ReviewCerebellum (London, England)2005
The robotic mouse: unravelling the function of AF4 in the cerebellum.
Review in Cerebellum (London, England), 2005. 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, 24 citations in OpenAlex.
- AFF4 Loss Compromises Osteogenesis of Orofacial Mesenchymal Stem Cells During Alveolar Bone Repair via AMPK-Mediated Mitophagy.Cell proliferation · 2026Article
- The Biological Significance of AFF4: Promoting Transcription Elongation, Osteogenic Differentiation and Tumor Progression.Combinatorial chemistry & high throughput screening · 2024Review
- Comment on Herring et al. The Use of "Retardation" in FRAXA, FMRP, FMR1 and Other Designations.Cells · 2022Article
- Transcription Pause and Escape in Neurodevelopmental Disorders.Frontiers in neuroscience · 2022Review
- Variants in the degron of AFF3 are associated with intellectual disability, mesomelic dysplasia, horseshoe kidney, and epileptic encephalopathy.American journal of human genetics · 2021Article
- Acute perturbation strategies in interrogating RNA polymerase II elongation factor function in gene expression.Genes & development · 2021Article
- AFF1 and AFF4 differentially regulate the osteogenic differentiation of human MSCs.Bone research · 2017Article
- MLL-Rearranged Leukemias-An Update on Science and Clinical Approaches.Frontiers in pediatrics · 2017Review
- Laf4/Aff3, a gene involved in intellectual disability, is required for cellular migration in the mouse cerebral cortex.PloS one · 2014Article
- The super elongation complex (SEC) family in transcriptional control.Nature reviews. Molecular cell biology · 2012Review
- The super elongation complex family of RNA polymerase II elongation factors: gene target specificity and transcriptional output.Molecular and cellular biology · 2012Article
- Protein network study of human AF4 reveals its central role in RNA Pol II-mediated transcription and in phosphorylation-dependent regulatory mechanisms.The Biochemical journal · 2011Article
- The identification of transcription factors expressed in the notochord of Ciona intestinalis adds new potential players to the brachyury gene regulatory network.Developmental dynamics : an official publication of the American Association of Anatomists · 2011Article
- AF4 is a critical regulator of the IGF-1 signaling pathway during Purkinje cell development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- The robotic mouse: understanding the role of AF4, a cofactor of transcriptional elongation and chromatin remodelling, in purkinje cell function.Cerebellum (London, England) · 2009Review
- A role for the MLL fusion partner ENL in transcriptional elongation and chromatin modification.Blood · 2007Article
- Comparative genetic analysis: the utility of mouse genetic systems for studying human monogenic disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2007Review
- MCEF is localized to the nucleus by protein sequences encoded within three distinct exons, where it represses HIV-1 Tat-transactivation of LTR-directed transcription.International journal of biological sciences · 2007Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The devastating nature and lack of effective treatments associated with neurodegenerative diseases have stimulated a world-wide search for the elucidation of their molecular basis to which mouse models have made a major contribution. In combination with transgenic and knockout technologies, large-scale mouse mutagenesis is a powerful approach for the identification of new genes and associated signalling pathways controlling neuronal cell death and survival. Here we review the characterization of the robotic mouse, a novel model of autosomal dominant cerebellar ataxia isolated from an ENU-mutagenesis programme, which develops adult-onset region-specific Purkinje cell loss and cataracts, and displays defects in early T-cell maturation and general growth retardation. The mutated protein, Af4, is a member of the AF4/LAF4/FMR2 (ALF) family of putative transcription factors previously implicated in childhood leukaemia and FRAXE mental retardation. The mutation, which lies in a highly conserved region among the ALF family members, significantly reduces the binding affinity of Af4 to the E3 ubiquitin-ligase Siah-1a, isolated with Siah-2 as interacting proteins in the brain. This leads to a markedly slower turnover of mutant Af4 by the ubiquitin-proteasome pathway and consequently to its abnormal accumulation in the robotic mouse. Importantly, the conservation of the Siah-binding domain of Af4 in all other family members reveals that Siah-mediated proteasomal degradation is a common regulatory mechanism that controls the levels, and thereby the function, of the ALF family. The robotic mouse represents a unique model in which to study the newly revealed role of Af4 in the maintenance of vital functions of Purkinje cells in the cerebellum and further the understanding of its implication in lymphopoeisis.
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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.