Application Note
*Optimal dilutions/concentrations should be determined by the researcher.
Application |
Recommended Dilution |
1:500-1:3000 |
1:100-1:1000 |
Not tested in other applications.
Calculated MW
Positive Control
A431
Predict Reactivity
Mouse, Rat, Bovine, Pig(>80% identity)
Form
Liquid
Buffer
0.1M Tris-Glycine (pH7), 10% Glycerol
Preservative
0.01% Thimerosal
Storage
Store as concentrated solution. Centrifuge briefly prior to opening vial. For short-term storage (1-2 weeks), store at 4ºC. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles.
Concentration
0.53 mg/ml (Please refer to the vial label for the specific concentration.)
Antigen Species
Human
Immunogen
Recombinant protein encompassing a sequence within the center region of human ITPK1. The exact sequence is proprietary.
Purification
Purified by antigen-affinity chromatography.
Conjugation
Unconjugated
RRID
AB_1950605
Note
For laboratory use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
Synonyms
inositol-tetrakisphosphate 1-kinase , ITRPK1
Background
Kinase that can phosphorylate various inositol polyphosphate such as Ins(3,4,5,6)P4 or Ins(1,3,4)P3. Phosphorylates Ins(3,4,5,6)P4 at position 1 to form Ins(1,3,4,5,6)P5. This reaction is thought to have regulatory importance, since Ins(3,4,5,6)P4 is an inhibitor of plasma membrane Ca(2+)-activated Cl(-) channels, while Ins(1,3,4,5,6)P5 is not. Also phosphorylates Ins(1,3,4)P3 on O-5 and O-6 to form Ins(1,3,4,6)P4, an essential molecule in the hexakisphosphate (InsP6) pathway. Also acts as an inositol polyphosphate phosphatase that dephosphorylate Ins(1,3,4,5)P4 and Ins(1,3,4,6)P4 to Ins(1,3,4)P3, and Ins(1,3,4,5,6)P5 to Ins(3,4,5,6)P4. May also act as an isomerase that interconverts the inositol tetraphosphate isomers Ins(1,3,4,5)P4 and Ins(1,3,4,6)P4 in the presence of ADP and magnesium. Probably acts as the rate-limiting enzyme of the InsP6 pathway. Modifies TNF-alpha-induced apoptosis by interfering with the activation of TNFRSF1A-associated death domain.
Database
Research Area