HCSGD entry for PDLIM7


1. General information

Official gene symbolPDLIM7
Entrez ID9260
Gene full namePDZ and LIM domain 7 (enigma)
Other gene symbolsLMP1 LMP3
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:0001503OssificationIEAbiological_process
GO:0001725Stress fiberIEAcellular_component
GO:0001726RuffleIEAcellular_component
GO:0005515Protein bindingIPImolecular_function
GO:0005737CytoplasmIEAcellular_component
GO:0005925Focal adhesionIDAcellular_component
GO:0006898Receptor-mediated endocytosisTASbiological_process
GO:0007275Multicellular organismal developmentIEAbiological_process
GO:0008270Zinc ion bindingIEAmolecular_function
GO:0015629Actin cytoskeletonIDAcellular_component
GO:0030036Actin cytoskeleton organizationIEAbiological_process
GO:0030054Cell junctionIDAcellular_component
GO:0030154Cell differentiationIEAbiological_process
GO:0045669Positive regulation of osteoblast differentiationIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.96200927020.01449645530.99999024730.2367004963

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

Data sourceUp or downLog fold change
GSE11954Down-0.8932201220
GSE13712_SHEARUp0.3090568228
GSE13712_STATICUp0.2130215052
GSE19018Down-0.5502656549
GSE19899_A1Down-0.5929026866
GSE19899_A2Down-0.2954225672
PubMed_21979375_A1Up0.1250713394
PubMed_21979375_A2Down-0.0896287024
GSE35957Down-0.2819720318
GSE36640Down-0.0199793091
GSE54402Down-0.0376163122
GSE9593Down-0.4002248213
GSE43922Down-0.2575359714
GSE24585Up0.0654642692
GSE37065Down-0.2412873676
GSE28863_A1Down-0.2677689585
GSE28863_A2Down-0.3453111052
GSE28863_A3Down-0.0505524909
GSE28863_A4Down-0.1278930438
GSE48662Down-0.0843174344

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-1MIMAT0000416MIRT001351pSILAC//ProteomicsFunctional MTI (Weak)18668040
hsa-miR-1MIMAT0000416MIRT001351Proteomics;MicroarrayFunctional MTI (Weak)18668037
hsa-miR-124-3pMIMAT0000422MIRT002914Proteomics;MicroarrayFunctional MTI (Weak)18668037
hsa-miR-30a-5pMIMAT0000087MIRT028432ProteomicsFunctional MTI (Weak)18668040
hsa-miR-24-3pMIMAT0000080MIRT030427MicroarrayFunctional MTI (Weak)19748357
hsa-miR-132-3pMIMAT0000426MIRT045848CLASHFunctional 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: 3 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

26498461Epstein-Barr virus (EBV) latent membrane protein-1 (LMP-1) and ligand-independent signaling by overexpressed CD30 are known to cause permanent activation of NF-kappaB in lymphomas
26498461Expression of LMP-1 and CD30 increased IkappaB-zeta expression at the transcriptional level
26498461Interestingly, IkappaB-zeta inhibited NF-kappaB activation by LMP-1 and CD30
15064751Epstein-Barr virus latent membrane protein 1 (LMP1) upregulates Id1 expression in nasopharyngeal epithelial cells
15064751Many of the downstream events of LMP1 expression are mediated through its ability to activate NF-kappaB
15064751In this study, we report a novel function of LMP1 to induce Id1 expression in nasopharyngeal epithelial cells (NP69) and human embryonal kidney cells (HEK293)
15064751With the combination of both specific chemical inhibitors and genetic inhibitors of cell signaling, we showed that induction of Id1 by LMP1 was dependent on its NF-kappaB activation domain at the carboxy-terminal region, CTAR1 and CTAR2
15064751Induction of Id1 by LMP1 may facilitate clonal expansion of premalignant nasopharyngeal epithelial cells infected with EBV and may promote their malignant transformation
10803461LMP1 of Epstein-Barr virus suppresses cellular senescence associated with the inhibition of p16INK4a expression
10803461Studies indicate that latent membrane protein LMP1 is one of the viral proteins essential for this process
10803461In this report, LMP1 was shown to prevent primary mouse embryonic fibroblasts from entering into replicative senescence in vitro
10803461In addition, LMP1 was shown to prevent premature senescence provoked by oncogenic ras in mouse embryonic fibroblasts, and to inhibit the oncogene ras-mediated induction of p16INK4a and p21WAF1
10803461In parallel, LMP1 also prevents ras-induced premature senescence in rat embryonic fibroblasts REF52 and human diploid fibroblasts IMR90
10803461Moreover, LMP1 is capable of suppressing the p16INK4a promoter in REF52 and Saos-2 cells in a promoter reporter assay
10803461Our findings suggest that with the expression of p16INK4a and replicative senescence being suppressed, LMP1 may play a key role in Epstein-Barr virus-associated proliferative diseases, and it may further contribute to cancer development by preventing premature senescence induced by mitogenic oncogenes
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