HCSGD entry for ELAVL1
1. General information
| Official gene symbol | ELAVL1 |
|---|---|
| Entrez ID | 1994 |
| Gene full name | ELAV (embryonic lethal, abnormal vision, Drosophila)-like 1 (Hu antigen R) |
| Other gene symbols | ELAV1 HUR Hua MelG |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
This gene isn't in PPI subnetwork.
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000166 | Nucleotide binding | IEA | molecular_function |
| GO:0003723 | RNA binding | IDA IEA | molecular_function |
| GO:0003725 | Double-stranded RNA binding | IDA | molecular_function |
| GO:0003729 | MRNA binding | TAS | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005634 | Nucleus | IDA | cellular_component |
| GO:0005654 | Nucleoplasm | TAS | cellular_component |
| GO:0005737 | Cytoplasm | IDA | cellular_component |
| GO:0005829 | Cytosol | TAS | cellular_component |
| GO:0006417 | Regulation of translation | IMP | biological_process |
| GO:0007275 | Multicellular organismal development | TAS | biological_process |
| GO:0010467 | Gene expression | TAS | biological_process |
| GO:0016070 | RNA metabolic process | TAS | biological_process |
| GO:0016071 | MRNA metabolic process | TAS | biological_process |
| GO:0017091 | AU-rich element binding | IDA | molecular_function |
| GO:0019901 | Protein kinase binding | IPI | molecular_function |
| GO:0035925 | MRNA 3'-UTR AU-rich region binding | IDA | molecular_function |
| GO:0045727 | Positive regulation of translation | IDA | biological_process |
| GO:0048255 | MRNA stabilization | IDA IMP | biological_process |
| GO:0070935 | 3'-UTR-mediated mRNA stabilization | IDA IMP | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.9475895103 | 0.0731649481 | 0.9999902473 | 0.5099509929 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Down | -0.0548875786 |
| GSE13712_SHEAR | Down | -0.0178643075 |
| GSE13712_STATIC | Down | -0.2254652944 |
| GSE19018 | Down | -0.3022635497 |
| GSE19899_A1 | Down | -0.2399801925 |
| GSE19899_A2 | Up | 0.3680050611 |
| PubMed_21979375_A1 | Down | -0.5189395275 |
| PubMed_21979375_A2 | Down | -0.5820323588 |
| GSE35957 | Down | -0.1569838009 |
| GSE36640 | Down | -0.6121973984 |
| GSE54402 | Up | 0.2319032987 |
| GSE9593 | Down | -0.3138992063 |
| GSE43922 | Down | -0.0982122673 |
| GSE24585 | Down | -0.1836880141 |
| GSE37065 | Down | -0.1329836617 |
| GSE28863_A1 | Up | 0.3335822172 |
| GSE28863_A2 | Up | 0.3349943351 |
| GSE28863_A3 | Down | -0.1462931916 |
| GSE28863_A4 | Up | 0.1658927774 |
| GSE48662 | Down | -0.6038537512 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-519b-3p | MIMAT0002837 | MIRT003731 | qRT-PCR//Western blot | Functional MTI | 19088191 |
| hsa-miR-519c-3p | MIMAT0002832 | MIRT003732 | qRT-PCR//Western blot | Functional MTI | 19088191 |
| hsa-miR-519a-3p | MIMAT0002869 | MIRT003733 | qRT-PCR//Western blot | Functional MTI | 19088191 |
| hsa-miR-125a-5p | MIMAT0000443 | MIRT005421 | Luciferase reporter assay//Western blot | Functional MTI | 19875930 |
| hsa-miR-340-5p | MIMAT0004692 | MIRT019606 | Sequencing | Functional MTI (Weak) | 20371350 |
| hsa-miR-93-5p | MIMAT0000093 | MIRT048754 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
- mirRecord
MicroRNA name | mirBase ID | Target site number | MiRNA mature ID | Test method inter | MiRNA regulation site | Reporter target site | Pubmed ID |
|---|---|---|---|---|---|---|---|
| hsa-miR-125a-5p | MIMAT0000443 | 1 | hsa-miR-125a-5p | {Western blot} | {overexpression by miRNA precursor transfection} | 19875930 | |
| hsa-miR-125b-5p | MIMAT0000423 | 1 | hsa-miR-125b | {Western blot} | {overexpression by miRNA precursor transfection} | 19875930 |
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6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 6 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 25104461 | HuR and post-transcriptional regulation in vascular aging |
