HCSGD entry for ANG
1. General information
| Official gene symbol | ANG |
|---|---|
| Entrez ID | 283 |
| Gene full name | angiogenin, ribonuclease, RNase A family, 5 |
| Other gene symbols | ALS9 HEL168 RNASE4 RNASE5 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0001525 | Angiogenesis | IDA IMP TAS | biological_process |
| GO:0001541 | Ovarian follicle development | NAS | biological_process |
| GO:0001556 | Oocyte maturation | NAS | biological_process |
| GO:0001666 | Response to hypoxia | IDA NAS | biological_process |
| GO:0001890 | Placenta development | NAS | biological_process |
| GO:0001938 | Positive regulation of endothelial cell proliferation | IDA | biological_process |
| GO:0003677 | DNA binding | IC | molecular_function |
| GO:0003779 | Actin binding | IDA | molecular_function |
| GO:0004519 | Endonuclease activity | TAS | molecular_function |
| GO:0004540 | Ribonuclease activity | IDA | molecular_function |
| GO:0005102 | Receptor binding | IDA | molecular_function |
| GO:0005507 | Copper ion binding | IDA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005605 | Basal lamina | IDA | cellular_component |
| GO:0005615 | Extracellular space | IDA | cellular_component |
| GO:0005634 | Nucleus | IDA | cellular_component |
| GO:0005730 | Nucleolus | ISS | cellular_component |
| GO:0006651 | Diacylglycerol biosynthetic process | IDA | biological_process |
| GO:0007154 | Cell communication | NAS | biological_process |
| GO:0007202 | Activation of phospholipase C activity | IMP | biological_process |
| GO:0008201 | Heparin binding | IDA | molecular_function |
| GO:0008219 | Cell death | IEA | biological_process |
| GO:0009303 | RRNA transcription | IMP | biological_process |
| GO:0009725 | Response to hormone | IDA | biological_process |
| GO:0016477 | Cell migration | IMP | biological_process |
| GO:0016892 | Endoribonuclease activity, producing 3'-phosphomonoesters | IEA | molecular_function |
| GO:0017148 | Negative regulation of translation | IEA | biological_process |
| GO:0019843 | RRNA binding | TAS | molecular_function |
| GO:0030041 | Actin filament polymerization | ISS | biological_process |
| GO:0030426 | Growth cone | ISS | cellular_component |
| GO:0032148 | Activation of protein kinase B activity | IMP | biological_process |
| GO:0032311 | Angiogenin-PRI complex | IPI | cellular_component |
| GO:0032431 | Activation of phospholipase A2 activity | IMP | biological_process |
| GO:0042277 | Peptide binding | IDA | molecular_function |
| GO:0042327 | Positive regulation of phosphorylation | IDA | biological_process |
| GO:0042592 | Homeostatic process | NAS | biological_process |
| GO:0043025 | Neuronal cell body | ISS | cellular_component |
| GO:0048662 | Negative regulation of smooth muscle cell proliferation | IDA | biological_process |
| GO:0050714 | Positive regulation of protein secretion | IDA ISS | biological_process |
| GO:0090305 | Nucleic acid phosphodiester bond hydrolysis | IDA TAS | biological_process |
| GO:0090501 | RNA phosphodiester bond hydrolysis | IDA | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.9227993997 | 0.0274931120 | 0.9999902473 | 0.3156787271 |
- 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 | -0.0663400320 |
| GSE13712_SHEAR | Down | -1.6055466647 |
| GSE13712_STATIC | Down | -0.2709701221 |
| GSE19018 | Up | 0.7412386918 |
| GSE19899_A1 | Down | -0.0819184136 |
| GSE19899_A2 | Down | -0.4315687363 |
| PubMed_21979375_A1 | Up | 0.8367160196 |
| PubMed_21979375_A2 | Down | -0.5632982194 |
| GSE35957 | Down | -1.1821336788 |
| GSE36640 | Down | -0.7882302734 |
| GSE54402 | Down | -0.2591722036 |
| GSE9593 | Down | -0.1364172934 |
| GSE43922 | - | - |
| GSE24585 | - | - |
| GSE37065 | - | - |
| GSE28863_A1 | - | - |
| GSE28863_A2 | - | - |
| GSE28863_A3 | - | - |
| GSE28863_A4 | - | - |
| GSE48662 | Up | 0.0268112525 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-409-3p | MIMAT0001639 | MIRT006649 | Immunofluorescence//Immunohistochemistry//Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 22531314 |
| hsa-miR-335-5p | MIMAT0000765 | MIRT018344 | Microarray | Functional MTI (Weak) | 18185580 |
| hsa-miR-215-5p | MIMAT0000272 | MIRT024617 | Microarray | Functional MTI (Weak) | 19074876 |
| hsa-miR-192-5p | MIMAT0000222 | MIRT026610 | Microarray | Functional MTI (Weak) | 19074876 |
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- mirRecord
No target information from mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 16 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 25952632 | Under these conditions, the anti-senescence genes TERT, bFGF, VEGF, and ANG were increased, whereas the senescence-related genes ATM, p21, and p53 were decreased |
| 25078983 | LY294002 pre-treatment significantly alleviated Ang II-induced HUVEC senescence, and partly reversed the elevation of TERT, UCP2, p-Akt, c-myc and p53 protein levels |
| 25073698 | OBJECTIVE: To observe the time-effect relation of extracts from ginseng, notoginseng and chuanxiong on angiotensin II (Ang II)-induced senescence of vascular endothelial cells and explore the feature of Chinese medicine against vascular diseases |
| 25073698 | CONCLUSION: Extracts from ginseng, notoginseng and chuanxiong can delay Ang II-induced aging of HUVECs and may play an important role in early senescence |
