Target intelligence / Profile preview

Macrophage immunometabolism regulator (MACIR)

Target
MACIR
Molecular classification
Other, Signal transducing adaptor protein, Membrane-associated protein
01

Overview

Macrophage immunometabolism regulator (MACIR), also known as C5orf30, is a highly conserved, vertebrate-specific protein that regulates macrophage function by promoting the resolution of inflammation and wound healing, primarily through M2 macrophages. It is involved in negatively regulating tissue damage and modulates both macrophages and synovial fibroblasts, especially within the context of rheumatoid arthritis, where lower MACIR activity correlates with increased disease severity and joint damage. MACIR is classified as a disordered protein with no significant homology to other characterized human proteins and appears to act as an adaptor or signal transduction protein with cellular interactions involving nuclear transport and trafficking proteins such as TNPO1 and UNC119. It is not a classical receptor, enzyme, or transporter, distinguishing it among therapeutic targets related to immune regulation. No direct drug ligands are known. Expression or dysfunction of MACIR serves as a biomarker for inflammatory disease severity.

Other names
C5orf30FLJ25291UNC119-binding proteinUNC119-binding protein C5orf30UPF0684 protein C5orf30
02

Mechanism of action

Not applicable (no known drugs interact directly; biological mechanism is modulation of macrophage and fibroblast activity via negative regulation of inflammation and tissue damage)

03

Biological functions

Negative regulation of tissue damageRegulation of macrophage biology and immunometabolismPromotes resolution of inflammation and enhances wound repair (M2 macrophage–mediated)Modulates activity of synovial fibroblasts
04

Disease associations

Rheumatoid arthritis (risk and tissue damage severity association)InflammationPotential roles in autoimmune diseases (based on macrophage biology link)
05

Safety considerations

No specific drug-related safety concerns reported; gene knockout or inhibition may increase inflammation and tissue damage in models
06

Biomarkers

Rheumatoid arthritis severity (expression levels associated with disease severity and risk)

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