Substrate-recognition component of a Cul2-RING (CRL2) E3 ubiquitin-protein ligase complex of the DesCEND (destruction via C-end degrons) pathway, which recognizes a C-degron located at the extreme C terminus of target proteins, leading to their ubiquitination and degradation (By similarity). The C-degron recognized by the DesCEND pathway is usually a motif of less than ten residues and can be present in full-length proteins, truncated proteins or proteolytically cleaved forms (By similarity). The CRL2(FEM1A) complex specifically recognizes proteins with an arginine at the C-terminus: recognizes and binds proteins ending with -Lys/Arg-Xaa-Arg and -Lys/Arg-Xaa-Xaa-Arg C-degrons, such as SIL1 or OR51B2, leading to their ubiquitination and degradation (By similarity). Involved in PGE2-EP4-mediated inhibition of inflammation of macrophages via interaction with NFKB1 and PTGER4 (PubMed:18270204, PubMed:26439841). Promotes inflammation in brain microglia through MAP2K4/MKK4-mediated signaling (PubMed:27315781). Protein modification; protein ubiquitination. Component of a CRL2 E3 ubiquitin-protein ligase complex, also named ECS (Elongin BC-CUL2/5-SOCS-box protein) complex, composed of CUL2, Elongin BC (ELOB and ELOC), RBX1 and substrate-specific adapter FEM1A (By similarity). Interacts with PTGER4 (PubMed:18270204). Interacts with NFKB1; the interaction is direct (PubMed:18270204). Preferentially expressed in cardiac muscle, brain and liver (at protein level) (PubMed:9828124, PubMed:19406122). Also expressed in skeletal muscle (PubMed:9828124). Expressed during embryogenesis. Up-regulated in ischemic hearts. Phosphorylated; highly phosphorylated in myoblasts and myotubes (PubMed:19406122). Phosphorylation at Ser-108 and Ser-608 promote PGE2-EP4-mediated inhibition of inflammation (PubMed:27799315). Dephosphorylated by protein phosphatase 2A (PP2A) (PubMed:27799315). No visible phenotype in normal conditions: mice are fertile and develop normally without any apparent malformation (PubMed:26439841, PubMed:27315781). In mice model of chronic inflammation, mice develop more severe colitis induced by dextran sodium sulfate (DSS) (PubMed:26439841). Mice display less microglial accumulation; decreased microglial activation is observed in the brain after systemic lipopolysaccharide administration (PubMed:27315781). Mice also show behavioral abnormalities, possibly caused by monoamine deficits (PubMed:28336432). Mice display reduced anxiety-like behavior and brain inflammation in a model of Alzheimer disease (PubMed:28624505). Belongs to the fem-1 family.