ELAVL2/ELAVL4 Antibody
Description
Structure and Function of ELAVL2/ELAVL4
ELAVL2 and ELAVL4 are paralogs in the ELAVL family, characterized by their RNA recognition motifs (RRMs) that bind AU-rich elements (AREs) in mRNA 3’ untranslated regions (3’UTRs). This binding stabilizes mRNA transcripts, regulating genes involved in neuronal differentiation, synaptic plasticity, and tumor suppression .
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ELAVL2: Expressed in retinal progenitor cells, ganglion cells, and amacrine cells, with roles in maintaining retinal function and visual acuity . It regulates transcription factors critical for neuronal differentiation .
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ELAVL4: Enriched in cortical neurons and radial glial cells, influencing neuronal migration and axonogenesis . It stabilizes proto-oncogenic transcripts like N-myc and tumor suppressors like p27 .
Neurological Studies
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Retinal Development: ELAVL2-deficient mice exhibit reduced retinal ganglion cell activity and impaired visual acuity .
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Neurodegeneration: Dysregulation of ELAVL2/ELAVL4 correlates with Alzheimer’s disease and autism spectrum disorder .
Cancer Research
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Glioblastoma (GBM): ELAVL2 loss promotes mesenchymal transition and chemoresistance in GBM, while its overexpression improves survival .
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Small Cell Lung Cancer (SCLC): ELAVL4 is a diagnostic marker, with 100% positivity in SCLC cells .
Other Applications
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Immunohistochemistry: Detects neuronal markers in paraneoplastic encephalomyelitis .
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Co-Immunoprecipitation: Identifies protein complexes involving ELAVL4 in neuronal progenitors .
Key Research Findings
Clinical Relevance
Product Specs
Target Background
- ELAVL2-regulated co-expression networks are enriched for genes involved in neurodevelopment and synaptic function. These networks also include genes exhibiting human-specific expression patterns in the frontal pole. These findings indicate that ELAVL2's regulation of transcript expression is crucial for neuronal function and may have clinical relevance to autism. (PMID: 27260404)
- 17 proteins that interact with at least 10 other proteins (P < 0.05, FDR < 0.05) were identified as hub proteins. (PMID: 26366417)
- Analysis of gene-environment interaction between 33 genes and maternal smoking revealed evidence of interaction with two additional genes: GRID2 and ELAVL2, among European mothers. (PMID: 23512105)
- The timing of the switch from proliferation to neuronal differentiation is controlled by the mutually antagonistic action of two RNA-binding proteins, Hu and hnRNP K, through post-transcriptional regulation of p21 mRNA. (PMID: 15671036)
- Elevated levels of mRNA transcripts have been observed in Small Cell Lung Cancer patients. (PMID: 18607064)
