HCSGD entry for CDIPT

1. General information

Official gene symbolCDIPT
Entrez ID10423
Gene full nameCDP-diacylglycerol--inositol 3-phosphatidyltransferase
Other gene symbolsPIS PIS1
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000139Golgi membraneIEAcellular_component
GO:0003881CDP-diacylglycerol-inositol 3-phosphatidyltransferase activityIDA TASmolecular_function
GO:0005789Endoplasmic reticulum membraneTAScellular_component
GO:0005886Plasma membraneIEAcellular_component
GO:0006644Phospholipid metabolic processTASbiological_process
GO:0006661Phosphatidylinositol biosynthetic processIDA TASbiological_process
GO:0008654Phospholipid biosynthetic processIEAbiological_process
GO:0016020MembraneIEAcellular_component
GO:0016021Integral component of membraneIDAcellular_component
GO:0016740Transferase activityIEAmolecular_function
GO:0016780Phosphotransferase activity, for other substituted phosphate groupsIEAmolecular_function
GO:0019992Diacylglycerol bindingIEAmolecular_function
GO:0030145Manganese ion bindingIEAmolecular_function
GO:0030246Carbohydrate bindingIEAmolecular_function
GO:0043178Alcohol bindingIEAmolecular_function
GO:0044281Small molecule metabolic processTASbiological_process
GO:0046341CDP-diacylglycerol metabolic processIEAbiological_process
GO:0046474Glycerophospholipid biosynthetic processTASbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.16413169330.82518512210.80150469391.0000000000

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Up0.2169330005
GSE13712_SHEARDown-0.2200902204
GSE13712_STATICDown-0.1592627346
GSE19018Up0.3223107380
GSE19899_A1Down-0.0293479065
GSE19899_A2Up0.3954901804
PubMed_21979375_A1Down-0.0118953565
PubMed_21979375_A2Up0.2404007282
GSE35957Up0.1882218388
GSE36640Up0.7646313760
GSE54402Down-0.1377239946
GSE9593Up0.2921100613
GSE43922Up0.1037373213
GSE24585Down-0.3446622673
GSE37065Down-0.1396219772
GSE28863_A1Up0.0183951082
GSE28863_A2Up0.1686148529
GSE28863_A3Down-0.3735601567
GSE28863_A4Up0.0582980403
GSE48662Up0.6353176669

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Name

Drug

Accession number

Myo-InositolDB03106 EXPT01892

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-let-7b-5pMIMAT0000063MIRT001644pSILAC//Proteomics;OtherFunctional MTI (Weak)18668040
hsa-miR-26b-5pMIMAT0000083MIRT029083MicroarrayFunctional MTI (Weak)19088304
hsa-miR-16-5pMIMAT0000069MIRT031548ProteomicsFunctional MTI (Weak)18668040
hsa-miR-1229-3pMIMAT0005584MIRT036339CLASHFunctional MTI (Weak)23622248
hsa-miR-331-3pMIMAT0000760MIRT043315CLASHFunctional MTI (Weak)23622248
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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: 4 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

26724531BACKGROUND: 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
26724531RESULTS: 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
24336070Survival 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)
24336070Because NRTIs and PIs together prevent or attenuate HIV-1 replication, and prolong life, the population of aging patients with HIV/AIDS increases accordingly
24336070PIs may also have a role in premature aging in HIV/AIDS as they cause prelamin A accumulation
23795945HIV protease inhibitors (PIs) have been suspected to participate to bone loss, but the mechanisms involved are unknown
23795945In endothelial cells, some PIs have been shown to induce the accumulation of farnesylated prelamin-A, a biomarker of cell aging leading to cell senescence
23795945Herein, 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
23795945We 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
17612587As 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
17612587As 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
17612587Adipose 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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