ArticlebioRxiv : the preprint server for biology2026
Arrestin-3 sca-olds multiple MAP3Ks driving stress-induced JNK3 activation and cell death.
Article in bioRxiv : the preprint server for biology, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-visual arrestin-3 (a.k.a. β-arrestin-2) functions as a scaffold facilitating the activation of c-Jun N-terminal kinases (JNKs), an important pathway regulating cell fate. Here, we demonstrate that arrestin-3 scaffolds not only previously identified ASK1, but facilitates signaling by several MAP3Ks, including ZAKα, ZAKβ, MEKK1, and TAK1. We identified ZAK (sterile alpha motif and leucine zipper-containing kinase) as the predominant MAP3K mediating arrestin-3-dependent JNK3 signaling and chemotherapy drug-induced cell death in HEK293 cells. We also showed that a 16-residue-long arrestin-3-derived peptide binds ZAK and fulfills the scaffolding function of full-length arrestin-3, sensitizing cells to death induced by chemotherapy drugs. These findings demonstrate that arrestin-3 is a versatile facilitator of stress signaling and suggest that functional peptide mimics can be used therapeutically to facilitate drug-induced death of cancer cells.
Identifiers
What Socratic 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 Socratic graph.