MARCKS N-terminal sequence-derived inhibitor peptides impair monocytic ROS production and migration via

Friederike Kühl1, Jana Lea Kopper1, Lena Sofie Wriede1

  • 1Hannover Medical School, Institute of Clinical Chemistry and Central Laboratory, Carl-Neuberg-Str. 1, 30625, Hannover, Germany.

Molecular Biology Reports
|September 17, 2025
PubMed
Abstract

Insights

Myristoylated alanine-rich C kinase substrate (MARCKS) inhibitor peptides MANS and BIO-11006 reduce monocytic ROS production and migration. These effects appear to be MARCKS-independent, even in MARCKS-deficient cells.

Area of Science:

  • Cellular Biology
  • Immunology
  • Biochemistry

Background:

  • Myristoylated alanine-rich C kinase substrate (MARCKS) is a key protein in cellular processes and disease.
  • MARCKS inhibitor peptides MANS and BIO-11006 were investigated for their effects on monocytic cells.

Purpose of the Study:

  • To assess the impact of MANS and BIO-11006 on reactive oxygen species (ROS) production in monocytic cells.
  • To evaluate the effect of these peptides on monocytic cell migration.
  • To determine if these effects are dependent on MARCKS.

Main Methods:

  • CRISPR/Cas9 gene editing was used to create MARCKS knock-out (KO) monocytic cell lines.
  • ROS production was measured using a chemiluminescence-based assay.
  • Monocytic migration was assessed via transwell assays.

Main Results:

  • MARCKS KO cells showed significantly reduced ROS production compared to wild-type (WT) cells.
  • MANS inhibited ROS production in various monocytic cells, while BIO-11006 primarily affected PMA-induced ROS.
  • Both peptides showed inhibitory effects on ROS production and MANS affected migration even in MARCKS KO cells, suggesting a MARCKS-independent mechanism.

Conclusions:

  • MARCKS inhibitor peptides MANS and BIO-11006 can inhibit cellular processes in monocytic cells.
  • The inhibitory mechanisms of MANS and BIO-11006 appear to be independent of MARCKS.
  • Further research is needed to elucidate the precise MARCKS-independent pathways involved.

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