HCSGD entry for TBCE


1. General information

Official gene symbolTBCE
Entrez ID6905
Gene full nametubulin folding cofactor E
Other gene symbolsHRD KCS KCS1 pac2
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:0000226Microtubule cytoskeleton organizationIEAbiological_process
GO:0003735Structural constituent of ribosomeIEAmolecular_function
GO:0005737CytoplasmIEAcellular_component
GO:0005840RibosomeIEAcellular_component
GO:0005874MicrotubuleTAScellular_component
GO:0006412TranslationIEAbiological_process
GO:0006457Protein foldingTASbiological_process
GO:0007023Post-chaperonin tubulin folding pathwayIDAbiological_process
GO:0008344Adult locomotory behaviorIEAbiological_process
GO:0009791Post-embryonic developmentIEAbiological_process
GO:0014889Muscle atrophyIEAbiological_process
GO:0044267Cellular protein metabolic processTASbiological_process
GO:0048589Developmental growthIEAbiological_process
GO:0048936Peripheral nervous system neuron axonogenesisIEAbiological_process
GO:0051084'de novo' posttranslational protein foldingTASbiological_process
GO:0051087Chaperone bindingTASmolecular_function
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.43824373310.18390697540.99999024730.8315322171

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

Data sourceUp or downLog fold change
GSE11954Up0.1600515837
GSE13712_SHEARUp0.6036968769
GSE13712_STATICUp0.6061791327
GSE19018Down-0.1620991997
GSE19899_A1Up0.1213492800
GSE19899_A2Up0.2384307354
PubMed_21979375_A1Up0.0936712210
PubMed_21979375_A2Down-0.4630344727
GSE35957Down-0.5972263176
GSE36640Down-0.3805207866
GSE54402Up0.3034797604
GSE9593Up0.2046202045
GSE43922Up0.0189105302
GSE24585Up0.0423701036
GSE37065Down-0.2322798241
GSE28863_A1Down-0.4279152287
GSE28863_A2Up0.3061035688
GSE28863_A3Down-0.5445550224
GSE28863_A4Down-0.1137245625
GSE48662Down-0.4093581886

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-423-3pMIMAT0001340MIRT042552CLASHFunctional 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: 2 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

15126325Changes in expression of different senescence-associated genes were analyzed in cultured human skin keratinocytes (KCs) that underwent replicative senescence or confluence-induced accelerated senescence
15126325Immunohistochemical analysis of 14 normal human skin samples (age range from 3 months to 84 years) showed that maspin is expressed by KCs in vivo and that the extent and intensity of maspin expression in the skin is significantly (P = 0
15126325Antiangiogenic activity of maspin secreted by senescent KCs was investigated in vitro by testing the effect of conditioned media from different KC cultures on endothelial cell migration in the presence or absence of several angiogenic factors
15126325Media conditioned by senescent cultures (undergoing replicative or accelerated senescence), but not by proliferating KCs, strongly inhibited the stimulation of endothelial cell migration by all of the tested angiogenic factors
15126325These findings indicate that senescent KCs exert a paracrine antiangiogenic activity, and maspin is the principal contributor to this potentially tumor-suppressive effect of cellular senescence
12507899During malignant transformation in skin, epidermal keratinocytes (KCs) frequently acquire the capacity to by-pass cellular senescence, a response that normally limits their unrestricted proliferation
12507899In this study, several molecular pathways are explored using cultured KCs and KCs freshly isolated from psoriatic plaques
12507899Although abnormal mitogenic signaling by oncogenic Ras is generally cited as being responsible for induction of premature senescence, our findings indicate that a broader perspective is warranted, to include confluency and cytokine-/TPA-induced pathways for KCs
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