ULK1 Kinase Assay Kit

Catalog #
78362
$850 *
Size: 96 reactions
Qty
*US Pricing only. For international pricing, please contact your local distributor.
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Description

The ULK1 Kinase Assay Kit is designed to measure ULK1 activity for screening and profiling applications, using Kinase-Glo® MAX as a detection reagent. The ULK1 Assay Kit comes in a convenient 96-well format, with enough purified ULK1, MBP substrate, ATP, and kinase assay buffer for 96 enzyme reactions.

Synonyms
Serine/threonine-protein kinase ULK1, Autophagy-related protein 1 homolog, ATG1, hATG1, Unc-51-like kinase 1, ULK1, KIAA0722, ULK-1
Product Info
Storage and Usage
Citations
Assay Kit Format
Luminescent
Materials Required But Not Supplied
  • Kinase-Glo MAX (Promega, #V6071)
  • Microplate reader capable of reading luminescence
  • Adjustable micropipettor and sterile tips
  • 30°C incubator
Format
Catalog # Name Amount Storage
40099 ULK1* 20 µg -80°C
79334 Kinase Buffer 1 (5X) 1.5 ml -20°C
79686 ATP (500 µM) 100 µl -20°C
78514 Myelin basic protein (MBP), 5 mg/ml 200 µl -20°C
79696 96-well plate, white 1 Room Temp

*The concentration of the protein is lot-specific and will be indicated on the tube.

UniProt #
O75385
Background

ULK1  (unc-51 like autophagy activating kinase 1) is a serine/threonine protein kinase that plays a critical role during the initial stages of autophagy in response to nutrient starvation. The conserved C-terminal domain of ULK1 controls the  function and the localization of the protein. Knockdown of ULK1 inhibits the autophagic response  and prevents rapamycin-induced autophagy, consistent with a role downstream of mTOR. ULK1 forms a complex with FIP200 and ATG13 and this complex is essential for starvation-induced autophagy (1). Both FIP200 and ATG13 are critical for correct localization of ULK1 to the pre-autophagosome and stability of the ULK1 protein (2). ULK1 is phosphorylated upon activation of the mTOR pathway in a nutrient starvation-regulated manner. Alterations in ULK signaling pathways may be involved in the formation of autophagy-regulated Lewi bodies, which have been associated with Parkinson’s disease (3).