HCSGD entry for TRIM32

1. General information

Official gene symbolTRIM32
Entrez ID22954
Gene full nametripartite motif containing 32
Other gene symbolsBBS11 HT2A LGMD2H TATIP
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:0000209Protein polyubiquitinationIDAbiological_process
GO:0003713Transcription coactivator activityTASmolecular_function
GO:0003723RNA bindingIEA ISSmolecular_function
GO:0004842Ubiquitin-protein ligase activityIDA IEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIEA ISScellular_component
GO:0005737CytoplasmIDAcellular_component
GO:0005829CytosolTAScellular_component
GO:0005863Striated muscle myosin thick filamentIEA ISScellular_component
GO:0008270Zinc ion bindingIEAmolecular_function
GO:0009411Response to UVIEA ISSbiological_process
GO:0016567Protein ubiquitinationIDAbiological_process
GO:0017022Myosin bindingIEA ISSmolecular_function
GO:0030307Positive regulation of cell growthIDAbiological_process
GO:0030335Positive regulation of cell migrationIDAbiological_process
GO:0030957Tat protein bindingTASmolecular_function
GO:0031369Translation initiation factor bindingIEA ISSmolecular_function
GO:0032479Regulation of type I interferon productionTASbiological_process
GO:0032481Positive regulation of type I interferon productionTASbiological_process
GO:0034612Response to tumor necrosis factorIEA ISSbiological_process
GO:0042787Protein ubiquitination involved in ubiquitin-dependent protein catabolic processIMPbiological_process
GO:0043130Ubiquitin bindingIDAmolecular_function
GO:0043621Protein self-associationIDAmolecular_function
GO:0045087Innate immune responseTASbiological_process
GO:0045444Fat cell differentiationIEA ISSbiological_process
GO:0045666Positive regulation of neuron differentiationIEA ISSbiological_process
GO:0045732Positive regulation of protein catabolic processIEA ISSbiological_process
GO:0045787Positive regulation of cell cycleIDAbiological_process
GO:0045862Positive regulation of proteolysisIDAbiological_process
GO:0048147Negative regulation of fibroblast proliferationIEA ISSbiological_process
GO:0050769Positive regulation of neurogenesisIEA ISSbiological_process
GO:0051092Positive regulation of NF-kappaB transcription factor activityIEA ISSbiological_process
GO:1902230Negative regulation of intrinsic apoptotic signaling pathway in response to DNA damageIDAbiological_process
GO:2000147Positive regulation of cell motilityIEA ISSbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.02443079670.84320001140.36977614941.0000000000

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

Data sourceUp or downLog fold change
GSE11954Up0.1240676352
GSE13712_SHEARUp0.1636868412
GSE13712_STATICUp0.3049019711
GSE19018Down-0.4268622188
GSE19899_A1Up0.3308712881
GSE19899_A2Up1.1881307438
PubMed_21979375_A1Up1.3344160583
PubMed_21979375_A2Up2.0632220167
GSE35957Up0.1823804402
GSE36640Up0.2971548204
GSE54402Up0.0773199038
GSE9593Up0.0102667494
GSE43922Up0.3838412927
GSE24585Down-0.0759409233
GSE37065Up0.1056811177
GSE28863_A1Up0.4104311124
GSE28863_A2Down-0.0436413000
GSE28863_A3Down-0.6488003911
GSE28863_A4Up0.0182752729
GSE48662Down-0.1855292455

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-155-5pMIMAT0000646MIRT001492pSILAC//Proteomics;OtherFunctional MTI (Weak)18668040
hsa-miR-16-5pMIMAT0000069MIRT031385ProteomicsFunctional MTI (Weak)18668040
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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

25701873Previously, we generated and characterized a Trim32 knockout mouse (T32KO) that displays both neurogenic and myopathic features
25701873This satellite cell senescence is due to accumulation of the SUMO ligase PIASy, a substrate of TRIM32
25701873The goal of this investigation was to identify additional substrates of TRIM32 using 2D fluorescence difference gel electrophoresis (2D-DIGE) in order to further explore its role in skeletal muscle
25701873Follow-up analysis confirmed that both proteins were ubiquitinated by TRIM32 in vitro; however, only NDRG2 accumulated in skeletal muscle and myoblasts in the absence of TRIM32
25701873Thus, we identified NDRG2 as a novel target for TRIM32; these findings further corroborate the hypothesis that TRIM32 is involved in control of myogenic cells proliferation and differentiation
22505452Previously, we generated Trim32 knockout mice (Trim32-/- mice) and showed that they display a myopathic phenotype accompanied by neurogenic features
22505452Here, we used these mice to investigate the muscle-specific defects arising from the absence of TRIM32, which underlie the myopathic phenotype
22505452Using 2 models of induced atrophy, we showed that TRIM32 is dispensable for muscle atrophy
22505452Conversely, TRIM32 was necessary for muscle regrowth after atrophy
22505452Furthermore, TRIM32-deficient primary myoblasts underwent premature senescence and impaired myogenesis due to accumulation of PIAS4, an E3 SUMO ligase and TRIM32 substrate that was previously shown to be associated with senescence
22505452Trim32-/- muscles had substantially fewer activated satellite cells, increased PIAS4 levels, and growth failure compared with wild-type muscles
22505452Moreover, Trim32-/- muscles exhibited features of premature sarcopenia, such as selective type II fast fiber atrophy
22505452These results imply that premature senescence of muscle satellite cells is an underlying pathogenic feature of LGMD2H and reveal what we believe to be a new mechanism of muscular dystrophy associated with reductions in available satellite cells and premature sarcopenia
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