Efr3b antibodies are specialized immunological tools targeting the Efr3 homolog B protein, a key regulator of phosphatidylinositol 4-kinase IIIα (PI4KIIIα) localization at the plasma membrane . These antibodies enable researchers to study Efr3b's roles in neuronal excitability, lipid metabolism, and disease mechanisms, particularly in neurological and oncological contexts .
Efr3b is critical for maintaining hippocampal CA2 pyramidal neuron (PN) excitability and social behavior in mice . Key findings include:
CA2/CA3 Enrichment: Efr3b mRNA is highly enriched in hippocampal CA2/CA3 excitatory neurons, with minimal expression in inhibitory neurons .
Excitability Regulation: Knockout or knockdown of Efr3b reduces CA2 PN excitability, increasing rheobase (minimal current for spike initiation) and decreasing action potential frequency .
Social Deficits: Efr3b-deficient mice exhibit impaired social novelty recognition while retaining normal sociability and anxiety-related behaviors .
Efr3b antibodies have been instrumental in:
Mapping Efr3b expression in hippocampal subregions using RNAscope and immunostaining .
Demonstrating that Efr3b depletion reduces CA2 PN excitability, linking it to social behavior deficits .
Brain Tumors: EFR3B expression is significantly reduced in adult glioblastoma (GBM) and pediatric tumors (e.g., ATRT, schwannoma) .
Redundancy with EFR3A: EFR3A compensates for EFR3B loss in tumors with low EFR3B expression, highlighting its therapeutic relevance .
Top-tier Efr3b antibodies undergo:
Batch consistency: Standardized manufacturing ensures reproducibility .
Enhanced validation: Supported by RNA expression correlation and knockout controls .
Efr3b antibodies will remain vital for:
Investigating Efr3b's role in lipid signaling and synaptic plasticity.
Developing targeted therapies for EFR3B-associated cancers and neurodevelopmental disorders.