ArticleMolecular biology reports2025
MARCKS N-terminal sequence-derived inhibitor peptides impair monocytic ROS production and migration via MARCKS-independent effects.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- MARCKS as a mediator and target for pathological tunneling nanotubes between patient-derived glioblastoma cells and astrocytes.Cell death & disease · 2026Article
- Physiological, patho-physiological, and potential therapeutic roles for neutrophils in cancer & beyond.Frontiers in immunology · 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyristoylated alanine-rich C kinase substrate (MARCKS) is a versatile unstructured protein involved in numerous cellular processes and associated with various diseases. In this study, the effect of MARCKS' N-terminal sequence-derived inhibitor peptides MANS ("myristoylated N-terminal sequence") and BIO-11006 on monocytic ROS production and migration was assessed. METHODS AND
resultsStimulation of calcitriol-differentiated monocytic THP-1 cells with PMA, opsonized (ops.) E. coli, ops. S. aureus, and ops. zymosan led to considerable ROS production (as determined using a chemiluminescence-based assay), an effect significantly reduced in THP-1-derived MARCKS knock-out (KO) cells that were generated with the CRISPR/Cas9 technique. MANS similarly inhibited ROS production in monocytic THP-1 and PLB-985 cells as well as primary human monocytes induced by various stimuli, while BIO-11006 predominantly affected PMA-induced ROS levels. TNF preincubation enhanced monocytic ROS production, but was not able to compensate for MANS treatment or MARCKS deficiency. Unexpectedly, an inhibition of ROS formation by both inhibitor peptides could also be observed in MARCKS KO cells, indicating a target-independent effect of MANS and BIO-11006 at least in MARCKS-deficient monocytic cells. Comparable negative effects of MANS in both WT and KO cells could also be observed when monocytic migration was assessed in transwell assays.
conclusionOur data suggest that MARCKS inhibitor peptides MANS and (to a lesser extent) BIO-11006 are able to inhibit MARCKS-associated cellular processes in monocytic cells by MARCKS-independent mechanisms.
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.