ArticleOncotarget2016
FAM65B controls the proliferation of transformed and primary T cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 29 citations in OpenAlex.
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- Multiparameter flow cytometric and transcriptional analyis of CD20 positive T-cells in bone marrow in patients of multiple myeloma and monoclonal gammopathy of undetermined significance.Frontiers in immunology · 2025Article
- MEK inhibition prevents CAR-T cell exhaustion and differentiation via downregulation of c-Fos and JunB.Signal transduction and targeted therapy · 2024Article
- Comprehensive Molecular Profiling of NPM1-Mutated Acute Myeloid Leukemia Using RNAseq Approach.International journal of molecular sciences · 2024Article
- Characterizing Neutrophil Subtypes in Cancer Using scRNA Sequencing Demonstrates the Importance of IL1β/CXCR2 Axis in Generation of Metastasis-specific Neutrophils.Cancer research communications · 2024Article
- Single cell multi-omic analysis identifies key genes differentially expressed in innate lymphoid cells from COVID-19 patients.Frontiers in immunology · 2024Article
- Review
- Chronic Inhalation Exposure to Antimony Trioxide Exacerbates the MAPK Signaling in Alveolar Bronchiolar Carcinomas in B6C3F1/N Mice.Toxicologic pathology · 2023Article
- Role of RHO family interacting cell polarization regulators (RIPORs) in health and disease: Recent advances and prospects.International journal of biological sciences · 2022Review
- Genetic loci for lung function in Japanese adults with adjustment for exhaled nitric oxide levels as airway inflammation indicator.Communications biology · 2021Article
- RHO GTPases: from new partners to complex immune syndromes.Nature reviews. Immunology · 2021Review
- DNA methylation and cancer incidence: lymphatic-hematopoietic versus solid cancers in the Strong Heart Study.Clinical epigenetics · 2021Article
- Dynamics in protein translation sustaining T cell preparedness.Nature immunology · 2020Article
- The circular RNA ACR attenuates myocardial ischemia/reperfusion injury by suppressing autophagy via modulation of the Pink1/ FAM65B pathway.Cell death and differentiation · 2019Article
- FOXO1 transcription factor plays a key role in T cell-HIV-1 interaction.PLoS pathogens · 2019Article
- The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8The Journal of experimental medicine · 2018Article
- Fam65b Phosphorylation Relieves Tonic RhoA Inhibition During T Cell Migration.Frontiers in immunology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell quiescence is controlled by regulated genome-encoded programs that actively express genes which are often down-regulated or inactivated in transformed cells. Among them is FoxO1, a transcription factor that imposes quiescence in several cell types, including T lymphocytes. In these cells, the FAM65B encoding gene is a major target of FOXO1. Here, we show that forced expression of FAM65B in transformed cells blocks their mitosis because of a defect of the mitotic spindle, leading to G2 cell cycle arrest and apoptosis. Upon cell proliferation arrest, FAM65B is engaged in a complex containing two proteins well known to be involved in cell proliferation i.e. the HDAC6 deacetylase and the 14.3.3 scaffolding protein. In primary T cells, FAM65B is down-regulated upon T cell receptor engagement, and maintaining its expression blocks their proliferation, establishing that the decrease of FAM65B expression is required for proliferation. Conversely, inhibiting FAM65B expression in naive T lymphocytes decreases their activation threshold. These results identify FAM65B as a potential new target for controlling proliferation of both transformed and normal cells.
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What Socratic 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 Socratic graph.