HCSGD entry for MAPK3
1. General information
| Official gene symbol | MAPK3 |
|---|---|
| Entrez ID | 5595 |
| Gene full name | mitogen-activated protein kinase 3 |
| Other gene symbols | ERK-1 ERK1 ERT2 HS44KDAP HUMKER1A P44ERK1 P44MAPK PRKM3 p44-ERK1 p44-MAPK |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000165 | MAPK cascade | NAS TAS | biological_process |
| GO:0000186 | Activation of MAPKK activity | TAS | biological_process |
| GO:0000187 | Activation of MAPK activity | TAS | biological_process |
| GO:0001784 | Phosphotyrosine binding | IEA | molecular_function |
| GO:0001934 | Positive regulation of protein phosphorylation | IMP | biological_process |
| GO:0002224 | Toll-like receptor signaling pathway | TAS | biological_process |
| GO:0002755 | MyD88-dependent toll-like receptor signaling pathway | TAS | biological_process |
| GO:0002756 | MyD88-independent toll-like receptor signaling pathway | TAS | biological_process |
| GO:0004707 | MAP kinase activity | IDA IEA NAS TAS | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005524 | ATP binding | IEA | molecular_function |
| GO:0005634 | Nucleus | IDA IEA TAS | cellular_component |
| GO:0005654 | Nucleoplasm | TAS | cellular_component |
| GO:0005730 | Nucleolus | IDA | cellular_component |
| GO:0005739 | Mitochondrion | TAS | cellular_component |
| GO:0005769 | Early endosome | TAS | cellular_component |
| GO:0005770 | Late endosome | TAS | cellular_component |
| GO:0005794 | Golgi apparatus | TAS | cellular_component |
| GO:0005829 | Cytosol | IEA TAS | cellular_component |
| GO:0005856 | Cytoskeleton | TAS | cellular_component |
| GO:0005901 | Caveola | TAS | cellular_component |
| GO:0005925 | Focal adhesion | TAS | cellular_component |
| GO:0006351 | Transcription, DNA-templated | IEA | biological_process |
| GO:0006360 | Transcription from RNA polymerase I promoter | TAS | biological_process |
| GO:0006361 | Transcription initiation from RNA polymerase I promoter | TAS | biological_process |
| GO:0006468 | Protein phosphorylation | IDA | biological_process |
| GO:0006915 | Apoptotic process | IEA | biological_process |
| GO:0006974 | Cellular response to DNA damage stimulus | IEA | biological_process |
| GO:0006975 | DNA damage induced protein phosphorylation | IDA | biological_process |
| GO:0007049 | Cell cycle | IEA | biological_process |
| GO:0007173 | Epidermal growth factor receptor signaling pathway | TAS | biological_process |
| GO:0007264 | Small GTPase mediated signal transduction | TAS | biological_process |
| GO:0007265 | Ras protein signal transduction | TAS | biological_process |
| GO:0007411 | Axon guidance | TAS | biological_process |
| GO:0007596 | Blood coagulation | TAS | biological_process |
| GO:0008286 | Insulin receptor signaling pathway | TAS | biological_process |
| GO:0008543 | Fibroblast growth factor receptor signaling pathway | TAS | biological_process |
| GO:0009887 | Organ morphogenesis | IEA | biological_process |
| GO:0010467 | Gene expression | TAS | biological_process |
| GO:0015630 | Microtubule cytoskeleton | IDA | cellular_component |
| GO:0016032 | Viral process | IEA | biological_process |
| GO:0016310 | Phosphorylation | IDA | biological_process |
| GO:0019221 | Cytokine-mediated signaling pathway | TAS | biological_process |
| GO:0019233 | Sensory perception of pain | IEA | biological_process |
| GO:0019902 | Phosphatase binding | IPI | molecular_function |
| GO:0030168 | Platelet activation | TAS | biological_process |
| GO:0030509 | BMP signaling pathway | IMP | biological_process |
| GO:0031143 | Pseudopodium | IEA | cellular_component |
| GO:0031663 | Lipopolysaccharide-mediated signaling pathway | IEA | biological_process |
| GO:0032872 | Regulation of stress-activated MAPK cascade | TAS | biological_process |
| GO:0033129 | Positive regulation of histone phosphorylation | IMP | biological_process |
| GO:0034134 | Toll-like receptor 2 signaling pathway | TAS | biological_process |
| GO:0034138 | Toll-like receptor 3 signaling pathway | TAS | biological_process |
| GO:0034142 | Toll-like receptor 4 signaling pathway | TAS | biological_process |
| GO:0034146 | Toll-like receptor 5 signaling pathway | TAS | biological_process |
| GO:0034162 | Toll-like receptor 9 signaling pathway | TAS | biological_process |
