Phospho-Wee1 (Ser642) (D47G5) Rabbit Antibody

INQUIRY

CAT. NO.: AMA-0373

Target Information
UniProt ID	P30291

Product Details
Size	20 µL/100 µL
Reactivity	Human
Host	Rabbit
Source/Isotype	Rabbit IgG
Storage	Store at -20°C. Do not aliquot the antibody.
Purification	Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser642 of human wee1.

Usage
Application	WB, IP
Product Usage Information Dilution	Western Blotting (1:1000); Immunoprecipitation (1:50)
MW (Target)	95 kDa

Background
Entry of all eukaryotic cells into mitosis is regulated by activation of cdc2 kinase. The critical regulatory step in activating cdc2 during progression into mitosis appears to be dephosphorylation of Tyr15 and Thr14 Phosphorylation at Tyr15 and Thr14 and inhibition of cdc2 is carried out by Wee1 and Myt1 protein kinases, while Tyr15 dephosphorylation and activation of cdc2 is carried out by the cdc25 phosphatase. Hyperphosphorylation and inactivation of Myt1 in mitosis suggests that one or more kinases activated at the G2/M transition negatively regulates Myt1 activity. Kinases shown to phosphorylate Myt1 include cdc2, p90RSK, Akt, and Plk1Akt/PKB-dependent phosphorylation at Ser642 promotes a change in Wee1 localization from nuclear to cytoplasmic and is associated with G2/M arrest.

Background

Entry of all eukaryotic cells into mitosis is regulated by activation of cdc2 kinase. The critical regulatory step in activating cdc2 during progression into mitosis appears to be dephosphorylation of Tyr15 and Thr14 Phosphorylation at Tyr15 and Thr14 and inhibition of cdc2 is carried out by Wee1 and Myt1 protein kinases, while Tyr15 dephosphorylation and activation of cdc2 is carried out by the cdc25 phosphatase. Hyperphosphorylation and inactivation of Myt1 in mitosis suggests that one or more kinases activated at the G2/M transition negatively regulates Myt1 activity. Kinases shown to phosphorylate Myt1 include cdc2, p90RSK, Akt, and Plk1Akt/PKB-dependent phosphorylation at Ser642 promotes a change in Wee1 localization from nuclear to cytoplasmic and is associated with G2/M arrest.

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