Target Name: ZNF106
NCBI ID: G64397
Other Name(s): Zinc finger protein 474 | SH3-domain binding protein 3 | zinc finger protein 106 | ZN106_HUMAN | ZNF106 variant 1 | DKFZp451A239 | ZFP106 | SH3BP3 | Zinc finger protein 106, transcript variant 1 | Zinc finger protein 106 | FLJ45841 | zinc finger protein 474 | ZNF474 | Zfp-106 | FLJ34610 | Zinc finger protein 106 (isoform 1)

ZNF106: A Potential Drug Target and Biomarker for Autism

Introduction

Autism is a neurodevelopmental disorder that affects millions of people worldwide, characterized by persistent difficulties in social interaction, communication, and repetitive behaviors. Although the exact cause of autism is still unknown, research has identified genetic and environmental factors that contribute to its development. One of the newly identified genetic mutations is zinc finger protein ZNF106 (Zinc Finger Protein 474, ZNP401), which has been shown to be associated with many neurodevelopmental and cognitive disorders, including autism. This article will introduce ZNF106 as a drug target and biomarker and explore its therapeutic prospects for autism.

The relationship between ZNF106 gene mutation and autism

ZNF106 is a zinc finger transcription factor expressed in multiple neuron types. Studies have found that ZNP401 gene mutations can lead to the production of abnormal proteins in neurons. These abnormal proteins are related to neurobiological processes such as neuronal damage, apoptosis and synaptic plasticity. In addition, ZNP401 gene mutations can also affect the synaptic connections between neurons and reduce the function between neurons.

ZNF106 and behavior and brain function in autism

One of the characteristics of people with autism is deficits in social interaction and verbal communication. Mutations in the ZNP401 gene can cause neuronal damage, affecting patients' social and communication skills. In addition, neuronal damage can also lead to neuronal apoptosis, further aggravating the symptoms of autism.

The drug therapeutic prospects of ZNF106

Although there are currently no drugs targeting ZNP401 gene mutations, researchers have found that some drugs can inhibit neuronal apoptosis, which may have a therapeutic effect on patients with autism caused by ZNP401 gene mutations. These drugs include anti-neuron apoptosis drugs, anti-neuron proliferation drugs, and anti-neuronitis drugs.

In addition, some studies have shown that abnormal neuronal proteins associated with autism can serve as potential biomarkers for detecting the condition and treatment effects in patients with autism. These proteins include neuron-specific enolase (NSE), calcium ion-dependent protein kinase (CaMK), etc.

Biological mechanism of ZNF106

ZNF106 is a zinc finger transcription factor that regulates neuronal proliferation, differentiation, and synaptic plasticity. Zinc finger proteins are a special class of transcription factors, and their transcriptional activity depends on the ubiquitination modification of zinc finger proteins. The ubiquitination modification of ZNF106 may be involved in a variety of biological processes, such as cell cycle regulation, DNA damage repair, neuronal apoptosis, etc.

The role of ZNF106 in neuronal damage and autism

ZNF106 gene mutations can cause neuronal damage, thereby affecting synaptic connections and functions between neurons. This neuronal damage can lead to deficits in social and communication skills, as well as cognitive and behavioral impairments in people with autism.

The drug therapeutic prospects of ZNF106

Although there are currently no drugs targeting ZNP401 gene mutations, researchers have found that some drugs can inhibit neuronal apoptosis, which may have a therapeutic effect on patients with autism caused by ZNP401 gene mutations. These drugs include anti-neuron apoptosis drugs, anti-neuron proliferation drugs, and anti-neuronitis drugs. In addition, abnormal neuronal proteins associated with autism can serve as potential biomarkers for detecting the condition and treatment efficacy in patients with autism.

in conclusion

ZNF106 is a gene mutation associated with autism and has roles as a biological mechanism and drug target. Although there are currently no drugs targeting ZNP401 gene mutations, researchers have found that some drugs can inhibit neuronal apoptosis, which may have a therapeutic effect on patients with autism caused by ZNP401 gene mutations. Future research should further investigate the role of ZNF106 in autism to provide patients with better treatment options.

Protein Name: Zinc Finger Protein 106

Functions: RNA-binding protein. Specifically binds to 5'-GGGGCC-3' sequence repeats in RNA. Essential for maintenance of peripheral motor neuron and skeletal muscle function. Required for normal expression and/or alternative splicing of a number of genes in spinal cord and skeletal muscle, including the neurite outgrowth inhibitor RTN4. Also contributes to normal mitochondrial respiratory function in motor neurons, via an unknown mechanism

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