IL1RAPL1 (Interleukin-1 Receptor Accessory Protein-Like 1) is a transmembrane protein encoded by the IL1RAPL1 gene on the X chromosome. It regulates synapse formation, dendritic spine development, and AMPA receptor trafficking in neurons . Mutations in IL1RAPL1 are linked to X-linked intellectual disability (XLID) and autism .
IL1RAPL1 antibodies target specific epitopes of this protein, facilitating its detection in experimental models. Canonical IL1RAPL1 has a molecular weight of ~80 kDa, with isoforms detected in human, mouse, rat, and other species .
IL1RAPL1 antibodies are critical in studying:
Synaptic Mechanisms: IL1RAPL1 interacts with Mcf2l and RhoA-ROCK pathways to regulate excitatory synapse formation in cortical neurons . Antibodies confirmed IL1RAPL1’s colocalization with synaptic markers like VGLUT1 .
Disease Models: Mutations (e.g., Δex6, C31R) disrupt IL1RAPL1’s interaction with PTPδ, impairing synaptogenesis in intellectual disability models . Antibodies detected mislocalization and instability of mutant proteins .
Signaling Pathways: IL1RAPL1 antibodies identified interactions with PKCε, Rasal1, and PLCβ1, highlighting its role in JNK pathway activation .
Synaptogenesis: Overexpression of IL1RAPL1 in cortical neurons increased VGLUT1-positive excitatory synapses, an effect blocked by RhoA-ROCK inhibitors .
Pathogenic Mutations: Δex6 and C31R mutants failed to induce synaptic differentiation due to reduced PTPδ binding, confirmed via coimmunoprecipitation .
Subcellular Localization: IL1RAPL1 antibodies verified membrane and cytoplasmic localization, with postsynaptic enrichment in hippocampal neurons .