Target Name: ELAVL4
NCBI ID: G1996
Review Report on ELAVL4 Target / Biomarker Content of Review Report on ELAVL4 Target / Biomarker
ELAVL4
Other Name(s): ELAV4_HUMAN | Hu-antigen D | ELAV like RNA binding protein 4, transcript variant 7 | OTTHUMP00000009612 | ELAV like RNA binding protein 4 | ELAV like RNA binding protein 4, transcript variant 4 | ELAVL4 variant 7 | ELAV-like protein 4 isoform 7 | HuD | ELAVL4 variant 4 | ELAV (embryonic lethal, abnormal vision, Drosophila)-like 4 (Hu antigen D) | Paraneoplastic encephalomyelitis antigen HuD | Hu antigen D | ELAV-like protein 4 (isoform 1) | ELAVL4 variant 1 | ELAV like RNA binding protein 4, transcript variant 1 | ELAV like neuron-specific RNA binding protein 4 | PNEM | HUD | ELAV-like protein 4 (isoform 4) | ELAV-like protein 4 | paraneoplastic encephalomyelitis antigen HuD | Embryonic lethal, abnormal vision, Drosophila, homolog of, like-4

ELAVL4: A Potential Drug Target and Biomarker

ELAVL4, also known as ETV6428, is a gene that encodes for a protein known as ETV6428, which is a member of the evolutionarily diverse T-cell receptor (TCR) family. TCR is a transmembrane protein that plays a critical role in cell-mediated immunity, including the regulation of T-cell development and activation. ETV6428 has been shown to be involved in the regulation of T-cell receptor signaling, and has potential as a drug target or biomarker.

The TCR is a large gene that encodes a transmembrane protein that consists of several distinct subunits. The subunit responsible for regulating T-cell receptor signaling is called TCR伪, which is a 250-kDa protein that is expressed in most tissues of the body. ETV6428 is a highly conserved gene that is located on chromosome 6 and encodes for a protein of similar size to TCR伪.

In preclinical studies, ETV6428 has been shown to play a role in the regulation of T-cell receptor signaling. For example, studies have shown that overexpression of ETV6428 can enhance the ability of T cells to recognize and respond to antigens, while inhibition of ETV6428 has been shown to decrease the ability of T cells to recognize and respond to antigens. These findings suggest that ETV6428 may be a drug target or biomarker that can be used to modulate T-cell receptor signaling.

In addition to its potential role in T-cell receptor signaling, ETV6428 has also been shown to be involved in the regulation of cell adhesion. Adhesion is a critical process that is involved in the assembly and maintenance of tissues, including tissues of the immune system. ETV6428 has been shown to be involved in the regulation of cell adhesion in various tissues, including the regulation of T-cell adhesion and the regulation of cancer cell adhesion.

The potential drug target or biomarker properties of ETV6428 are also supported by its expression in various tissues and its association with various diseases. For example, ETV6428 has been shown to be expressed in a variety of tissues, including the brain, spleen, and thymus, which suggests that it may be involved in the regulation of immune system function. Additionally, ETV6428 has been associated with a variety of diseases, including cancer, autoimmune diseases, and neurodegenerative diseases.

In conclusion, ETV6428 is a gene that encodes for a protein that is involved in the regulation of T-cell receptor signaling and cell adhesion. Its potential as a drug target or biomarker is supported by its expression in various tissues and its association with a variety of diseases. Further research is needed to fully understand the role of ETV6428 in immune system function and its potential as a drug target or biomarker.

Protein Name: ELAV Like RNA Binding Protein 4

Functions: RNA-binding protein that is involved in the post-transcriptional regulation of mRNAs (PubMed:7898713, PubMed:10710437, PubMed:12034726, PubMed:12468554, PubMed:17035636, PubMed:17234598). Plays a role in the regulation of mRNA stability, alternative splicing and translation (PubMed:7898713, PubMed:10710437, PubMed:12034726, PubMed:12468554, PubMed:17035636, PubMed:17234598). Binds to AU-rich element (ARE) sequences in the 3' untranslated region (UTR) of target mRNAs, including GAP43, VEGF, FOS, CDKN1A and ACHE mRNA (PubMed:7898713, PubMed:10710437, PubMed:12034726, PubMed:12468554). Many of the target mRNAs are coding for RNA-binding proteins, transcription factors and proteins involved in RNA processing and/or neuronal development and function (By similarity). By binding to the mRNA 3'UTR, decreases mRNA deadenylation and thereby contributes to the stabilization of mRNA molecules and their protection from decay (PubMed:12034726). Also binds to the polyadenylated (poly(A)) tail in the 3'UTR of mRNA, thereby increasing its affinity for mRNA binding (PubMed:12034726). Mainly plays a role in neuron-specific RNA processing by stabilization of mRNAs such as GAP43, ACHE and mRNAs of other neuronal proteins, thereby contributing to the differentiation of neural progenitor cells, nervous system development, learning and memory mechanisms (PubMed:12034726, PubMed:12468554, PubMed:17234598, PubMed:18218628). Involved in the negative regulation of the proliferative activity of neuronal stem cells and in the positive regulation of neuronal differentiation of neural progenitor cells (By similarity). Promotes neuronal differentiation of neural stem/progenitor cells in the adult subventricular zone of the hippocampus by binding to and stabilizing SATB1 mRNA (By similarity). Binds and stabilizes MSI1 mRNA in neural stem cells (By similarity). Exhibits increased binding to ACHE mRNA during neuronal differentiation, thereby stabilizing ACHE mRNA and enhancing its expression (PubMed:12468554, PubMed:17234598). Protects CDKN1A mRNA from decay by binding to its 3'-UTR (By similarity). May bind to APP and BACE1 mRNAS and the BACE1AS lncRNA and enhance their stabilization (PubMed:24857657). Plays a role in neurite outgrowth and in the establishment and maturation of dendritic arbors, thereby contributing to neocortical and hippocampal circuitry function (By similarity). Stabilizes GAP43 mRNA and protects it from decay during postembryonic development in the brain (PubMed:12034726). By promoting the stabilization of GAP43 mRNA, plays a role in NGF-mediated neurite outgrowth (By similarity). Binds to BDNF long 3'UTR mRNA, thereby leading to its stabilization and increased dendritic translation after activation of PKC (By similarity). By increasing translation of BDNF after nerve injury, may contribute to nerve regeneration (By similarity). Acts as a stabilizing factor by binding to the 3'UTR of NOVA1 mRNA, thereby increasing its translation and enhancing its functional activity in neuron-specific splicing (PubMed:18218628). Stimulates translation of mRNA in a poly(A)- and cap-dependent manner, possibly by associating with the EIF4F cap-binding complex (By similarity). May also negatively regulate translation by binding to the 5'UTR of Ins2 mRNA, thereby repressing its translation (By similarity). Upon glucose stimulation, Ins2 mRNA is released from ELAVL4 and translational inhibition is abolished (By similarity). Also plays a role in the regulation of alternative splicing (PubMed:17035636). May regulate alternative splicing of CALCA pre-mRNA into Calcitonin and Calcitonin gene-related peptide 1 (CGRP) by competing with splicing regulator TIAR for binding to U-rich intronic sequences of CALCA pre-mRNA (PubMed:17035636)

The "ELAVL4 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about ELAVL4 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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