HCSGD entry for NELFCD


1. General information

Official gene symbolNELFCD
Entrez ID51497
Gene full namenegative elongation factor complex member C/D
Other gene symbolsNELF-C NELF-D TH1 TH1L
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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This gene isn't in Literature mining network.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0005515Protein bindingIPImolecular_function
GO:0005654NucleoplasmTAScellular_component
GO:0006366Transcription from RNA polymerase II promoterTASbiological_process
GO:0006368Transcription elongation from RNA polymerase II promoterTASbiological_process
GO:0010467Gene expressionTASbiological_process
GO:0016032Viral processTASbiological_process
GO:0032021NELF complexIDAcellular_component
GO:0045892Negative regulation of transcription, DNA-templatedIEAbiological_process
GO:0050434Positive regulation of viral transcriptionTASbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.90594834920.05951533380.99999024730.4595198299

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

Data sourceUp or downLog fold change
GSE11954Up0.0245580173
GSE13712_SHEARDown-0.2054136761
GSE13712_STATICDown-0.0578984044
GSE19018Down-0.2241767061
GSE19899_A1Down-0.3068140595
GSE19899_A2Up0.3645397072
PubMed_21979375_A1Up0.4571476765
PubMed_21979375_A2Up0.5795892871
GSE35957Down-0.6360759835
GSE36640Down-1.2787801439
GSE54402Up0.3758023089
GSE9593Down-0.2463386293
GSE43922Down-0.0373174011
GSE24585Down-0.3103415664
GSE37065Down-0.2885893791
GSE28863_A1Down-0.0402043900
GSE28863_A2Down-0.3184221950
GSE28863_A3Down-0.3171922260
GSE28863_A4Up0.0318968343
GSE48662Down-0.2088929014

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-1MIMAT0000416MIRT002804MicroarrayFunctional MTI (Weak)15685193
hsa-miR-1MIMAT0000416MIRT002804pSILAC//ProteomicsFunctional MTI (Weak)18668040
hsa-miR-1MIMAT0000416MIRT002804Proteomics;MicroarrayNon-Functional MTI (Weak)18668037
hsa-miR-375MIMAT0000728MIRT020019MicroarrayFunctional MTI (Weak)20215506
hsa-miR-34a-5pMIMAT0000255MIRT025484ProteomicsFunctional MTI (Weak)21566225
hsa-miR-98-5pMIMAT0000096MIRT027792MicroarrayFunctional MTI (Weak)19088304
hsa-miR-26b-5pMIMAT0000083MIRT030245MicroarrayFunctional MTI (Weak)19088304
hsa-miR-877-3pMIMAT0004950MIRT037145CLASHFunctional MTI (Weak)23622248
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  • mirRecord

MicroRNA name

mirBase ID

Target site number

MiRNA mature ID

Test method inter

MiRNA regulation site

Reporter target site

Pubmed ID

hsa-miR-1MIMAT0000416NAhsa-miR-115685193
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6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 5 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

24925089JMJD3 also interacts with T-bet factor and induces Th1 differentiation of CD4(+) T cells
22080947In accordance with these observations, ras-specific Th1 lymphocytes could be detected in mice, in which oncogene-induced senescence had been triggered by hepatic expression of Nras(G12V)
19458122The inflammatory response was found to be significantly decreased in bortezomib-treated mice as reflected by a decreased infiltration of CD4(+) T cells and a significantly decreased Th1 cytokine expression in the kidneys
16821141In inflamed portal tracts of PBC, CD4+ T cells of Th1 type expressing IFN-gamma or CXCR3 are aggregated and more commonly detected around injured bile ducts than Th2-type CD4+ T cells expressing IL-4 or CCR4, indicating that Th1-dominant cellular immunity plays a more-prominent role in recruitment of memory T-cell subsets in PBC and may be responsible for the progressive bile duct damage
11830522Germ-line p53-targeted disruption inhibits helicobacter-induced premalignant lesions and invasive gastric carcinoma through down-regulation of Th1 proinflammatory responses
11830522In sera from WT mice, IgG2a, considered a proinflammatory Th1 response, continued to rise throughout the 15-month study (P < 0
11830522Our results support the hypothesis that germ-line deletion of one p53 allele results in a down-regulated Th1 response to gastric helicobacter infection, possibly because of T-cell senescence, which may indirectly protect against the development of gastric cancer and other epithelial-derived neoplasms associated with chronic inflammation
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