ArticleThe Journal of biological chemistry2017
Biochemical characterization of purified mammalian ARL13B protein indicates that it is an atypical GTPase and ARL3 guanine nucleotide exchange factor (GEF).
Article in The Journal of biological chemistry, 2017. 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, 61 citations in OpenAlex.
- Article
- Exome sequencing reveals broad genetic heterogeneity for neuromuscular disorders in consanguineous Pakistani Families.European journal of human genetics : EJHG · 2025Article
- Ciliary ARL13B Is Essential for Vision and Morphogenesis of Cone Outer Segments.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Knocking out ARL13B completely abolishes primary ciliogenesis in cell lines.Scientific reports · 2025Article
- A novel recurrent ARL3 variant c.209G > A p.(Gly70Glu) causes variable non-syndromic dominant retinal dystrophy with defective lipidated protein transport in human retinal stem cell models.Human molecular genetics · 2025Article
- Unfolding ARF and ARL GTPases: from biophysics to systems-level insights.Frontiers in molecular biosciences · 2025Review
- Article
- Phosphoinositides in New Spaces.Cold Spring Harbor perspectives in biology · 2023Review
- Ciliary ARL13B inhibits developmental kidney cystogenesis in mouse.Developmental biology · 2023Article
- Structural insights into regulation of CNNM-TRPM7 divalent cation uptake by the small GTPase ARL15.eLife · 2023Article
- The Arf family GTPases: Regulation of vesicle biogenesis and beyond.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Review
- Unraveling the intricate cargo-BBSome coupling mechanism at the ciliary tip.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Protein kinase CK2 modulates the activity of Maf-family bZIP transcription factor NRL in rod photoreceptors of mammalian retina.Human molecular genetics · 2023Article
- Interactions between TULP3 tubby domain and ARL13B amphipathic helix promote lipidated protein transport to cilia.Molecular biology of the cell · 2023Article
- Structural insights into regulation of TRPM7 divalent cation uptake by the small GTPase ARL15.bioRxiv : the preprint server for biology · 2023Article
- Ciliogenesis membrane dynamics and organization.Seminars in cell & developmental biology · 2023Review
- Loss of ARL13 impedes BBSome-dependent cargo export from Chlamydomonas cilia.The Journal of cell biology · 2022Article
- Article
- Phylogenetic profiling and cellular analyses of ARL16 reveal roles in traffic of IFT140 and INPP5E.Molecular biology of the cell · 2022Article
- The ARF GAPs ELMOD1 and ELMOD3 act at the Golgi and cilia to regulate ciliogenesis and ciliary protein traffic.Molecular biology of the cell · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Primary cilia play central roles in signaling during metazoan development. Several key regulators of ciliogenesis and ciliary signaling are mutated in humans, resulting in a number of ciliopathies, including Joubert syndrome (JS). ARL13B is a ciliary GTPase with at least three missense mutations identified in JS patients. ARL13B is a member of the ADP ribosylation factor family of regulatory GTPases, but is atypical in having a non-homologous, C-terminal domain of ∼20 kDa and at least one key residue difference in the consensus GTP-binding motifs. For these reasons, and to establish a solid biochemical basis on which to begin to model its actions in cells and animals, we developed preparations of purified, recombinant, murine Arl13b protein. We report results from assays for solution-based nucleotide binding, intrinsic and GTPase-activating protein-stimulated GTPase, and ARL3 guanine nucleotide exchange factor activities. Biochemical analyses of three human missense mutations found in JS and of two consensus GTPase motifs reinforce the atypical properties of this regulatory GTPase. We also discovered that murine Arl13b is a substrate for casein kinase 2, a contaminant in our preparation from human embryonic kidney cells. This activity, and the ability of casein kinase 2 to use GTP as a phosphate donor, may be a source of differences between our data and previously published results. These results provide a solid framework for further research into ARL13B on which to develop models for the actions of this clinically important cell regulator.
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.