Substrate recognition component of a SCF (SKP1-CUL1-F-box protein) E3 ubiquitin-protein ligase complex which mediates the ubiquitination and subsequent proteasomal degradation of target proteins. Probably recognizes and binds to phosphorylated target proteins. SCF(FBXW11) mediates the ubiquitination of phosphorylated CTNNB1 and participates in Wnt signaling regulation. SCF(FBXW11) mediates the ubiquitination of phosphorylated NFKBIA, which degradation frees the associated NFKB1 to translocate into the nucleus and to activate transcription. SCF(FBXW11) mediates the ubiquitination of IFNAR1. SCF(FBXW11) mediates the ubiquitination of CEP68; this is required for centriole separation during mitosis (PubMed:25503564). Involved in the oxidative stress-induced a ubiquitin-mediated decrease in RCAN1. Mediates the degradation of CDC25A induced by ionizing radiation in cells progressing through S phase and thus may function in the intra-S-phase checkpoint. Has an essential role in the control of the clock-dependent transcription via degradation of phosphorylated PER1 and phosphorylated PER2. SCF(FBXW11) mediates the ubiquitination of CYTH1, and probably CYTH2 (PubMed:29420262). (Microbial infection) Target of human immunodeficiency virus type 1 (HIV-1) protein VPU to polyubiquitinate and deplete BST2 from cells and antagonize its antiviral action. Self-associates. Component of the SCF(FBXW11) complex formed of CUL1, SKP1, RBX1 and a FBXW11 dimer. Interacts with BTRC, BST2, PER1, RCAN1 and USP47. Interacts with phosphorylated ubiquitination substrates CTNNB1, NFKBIA, IFNAR1, PER1 and PER2; the interaction requires the phosphorylation of the two serine residues in the substrates' destruction motif D-S-G-X(2,3,4)-S. Interacts with TRIM21. Interacts with PER3. Interacts with phosphorylated ubiquitination substrate CEP68 (PubMed:25503564). Interacts with INAVA (PubMed:29420262). Interacts with REST (PubMed:18354482). (Microbial infection) Interact with Rift valley fever virus NSs (via omegaXaV motif); this interaction is important for EIF2AK2/PKR degradation. In the embryo, it is expressed in the developing eye, limbs and brain (PubMed:31402090). Expression is observed in the lens, retina, lips of the optic fissure closure and regions of the conjunctiva at Carnegie stages (CS) between CS15 and CS21. As eye development progresses, the stronger signal observed in the retina progressively shifts from the inner toward the outer retinal layers (PubMed:31402090). In the developing hand, expression is strong at CS15. At CS19 and CS21, after the digits have begun to form, strong expression is seen in the mesenchyme surrounding the developing cartilage (PubMed:31402090). In the brain, it is expressed in the primitive ventricles at CS17 and CS19, hypothalamus and medulla at CS17, and metencephalon at CS19 (PubMed:31402090). Strong expression is also observed in the pharyngeal arches, including the mandibular process and tongue at CS17 (PubMed:31402090). Expression is negatively regulated by Wnt/beta-catenin pathway. The N-terminal D domain mediates homodimerization. The disease is caused by variants affecting the gene represented in this entry. Extended N-terminus.