LATS1, Active(L01-11G)
FOR BULK ORDER REQUESTS PLEASE CONTACT US
Description :Recombinant human LATS1 (589-end) was expressed by baculovirus in Sf9 insect cells using an N-terminal GST tag.
Species :Human
Tag :GST tag
Expression System:Sf9 insect cells using baculovirus
Sequence :589-end
Genbank Number :NM_004690
Specific Activity :Sample Kinase Activity Plot. For specific information on a given lot, see related technical data sheet.
Purity :Sample Purity Data. For specific information on a given lot, see related technical data sheet.
Storage, Stability and Shipping :Store product at –70oC. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.
Applications :Kinase Assay, Western Blot
Molecular Weight :~95 kDa
Gene Aliases :WARTS; wts
Scientific Background :LATS1 is a putative serine/threonine kinase that localizes to the mitotic apparatus and complexes with cell cycle controller CDC2 kinase in early mitosis which is phosphorylated in a cell-cycle dependent manner. The N-terminal region of the protein binds CDC2 to form a complex showing reduced H1 histone kinase activity which indicating a role as a negative regulator of CDC2/cyclin A and the C-terminal kinase domain binds to its own N-terminal region, suggesting potential negative regulation through interference with complex formation via intramolecular binding (1). LATS1 act as a tumor suppressor and play an important role in the development of soft-tissue sarcomas, ovarian stromal cell tumors and a high sensitivity to carcinogenic treatments (2).
References :
1. Tao, W.et.al: Human homologue of the Drosophila melanogaster lats tumour suppressor modulates CDC2 activity. Nature Genet. 21: 177-181, 1999.
2. St. John. et.al: Mice deficient of Lats1 develop soft-tissue sarcomas, ovarian tumours and pituitary dysfunction. Nature Genet. 21: 182-186, 1999.
Product Sheets (By Lot #) :
Research Areas :Cell Cycle, Cardiovascular Disease, Cancer, Apoptosis/Autophagy, Ser/Thr Kinases, Cancer, Cardiovascular Disease, Apoptosis/Autophagy, Cell Cycle