| GO:0034166 | Toll-like receptor 10 signaling pathway | TAS | biological_process |
| GO:0035066 | Positive regulation of histone acetylation | IMP | biological_process |
| GO:0035666 | TRIF-dependent toll-like receptor signaling pathway | TAS | biological_process |
| GO:0038083 | Peptidyl-tyrosine autophosphorylation | IDA | biological_process |
| GO:0038095 | Fc-epsilon receptor signaling pathway | TAS | biological_process |
| GO:0038096 | Fc-gamma receptor signaling pathway involved in phagocytosis | TAS | biological_process |
| GO:0038123 | Toll-like receptor TLR1:TLR2 signaling pathway | TAS | biological_process |
| GO:0038124 | Toll-like receptor TLR6:TLR2 signaling pathway | TAS | biological_process |
| GO:0043330 | Response to exogenous dsRNA | IEA | biological_process |
| GO:0045087 | Innate immune response | TAS | biological_process |
| GO:0045944 | Positive regulation of transcription from RNA polymerase II promoter | IMP | biological_process |
| GO:0048011 | Neurotrophin TRK receptor signaling pathway | TAS | biological_process |
| GO:0051090 | Regulation of sequence-specific DNA binding transcription factor activity | IEA TAS | biological_process |
| GO:0051216 | Cartilage development | IEA | biological_process |
| GO:0051403 | Stress-activated MAPK cascade | TAS | biological_process |
| GO:0051493 | Regulation of cytoskeleton organization | TAS | biological_process |
| GO:0060397 | JAK-STAT cascade involved in growth hormone signaling pathway | TAS | biological_process |
| GO:0070374 | Positive regulation of ERK1 and ERK2 cascade | IMP | biological_process |
| GO:0070498 | Interleukin-1-mediated signaling pathway | IMP | biological_process |
| GO:0070849 | Response to epidermal growth factor | IDA | biological_process |
| GO:0071260 | Cellular response to mechanical stimulus | IEP | biological_process |
| GO:0072584 | Caveolin-mediated endocytosis | TAS | biological_process |
| GO:0090170 | Regulation of Golgi inheritance | TAS | biological_process |
| GO:2000641 | Regulation of early endosome to late endosome transport | TAS | biological_process |
| GO:2000657 | Negative regulation of apolipoprotein binding | IEA | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.1527820562 | 0.5523410585 | 0.7798500872 | 1.0000000000 |
- 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 | -0.0056717192 |
| GSE13712_SHEAR | Down | -0.1342312311 |
| GSE13712_STATIC | Down | -0.2439746984 |
| GSE19018 | Up | 0.4888880670 |
| GSE19899_A1 | Down | -0.0743740738 |
| GSE19899_A2 | Up | 0.5972932917 |
| PubMed_21979375_A1 | Up | 0.2615950478 |
| PubMed_21979375_A2 | Up | 0.5432638474 |
| GSE35957 | Up | 0.3942022087 |
| GSE36640 | Up | 0.5612631604 |
| GSE54402 | Down | -0.0566338517 |
| GSE9593 | Up | 0.0596963455 |
| GSE43922 | Down | -0.1503073515 |
| GSE24585 | Down | -0.0743803412 |
| GSE37065 | Down | -0.0758937161 |
| GSE28863_A1 | Up | 0.1054885361 |
| GSE28863_A2 | Down | -0.1056928020 |
| GSE28863_A3 | Down | -0.4355308151 |
| GSE28863_A4 | Down | -0.1903760281 |
| GSE48662 | Up | 0.6967101815 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-483-5p | MIMAT0004761 | MIRT006217 | Luciferase reporter assay//Microarray//qRT-PCR//Western blot | Functional MTI | 22465663 |
| hsa-miR-320b | MIMAT0005792 | MIRT036229 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-423-3p | MIMAT0001340 | MIRT042561 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-34a-5p | MIMAT0000255 | MIRT047369 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
No target information from mirRecord
- mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 35 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 26824319 | This is neither dependent on p65/NF-kappaB signaling nor RAF/MEK/ERK pathway activity as inhibition of MEK by GSK1120212 (trametinib) and induction of ERK1/2 activity by parthenolide itself do not interfere with parthenolide-triggered depletion of MITF-M in both wild-type BRAF and BRAF(V600E) melanoma populations |
| 26696133 | In addition, the levels of some senescence-associated proteins, such as phosphorylated ERK1/2, caveolin-1, p53, p16(ink4a), and p21(waf1), were elevated in PPKO-treated cells |
| 26690546 | Under such conditions, Chk2, cyclin A/CDK2 and ERK1/2 were aberrantly activated |
