ArticleScientific reports2025
Discovery of effectors for casein kinase signaling in the African trypanosome.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Extensive divergence of protein sequences from those of model eukaryotes makes recognition of well-studied signaling pathways impossible in Trypanosoma brucei. Consequently, substrates and effectors of most protein kinases are unknown. We addressed these general problems by developing workflows to (i) identify effectors for protein kinases, (ii) discover new effectors and substrates of CK1.2 as proof of principle, and (iii) decode linear motifs in CK1.2 substrates. Casein kinase CK1.2 promotes cytokinesis and division of mitochondrial DNA (kinetoplast) (kDNA). Applying our principles to CK1.2 we identified four new substrates, BBP59, LRRP1, CAP64, and BBP268, that harbored two unique linear motifs, S-x(1,3)-T-x(1,4)-S-x(2)-A-x(2)-[AIV] and S-x(1,3)-T-x(1,4)-S. Ectopic expression of BBP59 inhibited cytokinesis and kinetoplast DNA division, like knockdown of CK1.2. Phosphorylation of BBP59 was blocked after knockdown of CK1.2 or treatment with SB-431542 an inhibitor of CK1.2 (IC
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.