| 24673471 | Beclin-1 was indispensable to Ang II-induced autophagy, and its BH3 domain was required for the interaction with Bcl-2 to attenuate autophagy |
| 23000914 | The present study demonstrates that upregulation of SIRT1 by peroxisome proliferator-activated receptor (PPAR) delta attenuates premature senescence in angiotensin (Ang) II-treated human coronary artery endothelial cells (HCAECs) |
| 23000914 | Activation of PPARdelta by the specific ligand GW501516 significantly inhibited Ang II-induced premature senescence and generation of reactive oxygen species (ROS) in HCAECs |
| 23000914 | Down-regulation or inhibition of SIRT1 by siRNA or sirtinol abrogated the effects of PPARdelta on Ang II-induced premature senescence and ROS generation, respectively |
| 23000914 | Furthermore, resveratrol, a well-known activator of SIRT1, mimicked the action of PPARdelta on Ang II-induced premature senescence and ROS generation |
| 22427991 | We found that Ang II-induced senescence is a zinc-dependent pathway mediated by the downregulation of the zinc transporters ZnT3 and ZnT10, which work to reduce cytosolic zinc |
| 22427991 | Zinc increases Ang II-induced senescence, while the zinc chelator TPEN, as well as overexpression of ZnT3 or ZnT10, decreases ROS and prevents senescence |
| 22427991 | These data demonstrate that zinc homeostasis dysfunction by decreased expression of ZnT3 or ZnT10 promotes senescence and that Ang II-induced senescence is a zinc and ROS-dependent process |
| 22283774 | Activation of the classic RAS, ACE/Ang II/AT1R, has been strictly related to down regulation of pro-survival genes (Nampt and Sirt3), increase in ROS production and pro-inflammatory cytokines and chemokines release, leading to cell senescence, inflammation and development of autoimmune dysfunctions |
| 22217266 | In our study, the induction of angiotensin II (Ang II)-accelerated HMC senescence, as judged by increased senescence-associated beta-galactosidase (SA-beta-gal)-positive staining cells, morphological changes, and G0/G1 cell cycle arrest |
| 22217266 | Our results indicate that STAT1 is implicated in the mediation of Ang II-induced HMC senescence through p53/ p21(Cip1) pathway, and that losartan could attenuate HMC senescence by regulating STAT1 |
| 22072715 | Here, we demonstrate that peroxisome proliferator-activated receptor (PPAR) delta coordinates angiotensin (Ang) II-induced senescence of human vascular smooth muscle cells (VSMCs) |
| 22072715 | Activation of PPARdelta by GW501516, a specific ligand for PPARdelta, significantly attenuated Ang II-induced generation of superoxides and suppressed senescence of VSMCs |
| 21270817 | Angiotensin II (Ang II)-induced astrocyte senescence may be involved in cerebral ischemic injury and age-associated neurodegenerative disease |
| 21270817 | Pretreatment with CV11974 (100 nM) or tempol (3 mM) abolished Ang II-induced astrocyte beta-galactosidase staining |
| 18633188 | We investigated whether a peroxisome proliferator-activated receptor (PPAR) agonist would effect the angiotensin II (Ang II)-induced senescence of endothelial progenitor cells (EPCs) |
| 18633188 | In addition, pioglitazone also inhibited Ang II-induced peroxynitrite formation |
| 18633188 | Ang II-induced EPC senescence was significantly inhibited by co-treatment with pioglitazone |
| 18633188 | In conclusion, pioglitazone inhibited Ang II-induced senescence of EPCs via down-regulation of the expression of AT1R |
| 17991883 | This study tests the hypothesis that DNA is an important target for Ang II-induced ROS leading to senescence via telomere-dependent and independent pathways |
| 17991883 | SIPS was associated with increased p53 expression but was not dependent on telomere attrition because overexpression of human telomerase did not prevent Ang II-induced SIPS |
| 17402563 | This suggests that the paracrine action of Ang 1 in the pericytes is necessary to sustain normal retinal vasculature, and that Ang 1-triggered intracellular signaling is useful for the treatment of vascular cell pathology associated with pericyte loss |
| 16834928 | STAT3 antisense oligonucleotides could inhibit both Ang II-induced STAT3-DNA binding activity as well as TIMP-1 expression |
| 16097371 | We therefore investigated the potential effect of estrogen on Ang II-induced EPC oxidative stress and senescence in EPCs |
| 16097371 | Because we previously demonstrated that both the up-regulation of gp91phox and the acceleration of cellular senescence in Ang II-stimulated EPCs could be abolished by pre-treatment with the AT1R- specific antagonist, valsartan, we also explored the effect of estrogen on AT1R expression |
| 16097371 | In conclusion, estrogen reduces Ang II-induced acceleration of senescence in EPCs partially through down-regulation of AT1R expression |
| 15643130 | Valsartan as well as superoxide dismutase (SOD) also inhibited Ang II-induced peroxynitrite formation |
| 15643130 | Ang II-induced EPC senescence was significantly inhibited by pre-treatment of either valsartan or SOD (P < 0 |
| 15643130 | We examined whether Ang II-induced EPC senescence translates into an impairment of EPC proliferation |
| 15643130 | In addition, Ang II-induced EPC senescence leads to the impairment of proliferative activity |
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