Mouse Interleukin-1 Receptor Accessory Protein-Like 1 (IL1RAPL1) Protein (Active)

Este producto es parte de IL1RAPL - Interleukin-1 Receptor Accessory Protein-like
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1235€ (100 µg)

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935106861
info@markelab.com
name
Mouse Interleukin-1 Receptor Accessory Protein-Like 1 (IL1RAPL1) Protein (Active)
category
Proteins and Peptides
provider
Abbexa
reference
abx691177
tested applications
SDS-PAGE

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

CategoryProteins and Peptides
Immunogen TargetIL-1R8
HostHEK293 cells
OriginMouse
Observed MWMolecular Weight: 65 kDa Sequence Fragment: Met1-Thr357 Tag: C-terminal Fc tag Validity: The validity for this protein is 12 months.
ExpressionRecombinant
Purity> 95% (SDS-PAGE)
Size 1100 µg
Form
Tested ApplicationsSDS-PAGE
BufferLyophilized from sterile PBS, pH 7.4.
AvailabilityShipped within 5-15 working days.
StorageAliquot and store at -20°C or -80°C. Avoid repeated freeze/thaw cycles.
Dry IceNo
UniProt IDP59823
AliasIL1RAPL1,IL1R8, IL1RAPL, IL-1RAPL-1, IL-1-RAPL-1, IL1RAPL-1,OPHN4
BackgroundProtein IL1RAPL1
StatusRUO
NoteThis 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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