Evidence map›Paper›PMID 40001545›Full record

ReviewBiomolecules2025

Modulating PAK1: Accessory Proteins as Promising Therapeutic Targets.

Amin Mirzaiebadizi, Rana Shafabakhsh, Mohammad Reza Ahmadian

Abstract readReview
In one paragraph

Review in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
  2. Article
  3. A Novel Pak1 Activator Ameliorates ER Stress for HFpEF Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. PAK1 inhibitor NVS-PAK1-1 preserves dendritic spines in amyloid/tau exposed neurons and 5xFAD mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  8. Article
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Amin MirzaiebadiziInstitute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0000-0002-3340-586X
Rana ShafabakhshInstitute for Experimental Molecular Imaging, RWTH Aachen University Hospital, 52074 Aachen, Germany.
Mohammad Reza AhmadianInstitute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0000-0002-2034-8894

Funding

Deutsche Forschungsgemeinschaft AH 92/8-3
6 · The paper itself

Abstract

The p21-activated kinase (PAK1), a serine/threonine protein kinase, is critical in regulating various cellular processes, including muscle contraction, neutrophil chemotaxis, neuronal polarization, and endothelial barrier function. Aberrant PAK1 activity has been implicated in the progression of several human diseases, including cancer, heart disease, and neurological disorders. Increased PAK1 expression is often associated with poor clinical prognosis, invasive tumor characteristics, and therapeutic resistance. Despite its importance, the cellular mechanisms that modulate PAK1 function remain poorly understood. Accessory proteins, essential for the precise assembly and temporal regulation of signaling pathways, offer unique advantages as therapeutic targets. Unlike core signaling components, these modulators can attenuate aberrant signaling without completely abolishing it, potentially restoring signaling to physiological levels. This review highlights PAK1 accessory proteins as promising and novel therapeutic targets, opening new horizons for disease treatment.

Indexed as

Neoplasmsp21-Activated KinasesAnimalsHumansMolecular Targeted TherapySignal Transductionp21-Activated KinasesPAK1 protein, humanaccessory inhibitorsaccessory proteinsadaptor proteinsCKIP1GIT1GRB2merlinNCK1nischarinp21-activated kinasePAK1PAK1P1paxillinRIT1scaffold proteinsα/βPIX

Identifiers

PMID40001545
PMCPMC11852631

What OpenQuestion holds

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Registered trials

None linked

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.