruggable KRAS": druggable after all.Genes & development · 2025Review
- Microtubule regulation in cancer cells.Frontiers in cell and developmental biology · 2025Article
- Article
- RAS-dependent RAF-MAPK hyperactivation by pathogenic RIT1 is a therapeutic target in Noonan syndrome-associated cardiac hypertrophy.Science advances · 2023Article
- Review
- Defective protein degradation in genetic disorders.Biochimica et biophysica acta. Molecular basis of disease · 2022Review
- How can same-gene mutations promote both cancer and developmental disorders?Science advances · 2022Article
- The RAS GTPase RIT1 compromises mitotic fidelity through spindle assembly checkpoint suppression.Current biology : CB · 2021Article
- LZTR1: A promising adaptor of the CUL3 family.Oncology letters · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
RIT1 is a member of the Ras family of GTPases that direct broad cellular physiological responses through tightly controlled signaling networks. The canonical Ras GTPases are well-defined regulators of the RAF/MEK/ERK pathway and mutations in these are pathogenic in cancer and a class of developmental disorders termed RASopathies. Emerging clinical evidences have now demonstrated a role for RIT1 in RASopathies, namely Noonan syndrome, and various cancers including lung adenocarcinoma and myeloid malignancies. While RIT1 has been mostly described in the context of neuronal differentiation and survival, the mechanisms underlying aberrant RIT1-mediated signaling remain elusive. Here, we will review efforts undertaken to characterize the biochemical and functional properties of the RIT1 GTPase at the molecular, cellular, and organismal level, as well as provide a phenotypic overview of different human conditions caused by RIT1 mutations. Deeper understanding of RIT1 biological function and insight to its pathogenic mechanisms are imperative to developing effective therapeutic interventions for patients with RIT1-mutant Noonan syndrome and 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.