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The protein encoded by IL1RAPL1 is a member of the interleukin 1 receptor family and is similar to the interleukin 1 accessory proteins. Additionally we are shipping IL1RAPL1 Antibodies (18) and IL1RAPL1 Proteins (13) and many more products for this protein.
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It was indicated that a defect in IL1RAPL1 that controls excitatory synapsis formation results in the excitation-inhibition balance affecting various cerebral functions.
Novel IL1RAPL1 mutations associated with intellectual disability impair synaptogenesis.
The interaction of the IL1RAPL1 family of proteins with PTPdelta and RhoGAP2 (show CHN1 ELISA Kits) reveals a pathophysiological mechanism of cognitive impairment associated with a novel type of trans-synaptic signaling.
The IL1RAPL1 gene is of interest as a candidate gene for autism spectrum disorder as mutations or deletions in the gene have previously been reported in individuals from families with ASD (show ARSD ELISA Kits).
Nearly all patients with deletions involving DAX1 (show NR0B1 ELISA Kits), but not DMD (show DMD ELISA Kits), had mental retardation if IL1RAPL1 was deleted. If ILIRAPLI & DMD (show DMD ELISA Kits) were intact, the patients with DAX1 (show NR0B1 ELISA Kits) deletions only rarely had normal development.
Report confirms the role of the IL1RAPL1 gene in causing nonspecific mental retardation in males.
DMD (show DMD ELISA Kits) gene and its immediately distal neighbor, the 1.8 Mb IL1RAPL1 gene are abundantly expressed in normal brain but were dramatically underexpressed in every brain tumor cell line and xenograft.
Combined data suggested that IL1RAPL1 affected human cognitive ability to some extent, especially the memory and concentration capability.
The function of truncated IL1RAPL1 protein in an autistic female with Asperger syndrome is severely altered in hippocampal neurons, demonstrated by its effect on neurite outgrowth activity.
IL1RAPL1 plays an important role in the etiology of X-linked mental retardation.
These results thus reveal the decoding mechanism of splice-insert signaling codes for synaptic differentiation induced by trans-synaptic adhesion between PTPdelta and IL1RAPL1/IL-1RAcP (show IL1RAP ELISA Kits).
These results suggest that IL1RAPL1 ablation resulted in spine density decrease and affected not only learning but also behavioural flexibility, locomotor activity and anxiety.
IL1RAPL1 associated with mental retardation and autism regulates the formation and stabilization of glutamatergic synapses of cortical neurons through RhoA (show RHOA ELISA Kits) signaling pathway.
the results of this study suggested that constitutive absence of Il1rapl1 disrupts this balance, possibly explaining the deficit in LTP (show SCP2 ELISA Kits) induction in vivo and the behavioral deficits observed in KO mice.
results suggest that IL1RAPL1 mediates synapse formation through trans-synaptic interaction with PTPdelta.
Absence of IL1RAPL1 causes a transient disinhibition of deep cerebellar nuclei neurons between postnatal days 10 and 14.
The protein encoded by this gene is a member of the interleukin 1 receptor family and is similar to the interleukin 1 accessory proteins. It is most closely related to interleukin 1 receptor accessory protein-like 2 (IL1RAPL2). This gene and IL1RAPL2 are located at a region on chromosome X that is associated with X-linked non-syndromic mental retardation. Deletions and mutations in this gene were found in patients with mental retardation. This gene is expressed at a high level in post-natal brain structures involved in the hippocampal memory system, which suggests a specialized role in the physiological processes underlying memory and learning abilities.
interleukin 1 receptor accessory protein-like 1
, X-linked interleukin-1 receptor accessory protein-like 1
, interleukin 1 receptor-8
, interleukin-1 receptor accessory protein-like 1
, mental retardation, X-linked 10
, three immunoglobulin domain-containing IL-1 receptor-related 2