| 26690546 | Pharmacological inactivation of Chk2, CDK2 or ERK1/2 or depletion of CDK2 or Chk2 inhibited the centrosome amplification in ETO-treated ACT cells |
| 26463993 | Addition of U0126, an inhibitor of ERK1/2, prevented appearance of senescent features induced by excess NaCl |
| 26273429 | Analysis of the mechanisms of senescent MSCs and galectin-3 on LoVo cells signal transduction determined that senescent MSCs and exogenous galectin-3 promoted cell growth by activating the mitogen-activated protein kinase (MAPK) (extracellular signal-regulated kinase [ERK]1/2) pathway |
| 25744025 | Nesprin-2-dependent ERK1/2 compartmentalisation regulates the DNA damage response in vascular smooth muscle cell ageing |
| 25744025 | The extracellular signal-regulated kinases 1 and 2 (ERK1/2) have emerged as key players in the DDR and are known to enhance ataxia telangiectasia-mutated protein (ATM) activity at DNA lesions, and in this study, we identified a novel relationship between prelamin A accumulation and ERK1/2 nuclear compartmentalisation during VSMC ageing |
| 25744025 | We show both prelamin A accumulation and increased DNA damage occur concomitantly, before VSMC replicative senescence, and induce the localisation of ERK1/2 to promyelocytic leukaemia protein nuclear bodies (PML NBs) at the sites of DNA damage via nesprin-2 and lamin A interactions |
| 25414256 | Given that ERK1/2 is one of the major kinases controlling cell growth and proliferation, we examined the possible implication of ERK1/2 |
| 25414256 | Senescent cells displayed a blunted response to growth factor-induced cell proliferation, which was preceded by impaired ERK1/2 activation |
| 25414256 | Further analysis revealed that senescent cells expressed a significantly higher level of mitogen-activated protein phosphatase 3 (MKP-3, a cytosolic ERK1/2-targeted phosphatase), which was suppressed by blocking the transcriptional activity of the tumor suppressor p53 with pifithrin-alpha |
| 25414256 | Inhibition of MKP-3 activity with a specific inhibitor or siRNA enhanced basal ERK1/2 phosphorylation and promoted cell proliferation |
| 25414256 | Apart from its role in growth arrest, impairment of ERK1/2 also contributed to the resistance of senescent cells to oxidant-elicited cell injury |
| 25414256 | These results therefore indicate that p53-mediated up-regulation of MKP-3 contributes to the establishment of the senescent cellular phenotype through dephosphorylating ERK1/2 |
| 25414256 | Impairment of ERK1/2 activation could be an important mechanism by which p53 controls cellular senescence |
| 25338966 | Instead, phosphorylation of p53 was mediated by Erk1/2 MAP kinase |
| 25115457 | A549 non-small lung cancer cells were exposed to different concentrations of hecogenin acetate and reactive species production, ERK1/2 activation, matrix metalloproteinase expression, cell cycle arrest and cell senescence parameters were evaluated |
| 25115457 | In addition, hecogenin acetate blocked ERK1/2 phosphorylation and inhibited the increase in MMP-2 caused by H2O2 |
| 25115457 | These data indicate that hecogenin acetate is able to exert anti-cancer effects by modulating reactive species production, inducing cell cycle arrest and senescence and also modulating ERK1/2 phosphorylation and MMP-2 production |
| 24997994 | Proteomic analysis reveals a role for Bcl2-associated athanogene 3 and major vault protein in resistance to apoptosis in senescent cells by regulating ERK1/2 activation |
| 24997994 | We demonstrate that Bag3 and MVP contribute to apoptosis resistance in therapy-induced senescence by increasing the level of activation of extracellular signal-regulated kinase1/2 (ERK1/2) |
| 24997994 | Silencing of either Bag3 or MVP decreased ERK1/2 activation and promoted apoptosis in adriamycin-treated cells |
| 24997994 | We propose a model in which Bag3 binds to MVP and facilitates MVP accumulation in the nucleus, which sustains ERK1/2 activation |
| 24997994 | We confirmed that silencing of Bag3 or MVP shifts the response toward apoptosis and regulates ERK1/2 activation in a panel of diverse breast cancer cell lines |
