Evidence map›Paper›PMID 41763306›Full record

ArticleThe Journal of biological chemistry2026

AKAP2 is required for assembly of cytoskeletal signaling complexes that promote growth and metastasis of triple-negative breast cancer.

Kacey J Rosenthal, Pamela Felix-Sanchez, Katherine Forbush, Nicole Rhoads, Mingu Kang, Juan Jesus Vicente, F Donelson Smith, Linda Wordeman, Shao-En Ong, Kevin J Cheung and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Kacey J RosenthalDepartment of Pharmacology, University of Washington School of Medicine, Seattle, Washington, USA.
Pamela Felix-SanchezDepartment of Pharmacology, University of Washington School of Medicine, Seattle, Washington, USA.
Katherine ForbushDepartment of Pharmacology, University of Washington School of Medicine, Seattle, Washington, USA.
Nicole RhoadsTranslational Research Program, Public Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, Washington, USA; Human Biology Division, Fred Hutchinson Cancer Center, Seattle, Washington, USA.
Mingu KangDepartment of Pharmacology, University of Washington School of Medicine, Seattle, Washington, USA.
Juan Jesus VicenteDepartment of Neurobiology and Biophysics, University of Washington School of Medicine, Seattle, Washington, USA.
F Donelson SmithDepartment of Pharmacology, University of Washington School of Medicine, Seattle, Washington, USA.
Linda WordemanDepartment of Neurobiology and Biophysics, University of Washington School of Medicine, Seattle, Washington, USA.
Shao-En OngDepartment of Pharmacology, University of Washington School of Medicine, Seattle, Washington, USA.
Kevin J CheungTranslational Research Program, Public Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, Washington, USA; Human Biology Division, Fred Hutchinson Cancer Center, Seattle, Washington, USA.
John D ScottDepartment of Pharmacology, University of Washington School of Medicine, Seattle, Washington, USA. Electronic address: scottjdw@uw.edu.

Funding

Supplement to DEFINING PATHWAY-SPECIFIC KINASE SIGNALING MODULES WITH PROTEOMICSR01GM129090 · NIGMS · UNIVERSITY OF WASHINGTON · PI ONG, SHAO-EN · 2019 to 2022
$1.7M
A NanoLC-Orbitrap Tribrid Instrument for Comprehensive Proteomics AnalysesS10OD021502 · OD · UNIVERSITY OF WASHINGTON · PI ONG, SHAO-EN · 2017 to 2017
$906k
Proteomic signatures to predict drug response in cancerR21CA288806 · NCI · UNIVERSITY OF WASHINGTON · PI ONG, SHAO-EN, YEUNG, RAYMOND · 2024 to 2025
$400k
NCI NIH HHS R21 CA288806NIGMS NIH HHS R01 GM129090NIH HHS S10 OD021502
6 · The paper itself

Abstract

A Kinase Anchoring Proteins (AKAPs) that coordinate spatiotemporal signaling are increasingly implicated in cancer. Elevated AKAP2 protein correlates with an invasive phenotype in triple-negative breast cancer cell lines. A combination of biochemical, cellular, and omics approaches shows that AKAP2 cytoskeleton and focal adhesion-associated scaffolds contribute to the progression of basal-like triple-negative breast cancer. Proximity proteomics identifies AKAP2 as an element of focal adhesions in MDA-MB-231 cells. Molecular and immunofluorescent microscopy studies demonstrate that AKAP2 indirectly constrains focal adhesion kinase (FAK). Gene silencing of AKAP2 not only decreases FAK levels but also attenuates the phosphorylation of the cell motility adapter protein paxillin on Tyr118. Cell-derived xenograft studies in mice establish that AKAP2 is required for triple-negative breast cancer growth and metastasis, phenotypes that are linked to FAK action. These findings discover a new role for focal adhesion-associated AKAP2 in triple-negative breast cancer pathology.

Indexed as

A Kinase Anchor ProteinsCytoskeletonTriple Negative Breast NeoplasmsAnimalsCell ProliferationFemaleFocal AdhesionsHumansMDA-MB-231 CellsMiceNeoplasm MetastasisSignal TransductionA Kinase Anchor ProteinsA kinase anchoring proteincytoskeletonfocal adhesionkinase signalingprotein phosphorylationsignaling scaffolds

Identifiers

PMID41763306
PMCPMC13022629

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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 Socratic graph.