Target intelligence / Profile preview

Amyloid beta A4 precursor protein-binding family A member 1 (APBA1)

Target
APBA1
Molecular classification
Adaptor protein (or Adapter protein), PTB (phosphotyrosine-binding) domain-containing protein, Signal transducing protein, Scaffold protein, Other (neuronal adapter protein)
01

Overview

Amyloid beta A4 precursor protein-binding family A member 1 (APBA1, also known as X11 or MINT1) is a neuronal adaptor protein primarily expressed in the brain, where it interacts with the C-terminus of the amyloid precursor protein (APP). APBA1 stabilizes APP at the cell surface and inhibits its proteolytic cleavage, reducing generation of amyloid-beta peptide, which is implicated in the pathology of Alzheimer’s disease. As a member of the X11/Mint family, APBA1 is a multidomain scaffold protein containing a PTB domain and PDZ domains, enabling formation of multiprotein complexes involved in synaptic vesicle exocytosis, neuronal signaling, and synaptic plasticity. APBA1 is implicated in coupling vesicle exocytosis to cell adhesion at synapses, further influencing neurotransmitter release and neuronal connectivity. Loss or alteration of APBA1 disrupts these processes and is linked to altered APP processing, beta-amyloid accumulation, and synaptic dysfunction relevant to neurodegenerative disease, particularly Alzheimer’s disease.

Other names
X11X11alphaMINT1Mint-1Neuron-specific X11 proteinNeuronal Munc18-1-interacting protein 1LIN10D9S411EAdapter protein X11alpha
02

Biological functions

Signal transductionSynaptic vesicle exocytosisAPP (amyloid precursor protein) stabilization and processingModulation of neurotransmitter releaseSynaptic adhesionVesicular trafficking
03

Disease associations

Neurodegenerative diseaseAlzheimer’s diseaseIntellectual disability (Syndromic X-Linked Intellectual Disability Najm type)Other (potential role in other neurological conditions)
04

Safety considerations

Modulating synaptic function—potential risk of neurotoxicity or altered neurotransmission if disruptedInterference with APP metabolism could have broad, unpredictable CNS effects

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