ArticlePloS one2013
A novel predicted calcium-regulated kinase family implicated in neurological disorders.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 51 citations in OpenAlex.
- Genome-wide DNA methylation profiling in COVID-19 positive patients reveals alterations in pathways linked to neurological dysfunction.Clinical epigenetics · 2026Article
- Genome-wide DNA methylation profiling reveals diagnostic markers in parathyroid tumours.Journal of endocrinological investigation · 2026Article
- Novel regulators of heparan sulfate proteoglycans modulate cellular uptake of α-synuclein fibrils.Communications biology · 2025Article
- Social fear extinction susceptibility is associated with Microbiota-Gut-Brain axis alterations.Brain, behavior, and immunity · 2024Article
- Allnighter pseudokinase-mediated feedback links proteostasis and sleep in Drosophila.Nature communications · 2023Article
- Regulation of secretory pathway kinase or kinase-like proteins in human cancers.Frontiers in immunology · 2023Review
- Pan-kinome of Legionella expanded by a bioinformatics survey.Scientific reports · 2022Article
- High-resolution structure of a fish aquaporin reveals a novel extracellular fold.Life science alliance · 2022Article
- Diverse functions associate with non-coding polymorphisms shared between humans and chimpanzees.BMC ecology and evolution · 2022Article
- Methods for discovering catalytic activities for pseudokinases.Methods in enzymology · 2022Article
- Article
- DIPK2A promotes STX17- and VAMP7-mediated autophagosome-lysosome fusion by binding to VAMP7B.Autophagy · 2020Article
- A fetus with Kabuki syndrome 2 detected by chromosomal microarray analysis.International journal of clinical and experimental pathology · 2020Article
- Breakdown of multiple sclerosis genetics to identify an integrated disease network and potential variant mechanisms.Physiological genomics · 2019Article
- PEAK3/C19orf35 pseudokinase, a new NFK3 kinase family member, inhibits CrkII through dimerization.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Genomic imbalances defining novel intellectual disability associated loci.Orphanet journal of rare diseases · 2019Article
- Thinking outside of the cell: Secreted protein kinases in bacteria, parasites, and mammals.IUBMB life · 2019Review
- Article
- Structure and evolution of the Fam20 kinases.Nature communications · 2018Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The catalogues of protein kinases, the essential effectors of cellular signaling, have been charted in Metazoan genomes for a decade now. Yet, surprisingly, using bioinformatics tools, we predicted protein kinase structure for proteins coded by five related human genes and their Metazoan homologues, the FAM69 family. Analysis of three-dimensional structure models and conservation of the classic catalytic motifs of protein kinases present in four out of five human FAM69 proteins suggests they might have retained catalytic phosphotransferase activity. An EF-hand Ca(2+)-binding domain in FAM69A and FAM69B proteins, inserted within the structure of the kinase domain, suggests they may function as Ca(2+)-dependent kinases. The FAM69 genes, FAM69A, FAM69B, FAM69C, C3ORF58 (DIA1) and CXORF36 (DIA1R), are by large uncharacterised molecularly, yet linked to several neurological disorders in genetics studies. The C3ORF58 gene is found deleted in autism, and resides in the Golgi. Unusually high cysteine content and presence of signal peptides in some of the family members suggest that FAM69 proteins may be involved in phosphorylation of proteins in the secretory pathway and/or of extracellular proteins.
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.