U9382
Ubiquitin-Carrier Protein H10 human
≥95% (SDS-PAGE), recombinant, expressed in E. coli (histidine-tagged), buffered aqueous glycerol solution
Synonym(s):
UbcH10
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This Item | U9132 | U5382 | P3988 |
|---|---|---|---|
| recombinant expressed in E. coli (histidine-tagged) | recombinant expressed in E. coli | recombinant expressed in E. coli (N-terminal FLAG® tagged) | recombinant - |
| assay ≥95% (SDS-PAGE) | assay ≥95% (SDS-PAGE) | assay ≥95% (SDS-PAGE) | assay ≥95% (SDS-PAGE) |
| technique(s) ligand binding assay: suitable | technique(s) - | technique(s) mass spectrometry (MS): suitable | technique(s) - |
| biological source human | biological source - | biological source human | biological source rabbit |
| form buffered aqueous glycerol solution | form liquid | form lyophilized powder | form solution |
| mol wt ~20 kDa | mol wt 18 kDa | mol wt 10 kDa | mol wt 700 kDa |
General description
Manufactured for Sigma by Boston Biochem., Inc.
Application
Ubiquitin-Carrier Protein H10 (UbcH10) human may be used to study the role of ubiquitin-proteasome system in pathogenesis of human diseases.
Biochem/physiol Actions
In conjunction with anaphase-promoting complex, catalyzes both cyclin A and cyclin B destruction.
In conjunction with the anaphase-promoting complex, the protein catalyzes the destruction of both cyclin A and cyclin B.
Ubiquitin-Carrier Protein H10 human also referred to as UbcH10 is a recombinant protein that catalyzes the destruction of cyclin A as well as cyclin B along with the anaphase promoting complex and hence plays a pivotal role in controlling the cell exit from mitosis.[1]
Physical form
Solution in 50 mM HEPES, pH 8.0, 125 mM NaCl, and 1 mM DTT in 10% glycerol.
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Li Zhu et al.
The Journal of biological chemistry, 288(44), 32050-32063 (2013-09-21)
Recent studies link synaptojanin 1 (synj1), the main phosphoinositol (4,5)-biphosphate phosphatase (PI(4,5)P2-degrading enzyme) in the brain and synapses, to Alzheimer disease. Here we report a novel mechanism by which synj1 reversely regulates cellular clearance of amyloid-β (Aβ). Genetic down-regulation of
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Zou, L; Wang, Z; Shen, L; Bao, GB; Wang, T; Kang, JH; Pei, G
Cell research null
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