Anti-ENSA antibody
Description
Application Data
Description
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An antibody raised against Alpha-endosulfine (ENSA); the phosphorylated form is a negative regulator of the mitotic serine/threonine phosphatase PP2A.
Application Data
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Data Sheet Data Sheet Data Sheet Material Safety Data Sheet (MSDS)Catalogue number crb2005720 Antibody Anti-ENSA antibody Antigen Peptide KLH conjugated synthetic peptide crb1200929 Protein ID UniProtKB - O43768, P60841, P60840 Aliases Alpha-endosulfine, ARPP-19e Cross-Reactivity Human, Rat, Mouse Host Species Rabbit Antibody Type Polyclonal Concentration 2.0 mg/mL Glycine (R1G), 2.0 mg/mL Glycine (R2G), 0.5 mg/mL TEA (R2T) Target ENSA, Ensa Family Endosulfine family Storage This material is supplied in PBS containing 0.01% sodium azide and 1% trehalose. The product should be stored at +4°C for short term storage and -20°C for long term storage. Avoid repeated freeze/thaw cycles. References Charrasse et al., (2017). Ensa controls S-phase length by modulating Treslin levels. Nat comms., 8(1): 1. doi: 10.1038/s41467-017-00339-4.
Heron et al., (1998). Human alpha-endosulfine, a possible regulator of sulfonylurea-sensitive KATP channel: molecular cloning, expression and biological properties. PNAS, 95(14): 8387. doi: 10.1073/pnas.95.14.8387.
Phosphorylation events allow the regulation of the mitotic proteins and thus the cell cycle. Most serine/threonine phosphatase activity in eukaryotic cells is carried out by protein phosphatase 1 (PP1) and 2A (PP2A). There are various specific inhibitors of PP2A and PP1 that allow constant phosphorylation of certain proteins creating a controllable cell cycle event that can be driven forward by phosphatase inhibitors. Alpha-endosulfine (ENSA) is a well-conserved PP2A negative regulator. In the cell cycle, late G2 requires cyclin-dependent kinase cdk1 to phosphorylate numerous targets. To enter mitosis and cdk1 reach full activation, PP2A needs to be inactivated by ENSA or paralogue ARPP-19.
When ENSA is phosphorylated at Ser-67 during mitosis, it specifically interacts with PPP2R2D (PR55-delta) and inhibits its activity, leading to the inactivation of PP2A. This is an essential condition to keep cyclin-B1-cdk11 activity high during M phase. This is known as the Greatwall/Ensa/PP2A-B55 pathway. Knockdowns of ENSA shows an increase of S phase due to a reduction in the number of replication forks. This was linked to a depletion of the firing of replication forks as there is an increased turnover of Treslin proteins, a vital replication origin protein.
ENSA also acts as a stimulator of insulin secretion by interacting with the sulfonylurea receptor (ABCC8), thereby preventing sulfonylurea from binding to its receptor and reducing K(ATP) channel currents.