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Human Alpha-endosulfine / ENSA Protein  pdf  pdf  pdf


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Synonym

ENSA,Alpha-endosulfine,ARPP-19e,endosulfine Alpha

Source

Recombinant Human ENSA /Alpha-endosulfine Protein (rh ENSA /Alpha-endosulfine) Ser 2 - Glu 121 (Accession # AAH00436) was produced in E.coli cells at ACROBiosystems.

Molecular Characterization

rh ENSA /Alpha-endosulfine is fused with a polyhistidine tag at the N-terminus, and has a calculated MW of 14.2 kDa. The predicted N-terminus is Met. DTT-reduced Protein migrates as 18 kDa in SDS-PAGE .

Endotoxin

Less than 1.0 EU per μg of the rh ENSA /Alpha-endosulfine by the LAL method.

Purity

>90% as determined by SDS-PAGE.

Formulation

Lyophilized from 0.22 μm filtered solution in PBS, pH 7.4. Normally Mannitol or Trehalose are added as protectants before lyophilization.

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Reconstitution

See Certificate of Analysis for reconstitution instructions and specific concentrations.

Storage

Avoid repeated freeze-thaw cycles.

No activity loss was observed after storage at:
In lyophilized state for 1 year (4oC); After reconstitution under sterile conditions for 3 months (-70oC).

 

SDS-PAGE


Recombinant Human ENSA /Alpha-endosulfine Protein
The purity of rh ENSA /Alpha-endosulfine was determined by DTT-reduced (+) SDS-PAGE and staining overnight with Coomassie Blue.
 
 

Background

Alpha-endosulfine (ENSA),a member of the endosulfine family, is also known as ARPP-19e,which is widely expressed with high levels in skeletal muscle and brain and lower levels in the pancreas. ENSA is a protein phosphatase inhibitor that specifically inhibits protein phosphatase 2A (PP2A) during mitosis. When phosphorylated at Ser-67 during mitosis, ENSA is able to specifically interact with PPP2R2D (PR55-delta) and inhibit its activity, leading to inactivation of PP2A, an essential condition to keep cyclin-B1-CDK1 activity high during M phase (By similarity). ENSA acts as a stimulator of insulin secretion by interacting with sulfonylurea receptor (ABCC8), thereby preventing sulfonylurea from binding to its receptor and reducing K(ATP) channel currents.

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References

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