HCSGD entry for SOAT1
1. General information
| Official gene symbol | SOAT1 |
|---|---|
| Entrez ID | 6646 |
| Gene full name | sterol O-acyltransferase 1 |
| Other gene symbols | ACACT ACAT ACAT-1 ACAT1 SOAT STAT |
| 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:0000062 | Fatty-acyl-CoA binding | IDA | molecular_function |
| GO:0004772 | Sterol O-acyltransferase activity | IDA IEA IMP | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005783 | Endoplasmic reticulum | IDA | cellular_component |
| GO:0005789 | Endoplasmic reticulum membrane | IDA | cellular_component |
| GO:0008203 | Cholesterol metabolic process | IDA IEA IMP | biological_process |
| GO:0010742 | Macrophage derived foam cell differentiation | IC IMP NAS | biological_process |
| GO:0010878 | Cholesterol storage | IMP | biological_process |
| GO:0015485 | Cholesterol binding | IDA | molecular_function |
| GO:0016020 | Membrane | IDA | cellular_component |
| GO:0016021 | Integral component of membrane | IEA | cellular_component |
| GO:0033344 | Cholesterol efflux | IMP | biological_process |
| GO:0034379 | Very-low-density lipoprotein particle assembly | IMP | biological_process |
| GO:0034435 | Cholesterol esterification | IDA IMP | biological_process |
| GO:0034736 | Cholesterol O-acyltransferase activity | IDA IMP | molecular_function |
| GO:0042632 | Cholesterol homeostasis | TAS | biological_process |
| GO:0042986 | Positive regulation of amyloid precursor protein biosynthetic process | 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 |
|---|---|---|---|
| 0.2799525702 | 0.0290025227 | 0.9768834151 | 0.3229748521 |
- 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 | Up | 0.0143079748 |
| GSE13712_SHEAR | Up | 0.1690679682 |
| GSE13712_STATIC | Up | 0.5515467054 |
| GSE19018 | Down | -0.6980931263 |
| GSE19899_A1 | Down | -0.8481344516 |
| GSE19899_A2 | Down | -0.3876535098 |
| PubMed_21979375_A1 | Down | -0.4732490579 |
| PubMed_21979375_A2 | Down | -0.6068353528 |
| GSE35957 | Up | 0.1121854398 |
| GSE36640 | Down | -0.2019882809 |
| GSE54402 | Down | -0.8768781301 |
| GSE9593 | Up | 0.5082883352 |
| GSE43922 | Down | -0.2613621077 |
| GSE24585 | Up | 0.2111407528 |
| GSE37065 | Up | 0.0264639485 |
| GSE28863_A1 | Up | 0.7914539044 |
| GSE28863_A2 | Up | 1.4218542058 |
| GSE28863_A3 | Down | -0.4580981471 |
| GSE28863_A4 | Down | -0.0189748666 |
| GSE48662 | Down | -0.6701021466 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
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- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-193b-3p | MIMAT0002819 | MIRT016592 | Microarray | Functional MTI (Weak) | 20304954 |
| hsa-miR-215-5p | MIMAT0000272 | MIRT024321 | Microarray | Functional MTI (Weak) | 19074876 |
| hsa-miR-192-5p | MIMAT0000222 | MIRT026807 | Microarray | Functional MTI (Weak) | 19074876 |
| hsa-miR-98-5p | MIMAT0000096 | MIRT027734 | Microarray | Functional MTI (Weak) | 19088304 |
| hsa-miR-1303 | MIMAT0005891 | MIRT035871 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-500a-3p | MIMAT0002871 | MIRT041152 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-186-5p | MIMAT0000456 | MIRT045139 | 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: 10 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 28123872 | Thus, our study elucidates a new mechanism for IL-15 in the regulation of STAT signaling pathways and CD8+ T-cell senescence |
| 27241018 | Perspective: Targeting the JAK/STAT pathway to fight age-related dysfunction |
| 25982278 | The expression of Nox4/Nox1 required Janus kinase (JAK)/signal transducers and activators of transcription (STAT) signaling and the effect was mediated by downstream activation of transforming growth factor-beta (TGFbeta) secretion and consequent autocrine/paracrine activation of the TGFbeta/Smad pathway |
| 24416650 | The roles of other STAT members in premature senescence also will be discussed to show the multiple mechanisms leading to cytokine-induced senescence |
| 26201620 | Examples include the HLA class-II region and genes implicated in IL12-JAK/STAT signaling, and the NF-kappaB and TNF signaling pathways |
| 23385065 | Persistent cytokine signaling and activated DDR evoke senescence in normal bystander cells, accompanied by activation of the JAK/STAT, TGFbeta/SMAD and IL1/NFkappaB signaling pathways |
| 21472252 | To date, little is known regarding the relationship between AngII or STAT protein and aging human GMCs |
| 19802007 | Here, we show that genotoxic drugs capable of inducing premature senescence in normal and cancer cells, such as 5-bromo-2'-deoxyuridine (BrdU), distamycin A (DMA), aphidicolin and hydroxyurea, persistently activate Janus kinase-signal transducer and activator of transcription (JAK/STAT) signaling and expression of interferon-stimulated genes (ISGs), such as MX1, OAS, ISG15, STAT1, PML, IRF1 and IRF7, in several human cancer cell lines |
| 19802007 | JAK1/STAT-activating ligands, interleukin 10 (IL10), IL20, IL24, interferon gamma (IFNgamma), IFNbeta and IL6, were also expressed by senescent cells, supporting autocrine/paracrine activation of JAK1/STAT |
| 19802007 | The strongest inducer of JAK/STAT signaling, cytokine production and senescence was BrdU combined with DMA |
| 19802007 | Thus, although DNA damage signaling, p53 and RB activation, and the cytokine/chemokine secretory phenotype are apparently shared by all types of senescence, our data reveal so far unprecedented activation of the IFNbeta-STAT1-ISGs axis, and indicate a less prominent causative role of IL6-JAK/STAT signaling in genotoxic drug-induced senescence compared with reports on oncogene-induced or replicative senescence |
| 23598653 | Genetic and transgenic analyses have identified several conserved signaling pathways that function in the ovary to regulate stem cell maintenance, division and differentiation, including the wingless, hedgehog, JAK/STAT, insulin and TGF-beta pathways |
| 14563561 | Analysis of hPNPase(old-35) expression in cell lines defective in various IFN signaling molecules confirms that hPNPase(old-35) expression is dependent upon the Janus activated kinase (JAK)/signal transducers and activators of transcription (STAT) pathway |
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