HCSGD entry for TAGLN
1. General information
| Official gene symbol | TAGLN |
|---|---|
| Entrez ID | 6876 |
| Gene full name | transgelin |
| Other gene symbols | SM22 SMCC TAGLN1 WS3-10 |
| 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:0003779 | Actin binding | IEA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005737 | Cytoplasm | IEA | cellular_component |
| GO:0007517 | Muscle organ development | TAS | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.9750263060 | 0.0000133392 | 0.9999902473 | 0.0071627451 |
- 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 | -1.4848960920 |
| GSE13712_SHEAR | Down | -0.5825046629 |
| GSE13712_STATIC | Down | -0.4508716644 |
| GSE19018 | Down | -0.5568865745 |
| GSE19899_A1 | Down | -2.2641471959 |
| GSE19899_A2 | Down | -2.2067483545 |
| PubMed_21979375_A1 | Down | -3.1505746017 |
| PubMed_21979375_A2 | Down | -3.3941218421 |
| GSE35957 | Up | 0.6336087801 |
| GSE36640 | Up | 0.9399946556 |
| GSE54402 | Down | -1.3416596100 |
| GSE9593 | Down | -0.0781584210 |
| GSE43922 | Down | -2.4658149771 |
| GSE24585 | Down | -0.1069175100 |
| GSE37065 | Down | -1.4466333344 |
| GSE28863_A1 | Down | -1.6847900422 |
| GSE28863_A2 | Down | -1.6223900424 |
| GSE28863_A3 | Down | -0.1362864359 |
| GSE28863_A4 | Up | 0.0142158734 |
| GSE48662 | Down | -0.5613676281 |
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-9-5p | MIMAT0000441 | MIRT021406 | Microarray | Functional MTI (Weak) | 17612493 |
| hsa-miR-128-3p | MIMAT0000424 | MIRT022018 | Microarray | Functional MTI (Weak) | 17612493 |
| hsa-miR-7-5p | MIMAT0000252 | MIRT025891 | Microarray | Functional MTI (Weak) | 17612493 |
| hsa-miR-26b-5p | MIMAT0000083 | MIRT030313 | Microarray | Functional MTI (Weak) | 19088304 |
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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: 10 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 25342130 | The increase in calcification was accompanied by up-regulation of Cbfa1 (osteogenic transcription factor) and down-regulation of SM22alpha (VSMC lineage marker) |
| 20705054 | Smooth muscle protein 22-alpha (SM22alpha) is known as a transformation shape change-sensitive actin cross-linking protein found in smooth muscle tissue and fibroblasts; however, its functional role remains uncertain |
| 20705054 | We reported previously that SM22alpha overexpression confers resistance against anti-cancer drugs or radiation via induction of metallothionein (MT) isozymes in HepG2 cells |
| 20705054 | In this study, we demonstrate that SM22alpha overexpression leads cells to a growth arrest state and promotes cellular senescence caused by treatment with a subclinical dose of gamma-radiation (0 |
| 20705054 | SM22alpha overexpression in HepG2 cells elevated p16(INK4a) followed by pRB activation, but did not activate the p53/p21(WAF1/Cip1) pathway |
| 20705054 | Moreover, MT-1G, which is induced by SM22alpha overexpression, was involved in the activation of the p16(INK4a)/pRB pathway, which led to a growth arrest state and promoted cellular senescence caused by damaging agents |
| 20705054 | Our findings provide the first demonstration that SM22alpha modulates cellular senescence caused by damaging agents via regulation of the p16(INK4a)/pRB pathway in HepG2 cells and that these effects of SM22alpha are partially mediated by MT-1G |
| 20554622 | Levels of apolipoprotein J (Apo J), SM22, and osteonectin (SPARC) mRNA were determined by real-time PCR analysis |
| 20554622 | RESULTS: TGF-beta2 increased SA-beta-Gal activity, lipid peroxidation, and the mRNA expressions of Apo J, SM22, and SPARC |
| 20362703 | Here, we demonstrate that FGFR3 signaling is also capable of inducing premature senescence in chondrocytes, manifested as reversible, ERK-dependent growth arrest accompanied by alteration of cellular shape, loss of the extracellular matrix, upregulation of senescence markers (alpha-GLUCOSIDASE, FIBRONECTIN, CAVEOLIN 1, LAMIN A, SM22alpha and TIMP 1), and induction of senescence-associated beta-GALACTOSIDASE activity |
| 19171648 | Expression of senescence-associated genes (apolipoprotein J [Apo J], connective tissue growth factor [CTGF], fibronectin, and SM22) was examined by real-time PCR and induction of signal transduction proteins (p21, p16, and pRb) by Western blot analysis |
| 19171648 | RESULTS: H(2)O(2) markedly increased the number of SA-beta-Gal-positive cells to up to 89% and the expression of Apo J, CTGF, fibronectin, and SM22 by approximately three to fourfold |
| 18425358 | Thirdly, the mRNA levels of three senescence-associated genes, fibronectin, osteonectin and SM22, also increased |
| 15610763 | Genes specifically up-regulated by transdifferentiation but not by cellular senescence of PrSCs were metalloproteinase 1 tissue inhibitor (Timp1), transgelin (Tagln), gamma 2 actin (Actg2), plasminogen activator inhibitor 1 (Serpinel), insulin-like growth factor binding protein 3 (Igfbp3), parathyroid hormone-like hormone (Pthlp), Tgfb-1, four and a half LIM domains 2 (Fhl-2), hydrogen peroxide-inducible clone 5 (Hic5) and cartilage oligomeric matrix protein (Comp) |
| 11060295 | In this work, we show that transforming growth factor-beta1 (TGF-beta1) regulates the induction of several of these biomarkers in SIPS: cellular morphology, senescence-associated beta-galactosidase activity, increase in the steady-state level of fibronectin, apolipoprotein J, osteonectin, and SM22 mRNA |
| 11060295 | In the presence of each of these antibodies, the steady-state level of fibronectin, osteonectin, apolipoprotein J, and SM22 mRNA is no more increased at 72 h after stress |
| 9570922 | Construction of cDNA libraries from two conditional cell lines and application of differential screening and subtractive hybridization techniques have resulted in the cloning of eight senescence-induced genes (SGP-2/Apo J, alpha 1-procollagen, osteonectin, fibronectin, SM22, cytochrome C oxidase, GTP-alpha, and a novel gene) and a senescence-repressed gene (FRS-2) |
| 8706785 | Expression of senescence-induced protein WS3-10 in vivo and in vitro |
| 8706785 | In our efforts to characterize cellular senescence we have shown that the mRNA encoding WS3-10 protein is overexpressed in senescent human diploid fibroblasts (HDF) when compared with their younger counterparts, and that forced expression of the WS3-10 cDNA in young HDF results in suppression of calcium-dependent membrane currents, presumably due in part to the presence of a calcium binding domain within the WS3-10 protein |
| 8706785 | Western blot analysis utilizing these antibodies showed that WS3-10 protein is also overexpressed in senescent HDF when compared to young HDF, and in normal fetal lung HDF when compared to SV40-transformed fetal lung HDF |
| 8706785 | HeLa cells do not express WS3-10 protein |
| 8706785 | Analysis of WS3-10 immunologically related proteins in rat tissue extracts revealed two WS3-10 homologs, sized 22 kDa and 20 kDa |
| 8706785 | Two proteins immunologically related to WS3-10 with sizes of 39 kDa and 91 kDa were present in rat spleen and skeletal muscle, respectively |
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