| 24691968 | Chemokine C-C motif ligand 5 (CCL5) expression was found to be approximately 8-fold higher in old compared to that in young quiescent NHFs, which correlated with an increase in the ERK1/2-cyclin D1 pro-proliferative pathway in MB231 cells |
| 24691968 | Conditioned media treated with anti-CCL5 antibody suppressed the activation of the ERK1/2-cyclin D1 pathway and proliferation of MB231 cells |
| 24691968 | This inhibition was associated with NHFs inability to activate the ERK1/2-cyclin D1 pathway and enhance proliferation of MB231 cells |
| 24471649 | Interestingly, phosphorylation of ERK1/2 was induced upon PDGF stimulation of young, replicating cells but not senescent cells |
| 24471649 | Induction of ERK1/2 phosphorylation was impaired in senescent cells and PTRF-overexpressing presenescent cells |
| 24408923 | The extracellular signal-regulated kinase ERK1 and ERK2 (ERK1/2) cascade regulates a variety of cellular processes by phosphorylating multiple target proteins |
| 23941874 | Moreover, the ability of PDGF to promote cell proliferation/migration and regulate the phosphorylation-dependent activation of Akt and ERK1/2 appears to be attenuated as a function of diabetes |
| 23599344 | Surprisingly, attenuation of ERK/MAP kinase signaling by genetic inactivation of Erk2, RNAi-mediated knockdown of ERK1 or ERK2, or MEK inhibitors prevented the activation of the senescence mechanism, allowing oncogenic ras to transform primary cells |
| 22915839 | Sustained activation of survival (Akt) and proliferative (ERK1/2) kinases fosters robustness of cells |
| 22847612 | The Bach1-deficient cells showed diminished phosphorylation of MEK and ERK1/2 in response to H-Ras(V12), which was consistent with the alterations in the gene expression profile, including phosphatase genes |
| 22820504 | Our results demonstrated that MSCs from SLE patients were senescent and that p16 (INK4A) plays an essential role in the process by inhibiting ERK1/2 activation |
| 22427991 | Zinc, siZnT3 and siZnT10 downregulate catalase by a post-transcriptional mechanism mediated by decreased phosphorylation of ERK1/2 |
| 22008288 | Effects of low concentration of endosulfan on proliferation, ERK1/2 pathway, apoptosis and senescence in Nile tilapia (Oreochromis niloticus) splenocytes |
| 22008288 | The ERK family of MAPKs includes ERK1 and ERK2 |
| 22008288 | Phosphorylated ERK1/2 (pERK1/2) molecules are involved in many aspects of cellular survival, and are important for apoptosis or oxidative stress-induced senescence |
| 22008288 | In order to study the mechanisms by which endosulfan affects fish health, the present study was aimed at evaluating the in vitro effects of this insecticide on proliferation, the ERK1/2 pathway, apoptosis and cell senescence in splenocytes from Nile tilapia |
| 21934682 | Profiling the established molecular targets of SHP2 (ERK1/2 and STAT3) confirmed specificity of these siRNAs |
| 21788308 | 1), RASSF1A weakly reduces cell proliferation and anchorage-independent growth of uveal melanoma cells without effect on ERK1/2 activation, cyclin D1 and p27(Kip1) expression |
| 21788308 | This study explored biological functions and underlying mechanisms of RASSF1A in the ERK1/2 pathway in normal uveal melanocytes |
| 21788308 | We showed that siRNA-mediated depletion of RASSF1A increased ERK1/2 activation, cyclin D1 expression, and also decreased p27(Kip1) expression in normal uveal melanocytes |
| 20453494 | Angiopoietin-1 inhibits mouse glomerular endothelial cell senescence via Tie2 receptor-modulated ERK1/2 signaling |
| 20428768 | The results thus suggest that low doses of radiation suppress doxorubicin-induced replicative senescence through the inhibition of p38-dependent phosphorylation of p53 and by activation of ERK1/2, without genomic damage |
| 20032303 | Changes in cellular expression of phosphoprotein enriched in astrocytes of 15 kDa (PEA-15) are linked to insulin resistance, tumor cell invasion, and cellular senescence; these changes alter the activation of the extracellular signal-regulated kinase (ERK)1/2 mitogen-activated protein (MAP) kinase pathway |
| 20032303 | PEA-15 binding prevented ERK1/2 membrane recruitment and threonine phosphorylation of fibroblast receptor substrate 2alpha (FRS2alpha), a key link in fibroblast growth factor (FGF) receptor activation of ERK1/2 |