| 25104461 | HuR (ELAV11 (embryonic lethal, abnormal vision)-like 1), a ubiquitously expressed member of the ELAV-like RNA-binding protein family, has been shown to regulate the stability and translation of mRNAs that encode factors regulating cellular senescence, thereby impacting on aging |
| 25018007 | Loss of HuR leads to senescence-like cytokine induction in rodent fibroblasts by activating NF-kappaB |
| 25018007 | BACKGROUND: HuR (human antigen R) is a ubiquitously expressed member of the Hu/ELAV family of proteins that is involved in diverse biological processes |
| 25018007 | HuR has also been shown to play an important role in cell cycle arrest during replicative senescence in both human and mouse cells |
| 25018007 | METHODS: Senescence-associated phenotypes were analyzed in MEFs and other cell line in which HuR expression is inhibited by sh-RNA-mediated knockdown |
| 25018007 | RESULTS: RNAi-mediated HuR inhibition resulted in an increase in SASP-related cytokines |
| 25018007 | In the absence of HuR, cells were defective in the DNA-damage response, and single strand DNA breaks accumulated, which may have caused the activation of NF-kappaB and subsequent cytokine induction |
| 25018007 | CONCLUSIONS: In the absence of HuR, cells exhibit multiple senescence-associated phenotypes |
| 25018007 | Our findings suggest that HuR regulates not only the replicative lifespan, but also the expression of SASP-related cytokines in mouse fibroblasts |
| 22510478 | This inhibition in large part resulted from the downregulation of SIRT1, which in turn was because of decrease in the expression of the translation regulator HuR |
| 18585896 | Signalling pathways regulating nucleo-cytoplasmic shuttling of the mRNA-binding protein HuR |
| 18585896 | Accordingly, a large number of reports have documented that the Human antigen R (HuR), a ubiquitously expressed member of the ELAV protein family, is one of the major actors in this scenario |
| 18585896 | Consequently, HuR is implicated in a large variety of pathologies in which deregulated stabilisation of many short-lived key mRNAs is causally linked with the onset and course of disease |
| 18585896 | Since HuR is most abundantly localised within the cell nucleus, export of HuR to the cytoplasm seems a major prerequisite for its stabilising effects on its cognate target adenylate- and uridylate-rich elements (AREs) containing cargo mRNAs |
| 18585896 | Although, the list of reports demonstrating a critical involvement of different signalling cascades in HuR-triggered mRNA functions is steadily growing, the mechanisms underlying HuR trafficking are not well understood |
| 18585896 | For this reason, the review will cover the most recent advances of knowledge of signalling cascades involved in the stimulus-dependent nucleo-cytoplasmic HuR shuttling and a special emphasis will be put on the possible regulatory role of posttranslational HuR modification |
| 12730239 | Increased AMP:ATP ratio and AMP-activated protein kinase activity during cellular senescence linked to reduced HuR function |
| 12730239 | HuR function was previously shown to be implicated in the maintenance of a "young cell" phenotype in models of replicative cellular senescence |
| 11486028 | Loss of HuR is linked to reduced expression of proliferative genes during replicative senescence |
| 11486028 | Here, using two models of replicative senescence, we describe the influence of the RNA-binding protein HuR in regulating the expression of several genes whose expression decreases during senescence |
| 11486028 | We demonstrate that HuR levels, HuR binding to target mRNAs encoding proliferative genes, and the half-lives of such mRNAs are lower in senescent cells |
| 11486028 | Importantly, overexpression of HuR in senescent cells restored a "younger" phenotype, while a reduction in HuR expression accentuated the senescent phenotype |
| 11486028 | Our studies highlight a critical role for HuR during the process of replicative senescence |
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