ReviewCells2016
Atypical Rho GTPases of the RhoBTB Subfamily: Roles in Vesicle Trafficking and Tumorigenesis.
Review in Cells, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
40 citing papers in PubMed, 56 citations in OpenAlex.
- RHOBTB2 enhances cell proliferation of acute myeloid leukemia by modulating Hippo-YAP1 signaling and dependent of KLHL13.Scientific reports · 2025Article
- Circulating microRNAs and cross sectional and longitudinal measurements of physical functioning and frailty: An explorative study in older twins.Mechanisms of ageing and development · 2025Article
- Secretory Profile Analysis of Human Granulosa Cell Line Following Gonadotropin Stimulation.International journal of molecular sciences · 2025Article
- Deregulated ion channels contribute to RHOBTB2-associated developmental and epileptic encephalopathy.Human molecular genetics · 2025Article
- The small GTPase MRAS is a broken switch.Nature communications · 2025Article
- Evaluation of large language models for discovery of gene set function.Nature methods · 2025Article
- Genome-Wide Identification and Expression Analysis of theInternational journal of molecular sciences · 2024Article
- Article
- The 2023 Walter B. Cannon Award Lecture: Mechanisms Regulating Vascular Function and Blood Pressure by the PPARγ-RhoBTB1-CUL3 Pathway.Function (Oxford, England) · 2024Review
- Genotype-phenotype correlations in RHOBTB2-associated neurodevelopmental disorders.Genetics in medicine : official journal of the American College of Medical Genetics · 2023Article
- MicroRNA-142-3p promotes renal cell carcinoma progression by targeting RhoBTB3 to regulate HIF-1 signaling and GGT/GSH pathways.Scientific reports · 2023Article
- Structure and Function of RhoBTB1 Required for Substrate Specificity and Cullin-3 Ubiquitination.Function (Oxford, England) · 2023Article
- RhoBTB3 Regulates Proliferation and Invasion of Breast Cancer Cells via Col1a1.Molecules and cells · 2022Article
- Dynamics of huntingtin protein interactions in the striatum identifies candidate modifiers of Huntington disease.Cell systems · 2022Article
- Genomics and transcriptomics yields a system-level view of the biology of the pathogen Naegleria fowleri.BMC biology · 2021Article
- Review
- Golgi-associated Rab GTPases implicated in autophagy.Cell & bioscience · 2021Review
- Neurodevelopmental Disorders (NDD) Caused by Genomic Alterations of the Ubiquitin-Proteasome System (UPS): the Possible Contribution of Immune Dysregulation to Disease Pathogenesis.Frontiers in molecular neuroscience · 2021Review
- Review
- High Throughput strategies Aimed at Closing the GAP in Our Knowledge of Rho GTPase Signaling.Cells · 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
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RhoBTB proteins constitute a subfamily of atypical Rho GTPases represented in mammals by RhoBTB1, RhoBTB2, and RhoBTB3. Their characteristic feature is a carboxyl terminal extension that harbors two BTB domains capable of assembling cullin 3-dependent ubiquitin ligase complexes. The expression of all three RHOBTB genes has been found reduced or abolished in a variety of tumors. They are considered tumor suppressor genes and recent studies have strengthened their implication in tumorigenesis through regulation of the cell cycle and apoptosis. RhoBTB3 is also involved in retrograde transport from endosomes to the Golgi apparatus. One aspect that makes RhoBTB proteins atypical among the Rho GTPases is their proposed mechanism of activation. No specific guanine nucleotide exchange factors or GTPase activating proteins are known. Instead, RhoBTB might be activated through interaction with other proteins that relieve their auto-inhibited conformation and inactivated through auto-ubiquitination and destruction in the proteasome. In this review we discuss our current knowledge on the molecular mechanisms of action of RhoBTB proteins and the implications for tumorigenesis and other pathologic conditions.
Indexed as
Identifiers
What 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.