HCSGD entry for CDIPT
1. General information
| Official gene symbol | CDIPT |
|---|---|
| Entrez ID | 10423 |
| Gene full name | CDP-diacylglycerol--inositol 3-phosphatidyltransferase |
| Other gene symbols | PIS PIS1 |
| 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:0000139 | Golgi membrane | IEA | cellular_component |
| GO:0003881 | CDP-diacylglycerol-inositol 3-phosphatidyltransferase activity | IDA TAS | molecular_function |
| GO:0005789 | Endoplasmic reticulum membrane | TAS | cellular_component |
| GO:0005886 | Plasma membrane | IEA | cellular_component |
| GO:0006644 | Phospholipid metabolic process | TAS | biological_process |
| GO:0006661 | Phosphatidylinositol biosynthetic process | IDA TAS | biological_process |
| GO:0008654 | Phospholipid biosynthetic process | IEA | biological_process |
| GO:0016020 | Membrane | IEA | cellular_component |
| GO:0016021 | Integral component of membrane | IDA | cellular_component |
| GO:0016740 | Transferase activity | IEA | molecular_function |
| GO:0016780 | Phosphotransferase activity, for other substituted phosphate groups | IEA | molecular_function |
| GO:0019992 | Diacylglycerol binding | IEA | molecular_function |
| GO:0030145 | Manganese ion binding | IEA | molecular_function |
| GO:0030246 | Carbohydrate binding | IEA | molecular_function |
| GO:0043178 | Alcohol binding | IEA | molecular_function |
| GO:0044281 | Small molecule metabolic process | TAS | biological_process |
| GO:0046341 | CDP-diacylglycerol metabolic process | IEA | biological_process |
| GO:0046474 | Glycerophospholipid biosynthetic process | 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 |
|---|---|---|---|
| 0.1641316933 | 0.8251851221 | 0.8015046939 | 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 | Up | 0.2169330005 |
| GSE13712_SHEAR | Down | -0.2200902204 |
| GSE13712_STATIC | Down | -0.1592627346 |
| GSE19018 | Up | 0.3223107380 |
| GSE19899_A1 | Down | -0.0293479065 |
| GSE19899_A2 | Up | 0.3954901804 |
| PubMed_21979375_A1 | Down | -0.0118953565 |
| PubMed_21979375_A2 | Up | 0.2404007282 |
| GSE35957 | Up | 0.1882218388 |
| GSE36640 | Up | 0.7646313760 |
| GSE54402 | Down | -0.1377239946 |
| GSE9593 | Up | 0.2921100613 |
| GSE43922 | Up | 0.1037373213 |
| GSE24585 | Down | -0.3446622673 |
| GSE37065 | Down | -0.1396219772 |
| GSE28863_A1 | Up | 0.0183951082 |
| GSE28863_A2 | Up | 0.1686148529 |
| GSE28863_A3 | Down | -0.3735601567 |
| GSE28863_A4 | Up | 0.0582980403 |
| GSE48662 | Up | 0.6353176669 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Name | Drug | Accession number |
|---|---|---|
| Myo-Inositol | DB03106 | EXPT01892 |
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-let-7b-5p | MIMAT0000063 | MIRT001644 | pSILAC//Proteomics;Other | Functional MTI (Weak) | 18668040 |
| hsa-miR-26b-5p | MIMAT0000083 | MIRT029083 | Microarray | Functional MTI (Weak) | 19088304 |
| hsa-miR-16-5p | MIMAT0000069 | MIRT031548 | Proteomics | Functional MTI (Weak) | 18668040 |
| hsa-miR-1229-3p | MIMAT0005584 | MIRT036339 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-331-3p | MIMAT0000760 | MIRT043315 | 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: 4 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 26724531 | BACKGROUND: Some LMNA mutations responsible for lipodystrophies, and some HIV-protease inhibitors (PIs) induce accumulation of farnesylated prelamin A and premature senescence in some cell types |
| 26724531 | RESULTS: Fibroblasts from LMNA-mutated lipodystrophic patients (mutations R482W, D47Y or R133L) and peripheral blood mononuclear cells from PI-treated-HIV-infected patients expressed increased prelamin A and decreased ZMPSTE24, which was also observed in VSMCs overexpressing mutant LMNA or treated with PIs |
| 24336070 | Survival with HIV/AIDS has markedly improved by therapy combinations containing nucleoside reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse transcriptase inhibitors, and protease inhibitors (PIs) called HAART (highly active antiretroviral therapy) |
| 24336070 | Because NRTIs and PIs together prevent or attenuate HIV-1 replication, and prolong life, the population of aging patients with HIV/AIDS increases accordingly |
| 24336070 | PIs may also have a role in premature aging in HIV/AIDS as they cause prelamin A accumulation |
| 23795945 | HIV protease inhibitors (PIs) have been suspected to participate to bone loss, but the mechanisms involved are unknown |
| 23795945 | In endothelial cells, some PIs have been shown to induce the accumulation of farnesylated prelamin-A, a biomarker of cell aging leading to cell senescence |
| 23795945 | Herein, we hypothesized that these PIs could induce premature aging of osteoblast precursors, human bone marrow mesenchymal stem cells (MSCs), and affect their capacity to differentiate into osteoblasts |
| 23795945 | We have shown that some PIs alter osteoblast formation by affecting their differentiation potential in association with altered senescence in MSCs, with a beneficial effect of statin |
| 17612587 | As genetically altered lamin A maturation also results in premature ageing syndromes with lipodystrophy, we studied prelamin A expression and senescence markers in cultured human fibroblasts bearing six different LMNA mutations or treated with PIs |
| 17612587 | As compared to control cells, fibroblasts with LMNA mutations or treated with PIs had nuclear shape abnormalities and reduced proliferative activity that worsened with increasing cellular passages |
| 17612587 | Adipose tissue samples from patients with LMNA mutations or treated with PIs also showed retention of prelamin A, overexpression of the cell cycle checkpoint inhibitor p16 and altered mitochondrial markers |
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