Human Interleukin 1 Receptor Accessory Protein Like Protein 1 (IL1RAPL1) Protein

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Description
Human Interleukin 1 Receptor Accessory Protein Like Protein 1 is a recombinant Human protein expressed in E. coli.
Documents del producto
Product specifications
Category | Proteins and Peptides |
Immunogen Target | Interleukin 1 Receptor Accessory Protein Like Protein 1 (IL1RAPL1) |
Host | E. coli |
Origin | Human |
Conjugation | Unconjugated |
Observed MW | Molecular Weight: Calculated MW: 22.5 kDa Observed MW: 25 kDa Concentration: Prior to lyophilization: 80 µg/ml Sequence Fragment: Ser113-Asp276 Tag: N-terminal His tag |
Expression | Recombinant |
Purity | > 95% |
Size 1 | 10 µg |
Size 2 | 50 µg |
Size 3 | 100 µg |
Size 4 | 200 µg |
Size 5 | 500 µg |
Form | Lyophilized Reconstitute in ddH2O to a concentration of 0.1-1.0 mg/ml. Do not vortex. |
Tested Applications | WB, SDS-PAGE |
Buffer | Prior to lyophilization: PBS, pH 7.4, containing 0.01% Sarcosyl, 5% Trehalose. |
Availability | Shipped within 5-7 working days. |
Storage | Store at 2-8 °C for up to one month. Store at -80 °C for up to one year. Avoid repeated freeze/thaw cycles. |
Dry Ice | No |
UniProt ID | Q9NZN1 |
Gene ID | 11141 |
OMIM | 300143 |
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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