ArticleThe Journal of biological chemistry2026
Structural basis of the protein kinase PKN1 HR1 domain oligomerization and differential regulation by RhoA and Rac1.
Article in The Journal of biological chemistry, 2026. 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
3 authors.
Funding
Abstract
The protein kinase C-related kinase (PKN) family of serine/threonine kinases consists of PKN1, PKN2 and PKN3, all of which are Rho family GTPase effectors. PKNs have three N-terminal Homology Region 1 (HR1) domains (HR1a, HR1b and HR1c), which form antiparallel coiled coils, which in two cases interact with Rho family GTPases, activating the kinase. The PKNs are implicated in several important cellular processes, including cytoskeletal regulation, cell adhesion, gene expression and cell cycle progression, and are also implicated in cancer. Here, we have investigated the roles of the HR1 domains in PKN oligomerisation. We show that PKN1 HR1a is a dimer and that the HR1c domain drives further oligomerization. We have mapped the interactions between the HR1 domains and used an integrative approach to model HR1-containing PKN1 dimers. Biophysical analysis shows that RhoA forms a 1:2 complex with HR1a, resulting in a rearrangement of the HR1a dimer, an outcome supported by SAXS models. In contrast, Rac1 binds to monomeric HR1a, suggesting that this GTPase activates PKN1 via a different mechanism. These data provide structural insight into interactions between HR1 domains and the Rho family proteins and their potential consequences for PKN1 activation.
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.