IL1RAPL1 antibody

Este producto es parte de IL1RAPL - Interleukin-1 Receptor Accessory Protein-like
IL1RAPL1 antibody
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Name
IL1RAPL1 antibody
Category
Primary Antibodies
Provider
FineTest
Reference
FNab04245
Tested Applications
ELISA, WB, IHC, IF, IP

Description

May regulate secretion and presynaptic differentiation through inhibition of the activity of N-type voltage-gated calcium channel. May activate the MAP kinase JNK. Plays a role in presynaptic and postsynaptic differentiation and dendritic spine formation in neurons.

Documentos del producto

Instrucciones
Descargar
Data sheet
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Especificaciones del producto

Category
Primary Antibodies
Immunogen Target
interleukin 1 receptor accessory protein-like 1 (IL1RAPL1)
Host
Rabbit
Reactivity
Human, Mouse, Rat
Recommended Dilution
WB: 1:500-1:2000; IP: 1:200-1:1000; IHC: 1:20-1:200; IF: 1:20-1:200
Clonality
polyclonal
Conjugation
Unconjugated
Isotype
IgG
Observed MW
66-75 kDa
Purity
≥95% as determined by SDS-PAGE
Purification
Immunogen affinity purified
Size 1
100µg
Form
liquid
Tested Applications
ELISA, WB, IHC, IF, IP
Storage
PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months(Avoid repeated freeze / thaw cycles.)
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
Note
Mol. Weight 66-75 kDa

Background

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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