3.4.22.B26: calpain 6
This is an abbreviated version!
For detailed information about calpain 6, go to the full flat file.
Word Map on EC 3.4.22.B26
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3.4.22.B26
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non-proteolytic
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medicine
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myometrium
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leiomyomas
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nonlysosomal
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pinocytotic
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calpastatin
- 3.4.22.B26
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non-proteolytic
- medicine
-
myometrium
- leiomyomas
-
nonlysosomal
-
pinocytotic
- calpastatin
Reaction
A microtubule-stabilizing protein. The enzyme lacks the active-site catalytic cysteine residue and proteolytic activity has not been detected. =
Synonyms
calpain 6, calpain-6, CAPN6
ECTree
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Results | in table |
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2 | AA Sequence |
4 | Application |
141 | Disease/ Diagnostics |
4 | Expression |
9 | General Information |
2 | Inhibitors |
6 | Organism |
1 | Reaction |
6 | Reference |
18 | Source Tissue |
4 | Synonyms |
Application
Application on EC 3.4.22.B26 - calpain 6
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medicine
medicine
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calpain-6 is a possible therapeutic target in chemoresistant osteosarcoma
medicine
calpain-6 expression is associated with cancer stem cell features. Calpain-6 levels are especially high in tumors that have been successfully propagated in mouse to establish patient-derived xenografts. Calpain-6 levels are increased by hypoxia in vitro and calpain-6 is detected within hypoxic areas in tumors. Calpain-6 expression depends on the stem cell transcription network that involves Oct4, Nanog, and Sox2 and is activated by hypoxia. Calpain-6 expression in sarcomas inversely correlates with senescence markers. Calpain-6 knockdown suppresses hypoxia-dependent prevention of senescence entry and also promotion of autophagic flux
medicine
calpain-6 expression is associated with cancer stem cell features. In mouse models of bone sarcoma, calpain-6-expressing cells have unique tumor-initiating and metastatic capacities. Calpain-6 levels are especially high in tumors that have been successfully propagated in mouse to establish patient-derived xenografts. Calpain-6 levels are increased by hypoxia in vitro and calpain-6 is detected within hypoxic areas in tumors. Calpain-6 knockdown blocks tumor development in mouse and induces depletion of the cancer stem cell population. Calpain-6 expression depends on the stem cell transcription network that involves Oct4, Nanog, and Sox2 and is activated by hypoxia. Calpain-6 expression in sarcomas inversely correlates with senescence markers. Calpain-6 knockdown suppresses hypoxia-dependent prevention of senescence entry and also promotion of autophagic flux