Evidence map›Paper›PMID 42214129›Full record

ArticleStem cell research2026

Modeling stimulus-induced stress responses in microglia-like cells using a commercial iPSC-dCas9-KRAB line.

Devin M Saunders, Nicola A Kearns, Bernard Ng, Faraz Sultan, Himanshu Vyas, Ricardo A Vialle, Eric M Clark, Sashini De Tissera, Jishu Xu, David A Bennett and 1 more

Abstract read
In one paragraph

Article in Stem cell research, 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.

Devin M SaundersRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL 60612, USA.
Nicola A KearnsRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL 60612, USA; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Bernard NgRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL 60612, USA.
Faraz SultanRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL 60612, USA.
Himanshu VyasRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL 60612, USA.
Ricardo A VialleRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL 60612, USA.
Eric M ClarkRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL 60612, USA.
Sashini De TisseraRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL 60612, USA.
Jishu XuRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL 60612, USA.
David A BennettRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL 60612, USA; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Yanling WangRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL 60612, USA; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA. Electronic address: yanling_wang@rush.edu.

Funding

SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1991 to 2020
$49.1M
EPIDEMIOLOGY OF NEURAL RESERVE AND NEUROBIOLOGY IN AGINGR01AG017917 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 2001 to 2023
$43.3M
Rush Alzheimer's Disease Research CenterP30AG072975 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI Lisa L Barnes, Julie A. Schneider · 2021 to 2026
$24.7M
RISK FACTORS, PATHOLOGY, AND CLINICAL EXPRESSIONS OF ADR01AG015819 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1998 to 2024
$21.4M
Multi-omic network-directed proteoform discovery, dissection and functional validation to prioritize novel AD therapeutic targetsU01AG061356 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BENNETT, DAVID ALAN, DE JAGER, PHILIP L · 2018 to 2022
$13.7M
Investigating the Effect of APOE Alleles on Neuro-Immunity of Human Brain Borders in Normal Aging and Alzheimer's Disease Using Single-Cell Multi-Omics and In Vitro OrganoidsR01AG079223 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI Yanling Wang · 2022 to 2026
$3.7M
Uncovering cell-type-specific driver genes of Alzheimer's Disease by pathology-indexing scRNA-seq, spatial transcriptomics, and CRISPR screensR01AG074082 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI Yanling Wang · 2022 to 2026
$3.6M
NIA NIH HHS P30 AG010161NIA NIH HHS P30 AG072975NIA NIH HHS R01 AG015819NIA NIH HHS R01 AG017917NIA NIH HHS R01 AG074082NIA NIH HHS R01 AG079223NIA NIH HHS U01 AG061356
6 · The paper itself

Abstract

Commercially available human iPSC lines with inducible CRISPR interference (CRISPRi) systems offer scalable platforms for gene function studies. One widely available line, the AICS-0090 dCas9-KRAB iPSC line developed by the Allen Institute, has been extensively validated for genomic integrity and stem cell potency. However, its utility in modeling specialized immune cell types such as microglia - and in assessing their functional responses to disease-relevant stimuli - has not been fully established. Here, we evaluated the AICS-0090 line for its ability to differentiate into microglia-like cells, support efficient gene knockdown, and respond to environmental stressors. We assessed its differentiation capacity by qPCR, flow cytometry, and immunocytochemistry, confirming reproducible expression of microglial surface markers at early and late timepoints. Gene knockdown efficiency was validated both at the single-gene level and in pooled CRISPRi screens. Focusing on functional responsiveness, we exposed the microglia-like cells to two distinct stimuli: aggregated amyloid-β (Aβ), a disease-associated trigger in Alzheimer's disease, and lipopolysaccharide (LPS), a classical inflammatory signal. Transcriptomic and functional analyses revealed stimulus-specific responses: aggregated Aβ induced limited activation of stress and inflammation pathways, whereas LPS elicited broader transcriptional reprogramming and cytokine release. Signatures from both conditions partially overlapped with ex vivo human and mouse microglial states. Together, these findings support the use of the AICS-0090 dCas9-KRAB iPSC-derived microglia-like cells as a flexible and tractable model for gene function interrogation under defined inflammatory contexts, with potential for future applications in neuroimmune modeling and perturbation-based screening.

Indexed as

Induced Pluripotent Stem CellsMicrogliaStress, PhysiologicalAmyloid beta-PeptidesAnimalsCell DifferentiationCell LineHumansLipopolysaccharidesAmyloid beta-PeptidesLipopolysaccharidesaggregated AβCRISPR interferenceiPSCs, microglia-like cellsLPSsingle-cell RNA sequencingStress response

Identifiers

PMID42214129
PMCPMC13335154

What OpenQuestion holds

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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 OpenQuestion graph.