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Target intelligence / Profile preview
Protein fem-1 homolog A (FEM1A)
- Target
- FEM1A
- Molecular classification
- E3 ubiquitin-protein ligase substrate adaptor (component of the Cul2-RING complex), Protein-coding gene, Ubiquitin-like ligase-substrate adaptor
01
Overview
Protein fem-1 homolog A (FEM1A) is a substrate-recognition component of the Cul2-RING (CRL2) E3 ubiquitin ligase complex, active in mitochondria and responsible for recognizing proteins with specific C-terminal degrons for ubiquitination and subsequent degradation. As a molecular adaptor, it facilitates the negative regulation of inflammatory responses, notably through interactions with the prostaglandin E2 receptor EP4, and is implicated in both anti-inflammatory and pro-inflammatory signaling depending on the cellular context. FEM1A is associated with cancer (notably Rhabdomyosarcoma) and immune pathways, illustrating its importance in health and disease.
- Other names
- FEM1AEPRAPfem-1 homolog AProstaglandin E receptor 4-associated proteinFEM1-alphaprotein fem-1 homolog A
02
Mechanism of action
Inhibiting (or modulating) FEM1A may alter inflammatory signaling via the EP4 prostaglandin E2 receptor pathway. Targeting its E3 ubiquitin ligase substrate adaptor activity would modulate protein degradation pathways, affecting the stability of specific proteins.
03
Biological functions
Negative regulation of inflammatory response (PGE2-EP4-mediated inhibition in macrophages; promotes inflammation in brain microglia)Ubiquitin-dependent protein catabolic process via the C-end degron rule pathwaySubstrate recognition for the destruction via C-end degrons (DesCEND) pathwayProtein degradation: recognizes specific C-terminal motifs in proteins, leading to their ubiquitination and degradation (e.g., SIL1, OR51B2, SLBP)Binding to EP4 subtype prostaglandin E2 receptor
04
Disease associations
Cancer (associated with Rhabdomyosarcoma)Inflammation (regulation of inflammatory processes in macrophages and microglia)Other (possible roles in antigen processing and presentation)
05
Safety considerations
None explicitly reported. As a regulator of inflammation, manipulating FEM1A activity could theoretically affect immune and neuroinflammatory responses.Disruption of ubiquitin-proteasome pathways (such as via FEM1A) may have broad side effects due to protein turnover changes.
06
Interacting drugs
None explicitly listed in current search results. FEM1A interacts with the prostaglandin E2 receptor EP4 (PTGER4); drugs targeting EP4 may indirectly influence FEM1A function, but direct drug interactions are not affirmed in available data.
07
Biomarkers
None directly identified in search results. FEM1A has potential as a biomarker for inflammatory processes or Rhabdomyosarcoma, but this is not validated in currently cited sources.
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