| 20032303 | This is the dominant mechanism by which PEA-15 activates ERK1/2 because genetic deletion of FRS2alpha blocked the capacity of PEA-15 to activate the MAP kinase pathway |
| 20032303 | Thus, PEA-15 prevents ERK1/2 localization to the plasma membrane, thereby inhibiting ERK1/2-dependent threonine phosphorylation of FRS2alpha to promote activation of the ERK1/2 MAP kinase pathway |
| 19937729 | Notably, low concentrations of 5,6-secosterol caused a sustained activation of ERK1/2, inducing cell proliferation, this unexpected behavior should be better characterized by further studies |
| 19164294 | The Cspg2(Delta3/Delta3) fibroblasts showed a substantial increase of ERK1/2 phosphorylation and expression of senescence markers p53, p21, and p16 |
| 19164294 | Treatment of wild type fibroblasts with hyaluronidase and exogenous hyaluronan enhanced ERK1/2 phosphorylation, and treatment with an anti-CD44 antibody that blocks HA-CD44 interaction inhibited the phosphorylation |
| 19164294 | These results demonstrate that versican is essential for matrix assembly involving hyaluronan and that diminished versican deposition increases free hyaluronan fragments that interact with CD44 and increase phosphorylation of ERK1/2, leading to cellular senescence |
| 18765664 | S1P-induced Akt and ERK1/2 activation were comparable between ECs of different in vitro ages; however, PTEN (phosphatase and tensin homolog deleted on chromosome 10) activity was significantly elevated and Rac activation was inhibited in senescent ECs |
| 17092487 | Furthermore, overexpression of GNG11 activated ERK1/2 of the MAP kinase family, but did not Ras |
| 16600555 | By use of conditioned medium, we found a growth promoting impact of fibroblasts compared with control medium from epithelial cells associated with activation of ERK1/2, Akt, p70S6K, and EGF receptor |
| 15711127 | Although some of these differences between Taxol and discodermolide were dose dependent, only discodermolide produced a doxorubicin-like induction of a senescence phenotype, including a senescence-associated beta-galactosidase activity, up-regulation of PAI-1 and p66Shc, and a strong, sustained, Erk1/2 activation |
| 15331596 | The ERK1/2 mitogen-activated protein kinase pathway is required for the transforming effects of ras, and its activation is often sufficient to convey mitogenic stimulation |
| 15331596 | How the Ras/ERK1/2 pathway activates different cellular programs is not well understood |
| 12840032 | When the cells were pretreated with 10 mm N-acetyl-l-cysteine for 1 h, Erk1/2 activation was completely blocked |
| 12470826 | TCF is activated after phosphorylation by the Extracellular signals Regulated Kinase 1 and 2 (ERK1/2), two kinases of the Raf/MEK/ERK signaling pathway |
| 10748101 | Significance of nuclear relocalization of ERK1/2 in reactivation of c-fos transcription and DNA synthesis in senescent fibroblasts |
| 10748101 | Two of mitogen-activated protein kinases (MAPK), p44(mapk)/p42(mapk) extracellular signal-regulated kinases (ERK1/2), translocate into nuclei following activation and play critical roles in connecting the signal to gene expression and allowing cell-cycle entry |
| 10748101 | Here we found that the nuclear translocation of ERK1/2 in response to growth stimuli was significantly inhibited in senescent cells that were irreversibly growth arrested, compared with presenescent cells |
| 10748101 | The activation step of these enzymes was not impaired, since ERK1/2 were phosphorylated and activated in senescent cells as efficiently as in presenescent cells |
| 10748101 | Furthermore, the nuclear localization of ERK1/2 has been suggested to potentiate the proliferative activity of the senescent cells in collaboration with adenovirus E1A protein |
| 10748101 | More importantly, SV40 large T antigen, the strong inducer of DNA synthesis, had the inherent ability to restore nuclear relocalization of active ERK1/2 in senescent cells, which was essentially required for the reinitiation of DNA synthesis |
| 10748101 | Thus, manipulating the relocalization of ERK1/2 into nuclei was expected to open the way to overcome some of the senescent phenotypes |
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