Disease relevance of ELAVL3

• The PLE21/HuC neural protein is an autoantigen for anti-neuronal nuclear autoantibodies (ANNA-1/anti-Hu/Type IIa antibodies) from a patient with paraneoplastic limbic encephalomyelitis and small cell lung carcinoma [1].
• The serum of all patients with anti-Hu-associated paraneoplastic encephalomyelitis and sensory neuronopathy react with HuD and Hel-N1, but the reactivity with HuC is unknown [2].
• First, a partially transformed non-virus-producing cell line was obtained after infection of HUC with simian virus 40 (SV40) [3].
• To study the role of the epithelium in the innate response to herpes simplex virus 1 (HSV-1) infection of the cornea, we used a telomerase-immortalized human corneal epithelial cell (HCEC) line, HUCL, and primary HCECs as a model and infected the cells with HSV-1 (KOS strain) [4].

High impact information on ELAVL3

• Based on co-labeling with the pan-neuronal marker HuC/D we conclude that submucous nerve cells potentially express heteromeric 5-HT3A/B receptors [5].
• By contrast, generic neuronal differentiation seems to be unaffected, as the expression of elavl3 (HuC) is not reduced in hands off sympathetic ganglia [6].
• Whereas three of the Elav family members (Hel-N1, HuC, and HuD) are restricted to young and mature neurons, HuR is more broadly expressed, including proliferating cells of the developing CNS [7].
• The deduced amino acid sequence of the RBP9 proteins is highly similar to those of three other nervous system-specific genes, human HuC and HuD and Drosophila elav, which also encode proteins with three RRMs [8].
• RESULTS: Exposure of HUCL cells to live, but not heat-killed, S. aureus resulted in NF-kappaB activation in a time-dependent manner, as assessed by the increase in IkappaB-alpha phosphorylation and degradation [9].

Biological context of ELAVL3

• Localization of HuC (ELAVL3) to chromosome 19p13.2 by fluorescence in situ hybridization utilizing a novel tyramide labeling technique [10].
• Exposure of both HUCL and primary HCE cells to purified PA flagellin (250 ng/mL) resulted in IkappaB-alpha phosphorylation and degradation in a time-dependent manner [11].
• Finally, some CC-contacting cells expressed HuC/D - a marker of immature neurones - and fired action potentials [12].
• Toll-like receptor (TLR)-5, an innate immunity receptor for flagellin, was expressed in HUCL cells and located at the cell surface of the basal and wing, but not in superficial, cells of human corneal epithelium [11].
• Finally, recent findings generated using in vitro transformation systems with human uroepithelial cells provide strong evidence that loss of genes on 3p, which occurs in approximately 20% of bladder cancers, and/or gain of genes on 20q play an important role in blocking HUC cellular senescence [13].

Anatomical context of ELAVL3

• Moreover, the generation of neurons in sphere cultures induced immunoreactivity to the ELAV-like neuronal RNA-binding proteins HuC/D, which have been implicated in mechanisms of nerve cell differentiation [14].
• Purified flagellin was used to challenge HUCL, a telomerase-immortalized HCE cell line, and primarily cultured HCE cells [11].
• Normal human urinary tract epithelial cells (HUC) were neoplastically transformed in vitro using a step-wise strategy [3].
• METHODS: HUCL, a telomerase-immortalized HCEC line, and primary cultures of HCECs were challenged with live or heat-killed S. aureus, its exoproducts, or cell wall components lipoteichoic acid (LTA) and peptidoglycan (PGN) [9].
• Induction of cytotoxic T lymphocytes specific for paraneoplastic cerebellar degeneration-associated antigen in vivo by DNA immunization [15].

Associations of ELAVL3 with chemical compounds

• Those investigated displaying potential occupational utility included the induction of ornithine decarboxylase (ODC), DNA adducts, and altered proteins, as detected on HUC two-dimensional polyacrylamide gel electrophoresis protein maps [16].

Other interactions of ELAVL3

• HuC is a neural-specific member of the Elav family of RNA-binding proteins [10].
• Deletions of the internal or terminal amino acid residues of the first RRM (RRM1) of the HuC/ple21 ELAV-like protein completely abolished RNA binding [17].
• RNA-binding analyses of HuC and HuD with the VEGF and c-myc 3'-untranslated regions using a novel ELISA-based assay [18].

Analytical, diagnostic and therapeutic context of ELAVL3

• Northern blot analysis indicated that N cells express all three Hu genes, HuD, HuC and Hel-N1 [19].
• Fab GLN495 recognized HuD and other related proteins (HuC and Hel-N1, or Hu antigens) in immunoblots of these recombinant proteins and in immunohistochemical and Western blot analysis of SCLC and neurons [20].

References