Interleukin 1 Receptor Accessory Protein Like 1 (IL1RAPL1) Antibody (Biotin)
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Description
IL1RAPL1 Antibody (Biotin) is a Rabbit Polyclonal against IL1RAPL1.
Documents del producto
Product specifications
| Category | Primary Antibodies |
| Immunogen Target | Interleukin 1 Receptor Accessory Protein Like 1 (IL1RAPL1) |
| Host | Rabbit |
| Reactivity | Human |
| Recommended Dilution | Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Polyclonal |
| Conjugation | Biotin |
| Isotype | IgG |
| Purity | > 95% |
| Purification | Purified by Protein G. |
| Size 1 | 20 µg |
| Size 2 | 50 µg |
| Size 3 | 100 µg |
| Size 4 | 200 µg |
| Size 5 | 1 mg |
| Form | Liquid |
| Tested Applications | ELISA |
| Buffer | 0.01 M PBS, pH 7.4, 0.03% Proclin-300 and 50% Glycerol. |
| Availability | Shipped within 5-10 working days. |
| Storage | Aliquot and store at -20°C. Avoid exposure to light. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | Q9NZN1 |
| Gene ID | 11141 |
| Alias | IL1RAPL1,IL1R8, IL1RAPL, IL-1RAPL-1, IL-1-RAPL-1, IL1RAPL-1,OPHN4 |
| Background | Antibody anti-IL1RAPL1 |
| Status | RUO |
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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