Target intelligence / Profile preview

Neuronal tyrosine-phosphorylated phosphoinositide-3-kinase adaptor 1 (NYAP1)

Target
NYAP1
Molecular classification
Other
01

Overview

NYAP1 (neuronal tyrosine-phosphorylated phosphoinositide-3-kinase adaptor 1) is a neuron-specific adaptor protein encoded by a gene located on chromosome 7[1][2]. NYAP1 mediates tyrosine kinase signaling in developing neurons by being phosphorylated (notably by Fyn kinase) in response to upstream signals such as Contactin5[3][4]. Tyrosine-phosphorylated NYAP1 interacts directly with the regulatory subunit p85 of phosphoinositide 3-kinase (PI3K), activating the PI3K/Akt/Rac1 signaling axis. Simultaneously, NYAP1 participates in linking this pathway with the WAVE1 protein complex, which regulates actin cytoskeleton remodeling necessary for neuronal morphogenesis[1][3]. Functional studies in mice show that disruption of NYAP1 and its family members impairs neurite elongation, neuronal migration, and leads to reduced brain size, emphasizing its role in brain development[3][4]. NYAP1 does not belong to canonical therapeutic target classes such as receptors or enzymes but serves as a critical signaling adaptor in neurons. There are no approved or investigational drugs that directly target NYAP1, nor is it currently used as a clinical biomarker[5]. Genetic association studies indicate that the NYAP1 locus may be implicated in neurodevelopmental disorders such as autism, but clinical significance remains to be fully established[3].

Other names
C7orf51FLJ37538Chromosomal 7 open reading frame 51KIAA1486-likeKIAA1486Lneuronal tyrosine phosphorylated phosphoinositide-3-kinase adaptor 1neuronal tyrosine-phosphorylated phosphoinositide-3-kinase adapter 1LOC1009108386430598A04RikRGD1310964
02

Biological functions

Neuronal morphogenesisRegulation of actin cytoskeletonSignal transduction (PI3K/Akt pathway activation)Regulation of neuronal migration
03

Disease associations

Neurodevelopmental disorder (“suggestive association signals” with autism spectrum disorder in case-control genetic studies)[3]Other (Potential link to cortical development deficits such as microcephaly or neuronal migration disorders, based on knockout mouse studies)[3][4]
04

Safety considerations

Loss or dysregulation may contribute to brain size abnormalities (microcephaly or neuronal hypertrophy) and defects in neuronal migration or morphogenesis[3][4]

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