Mouse Interleukin-1 Receptor Accessory Protein-Like 1 (IL1RAPL1) Protein (Active)
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Description
Mouse IL-1R8 Protein is a recombinant protein from Mouse produced in HEK293 Cells. A DNA sequence encoding the mouse IL1RAPL1 (P59823) extracellular domain (Met 1-Thr 357) was fused with the Fc region of human IgG1 at the C-terminus.
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Product specifications
| Category | Proteins and Peptides |
| Immunogen Target | IL-1R8 |
| Host | HEK293 cells |
| Origin | Mouse |
| Observed MW | Molecular Weight: 65 kDa Sequence Fragment: Met1-Thr357 Tag: C-terminal Fc tag Validity: The validity for this protein is 12 months. |
| Expression | Recombinant |
| Purity | > 95% (SDS-PAGE) |
| Size 1 | 100 µg |
| Form | |
| Tested Applications | SDS-PAGE |
| Buffer | Lyophilized from sterile PBS, pH 7.4. |
| Availability | Shipped within 5-15 working days. |
| Storage | Aliquot and store at -20°C or -80°C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | P59823 |
| Alias | IL1RAPL1,IL1R8, IL1RAPL, IL-1RAPL-1, IL-1-RAPL-1, IL1RAPL-1,OPHN4 |
| Background | Protein IL1RAPL1 |
| Status | RUO |
| Note | This product is for research use only. Not for human consumption, cosmetic, therapeutic or diagnostic use. |
Descripción
IL1RAPL1, a neuronal protein in the IL-1 receptor family, regulates synapse formation, neuronal maturation, and cognitive processes critical for brain development and function. It interacts with postsynaptic density proteins, including PSD-95 and Rho GTPases, to modulate dendritic spine formation, excitatory synaptic activity, and synaptic plasticity, processes vital for learning and memory. IL1RAPL1 is primarily expressed in the brain, particularly in the cortex, hippocampus, and cerebellum, where it facilitates proper neural connectivity and neurotransmission. Mutations, deletions, or loss of IL1RAPL1 function are strongly linked to X-linked intellectual disability, autism spectrum disorders, and epilepsy, as disrupted synaptic organization leads to impaired cognitive function and abnormal behavior. Functional studies reveal defects in synaptic organization, dendritic arborization, and reduced synaptic plasticity in IL1RAPL1-deficient models. Knockout studies highlight impaired learning, memory deficits, and altered excitatory signaling, emphasizing its essential role in neuronal development, synapse regulation, and neurodevelopmental health.
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