HCSGD entry for TGIF1


1. General information

Official gene symbolTGIF1
Entrez ID7050
Gene full nameTGFB-induced factor homeobox 1
Other gene symbolsHPE4 TGIF
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

color bar
This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000122Negative regulation of transcription from RNA polymerase II promoterIEA TASbiological_process
GO:0001843Neural tube closureIEAbiological_process
GO:0003682Chromatin bindingIEAmolecular_function
GO:0003700Sequence-specific DNA binding transcription factor activityIEAmolecular_function
GO:0003714Transcription corepressor activityTASmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIEAcellular_component
GO:0005654NucleoplasmTAScellular_component
GO:0006351Transcription, DNA-templatedTASbiological_process
GO:0006367Transcription initiation from RNA polymerase II promoterTASbiological_process
GO:0007179Transforming growth factor beta receptor signaling pathwayTASbiological_process
GO:0007275Multicellular organismal developmentTASbiological_process
GO:0007368Determination of left/right symmetryIEAbiological_process
GO:0008285Negative regulation of cell proliferationIEAbiological_process
GO:0009953Dorsal/ventral pattern formationIEAbiological_process
GO:0010467Gene expressionTASbiological_process
GO:0010470Regulation of gastrulationIEAbiological_process
GO:0038092Nodal signaling pathwayIEAbiological_process
GO:0042493Response to drugIEAbiological_process
GO:0043565Sequence-specific DNA bindingIEAmolecular_function
GO:0045666Positive regulation of neuron differentiationIEAbiological_process
GO:0048146Positive regulation of fibroblast proliferationIEAbiological_process
GO:0048387Negative regulation of retinoic acid receptor signaling pathwayIEAbiological_process
GO:0060041Retina development in camera-type eyeIEAbiological_process
GO:0070410Co-SMAD bindingIEAmolecular_function
GO:0071363Cellular response to growth factor stimulusIEAbiological_process
Entries Per Page
Displaying Page of

4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.08227795680.91601981310.60495349161.0000000000

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

Data sourceUp or downLog fold change
GSE11954Up0.2658458697
GSE13712_SHEARUp0.2883452290
GSE13712_STATICDown-0.3168063010
GSE19018Up0.3115175759
GSE19899_A1Up0.0975401611
GSE19899_A2Up0.0394775555
PubMed_21979375_A1Up0.8927602513
PubMed_21979375_A2Up0.5548192946
GSE35957Down-0.3600309498
GSE36640Down-0.2332835692
GSE54402Up0.3172288090
GSE9593Up0.2461503508
GSE43922Up0.3858155149
GSE24585Up0.0436640567
GSE37065Up0.3092975686
GSE28863_A1Down-0.0072194590
GSE28863_A2Down-0.0688139172
GSE28863_A3Up0.0058289854
GSE28863_A4Up0.1069889675
GSE48662Down-0.0449305652

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-21-5pMIMAT0000076MIRT004287Western blotFunctional MTI19906824
Entries Per Page
Displaying Page of
    • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 1 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

22514746Premature senescence and increased TGFbeta signaling in the absence of Tgif1
22514746Here we demonstrate that primary mouse embryo fibroblasts (MEFs) lacking Tgif1 proliferate slowly, accumulate increased levels of DNA damage, and senesce prematurely
22514746We also provide evidence that the effects of loss of Tgif1 on proliferation and senescence are not limited to primary cells
22514746The increased DNA damage in Tgif1 null MEFs can be partially reversed by culturing cells at physiological oxygen levels, and growth in normoxic conditions also partially rescues the proliferation defect, suggesting that in the absence of Tgif1 primary MEFs are less able to cope with elevated levels of oxidative stress
22514746Additionally, we show that Tgif1 null MEFs are more sensitive to TGFbeta-mediated growth inhibition, and that treatment with a TGFbeta receptor kinase inhibitor increases proliferation of Tgif1 null MEFs
22514746We suggest that in the absence of Tgif1, a persistent increase in TGFbeta responsive transcription and a reduced ability to deal with hyperoxic stress result in premature senescence in primary MEFs
Entries Per Page
Displaying Page of