3.4.22.B73: SENP5 peptidase
This is an abbreviated version!
For detailed information about SENP5 peptidase, go to the full flat file.
Word Map on EC 3.4.22.B73
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3.4.22.B73
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senps
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desumoylation
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deconjugation
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isopeptidase
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mitosis
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fission
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nucleolus
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regulator-related
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medicine
- 3.4.22.B73
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senps
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desumoylation
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deconjugation
- isopeptidase
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mitosis
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fission
- nucleolus
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regulator-related
- medicine
Reaction
SENP5 additional information efficiently removes SUMO-2 and SUMO-3 than SUMO-1 from SUMO-modified target such as Ran GTPase-activating protein 1. Catalyzes desumoylation of mitochondrial fission GTPase DRP1. =
Synonyms
SENP5, SENP5 peptidase, sentrin/small ubiquitin-like modifier-specific protease5, SUMO isopeptidase, SUMO-specific protease 5
ECTree
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General Information on EC 3.4.22.B73 - SENP5 peptidase
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GENERAL INFORMATION 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
malfunction
metabolism
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SUMO conjugation is a dynamic posttranslational modification that can be readily reversed by the activity of sentrin-specific proteases (SENPs). Elevated expression of SENP5 in the failing human hearts, development of cardiomyopathy, overview
physiological function
malfunction
knockdown of SENP5 leads to an increase in cells with more than one nucleus or aberrant nuclear structure consistent with defects in mitosis and cytokinesis
malfunction
silencing of SENP5 results in a fragmented and altered morphology
malfunction
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H2O2 alone enhances mitochondrial network formation, whereas the combination of H2O2 and enzyme SENP5 silencing leads to mitochondrial fragmentation in the CAL-27 cells
malfunction
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SENP5 enzyme overexpression leads to cardiac dysfunction, accompanied by decreased cardiomyocyte proliferation and elevated apoptosis, overview. Transgenic SENP5-hearts, that are larger than wild-type, unveil a decrease in SUMO attachment to dynamin related protein (Drp1), a factor critical for mitochondrial fission, phenotype, overview
physiological function
SENP5 is a regulator of SUMO1 proteolysis from mitochondrial targets. SENP5 is required to maintain normal mitochondrial morphology and to control intracellular levels of reactive oxygen species. SENP5 expression affects the mitochondrial morphology by increasing the number of cells with elongated tubules
physiological function
SENP5 is required for cell division. SENP5 has nonredundant functions in vivo, likely due to distinct substrate specificities in SUMO maturation and deconjugation that are regulated by both the catalytic and noncatalytic domains of the enzyme
physiological function
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enzyme SENP5 protects the oral squamous cell carcinoma cells from oxidative stress-induced apoptosis. Cell with higher enzyme content show a higher resistance to H2O2, overview
physiological function
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SUMO isopeptidase SENP5 induces apoptosis and cardiomyopathy, which represents a major health issue and is a leading cause of heart failure. Significant increase in the level of enzyme SEN,P5 in human idiopathic failing hearts
physiological function
Senp5 is overexpressed in hepatocellular carcinoma samples and required for hepatocellular carcinoma cells proliferation both in vitro and in vivo. SENP5-depleted Hep-G2 cells exhibit hypersensitivity to IR and etoposide treatment with defective checkpoint activation including decreased activation of ATM and Rad3-related kinases ATR and phosphorylation of ATR targets. Senp5 interacts with ATR regulator ATRIP and promotes ATRIP deSUMOylation
physiological function
Senp5 is significantly repressed in clinical acute myeloid leukemia when compared to healthy neutrophil samples. SENP5 expression is induced during neutrophil differentiation of acute myeloid leukemia cells, and knocking down SENP5 results in significantly attenuated neutrophil differentiation
