Anti-BCKDK antibody,Abcam,AB151297

Host

Rabbit

Reactivity

Mouse, Rat, Human

Application

ICC/IF, WB

Platform ID

BAB222437530

Abcam

Headquarters

Discovery Drive Cambridge Biomedical Campus Cambridge CB2 0AX UK

Contact

Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215

Product Specifications
Scientific Background

Specifications

NameAnti-BCKDK antibody
Cat. No.AB151297
HostRabbit
IsotypeIgG
ReactivityMouse, Rat, Human
ApplicationICC/IF, WB
ClonalityPolyclonal
Concentration0.35 mg/mL Batch dependent concentration
ImmunogenRecombinant Fragment Protein within Human BCKDK aa 50-400. The exact immunogen used to generate this antibody is proprietary information.
PurityAffinity purification Immunogen
Appearance/FormLiquid
ShippingBlue Ice
FormulationpH: 7 Preservative: 0.025% Proclin 300 Constituents: PBS, 20% Glycerol (glycerin, glycerine), 1% BSA
Storage-20°C
Regulatory StatusResearch Use Only

Scientific Background

Target data Serine/threonine-protein kinase component of macronutrients metabolism. Forms a functional kinase and phosphatase pair with PPM1K, serving as a metabolic regulatory node that coordinates branched-chain amino acids (BCAAs) with glucose and lipid metabolism via two distinct phosphoprotein targets : mitochondrial BCKDHA subunit of the branched-chain alpha-ketoacid dehydrogenase (BCKDH) complex and cytosolic ACLY, a lipogenic enzyme of Krebs cycle (PubMed : 24449431, PubMed : 29779826, PubMed : 37558654). Phosphorylates and inactivates mitochondrial BCKDH complex a multisubunit complex consisting of three multimeric components each involved in different steps of BCAA catabolism : E1 composed of BCKDHA and BCKDHB, E2 core composed of DBT monomers, and E3 composed of DLD monomers. Associates with the E2 component of BCKDH complex and phosphorylates BCKDHA on Ser-337, leading to conformational changes that interrupt substrate channeling between E1 and E2 and inactivates the BCKDH complex (PubMed : 29779826, PubMed : 37558654). Phosphorylates ACLY on Ser-455 in response to changes in cellular carbohydrate abundance such as occurs during fasting to feeding metabolic transition. Refeeding stimulates MLXIPL/ChREBP transcription factor, leading to increased BCKDK to PPM1K expression ratio, phosphorylation and activation of ACLY that ultimately results in the generation of malonyl-CoA and oxaloacetate immediate substrates of de novo lipogenesis and glucogenesis, respectively (PubMed : 29779826). Recognizes phosphosites having SxxE/D canonical motif (PubMed : 29779826). See full target information BCKDK

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