ArticleMediators of inflammation2024
The Expression Profiles and Clinical Significance of Mixed Lineage Kinases in Glioma.
Article in Mediators of inflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- ZAK kinase at the crossroads of cellular stress: functional plasticity, human pathobiology, and precision therapeutics.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mixed lineage kinases (MLKs), comprising seven members: MLK1-4, dual leucine zipper kinase (DLK), leucine zipper kinase (LZK), and sterile alpha motif and leucine zipper containing kinase (ZAK), belong to the mitogen-activated protein kinase kinase kinase (MAP3K) family. These kinases are implicated in the progression of numerous cancers by activating mitogen-activated protein kinase (MAPK) cascades or functioning as ser/thr and tyr kinases. However, their specific roles in glioma remain elusive. In the present study, we utilized bioinformatics approaches to investigate the expression patterns of MLKs in low-grade gliomas (LGG) and glioblastoma multiforme (GBM). Additionally, we analyzed their clinical significance and delved into the potential mechanisms underlying MLK activity as well as their association with tumor-immune infiltrating cells (TIICs) in glioma. Furthermore, we conducted in vitro studies to elucidate the functional roles of MLK1-2 in glioma. Our findings revealed that the expressions of MLK1-2 were conspicuously downregulated in GBM and positively correlated with patients' overall survival. Conversely, ZAK exhibited an opposing trend. Notably, our newly devised risk score model exhibited superior performance in predicting patient prognoses. Moreover, we analyzed the potential mechanisms of MLK activity and its interplay with tumor immune infiltration. Last, we validated the antitumor effect of MLK1-2 at the in vitro level. In summary, our study sheds new insights into the roles of MLKs in glioma, particularly MLK1-2, and their potential as therapeutic targets.
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.