Catalytic subunit of AMP-activated protein kinase , an energy sensor protein kinase that plays a key role in regulating cellular energy metabolism . In response to reduction of intracellular ATP levels, AMPK activates energy-producing pathways and inhibits energy-consuming processes: inhibits protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation . AMPK acts via direct phosphorylation of metabolic enzymes, and by longer-term effects via phosphorylation of transcription regulators . Regulates lipid synthesis by phosphorylating and inactivating lipid metabolic enzymes such as ACACA, ACACB, GYS1, HMGCR and LIPE; regulates fatty acid and cholesterol synthesis by phosphorylating acetyl-CoA carboxylase and hormone-sensitive lipase enzymes, respectively . Promotes lipolysis of lipid droplets by mediating phosphorylation of isoform 1 of CHKA . Regulates insulin-signaling and glycolysis by phosphorylating IRS1, PFKFB2 and PFKFB3 . AMPK stimulates glucose uptake in muscle by increasing the translocation of the glucose transporter SLC2A4/GLUT4 to the plasma membrane, possibly by mediating phosphorylation of TBC1D4/AS160 . Regulates transcription and chromatin structure by phosphorylating transcription regulators involved in energy metabolism such as CRTC2/TORC2, FOXO3, histone H2B, HDAC5, MEF2C, MLXIPL/ChREBP, EP300, HNF4A, p53/TP53, SREBF1, SREBF2 and PPARGC1A . Acts as a key regulator of glucose homeostasis in liver by phosphorylating CRTC2/TORC2, leading to CRTC2/TORC2 sequestration in the cytoplasm . In response to stress, phosphorylates 'Ser-36' of histone H2B , leading to promote transcription . Acts as a key regulator of cell growth and proliferation by phosphorylating FNIP1, TSC2, RPTOR, WDR24 and ATG1/ULK1: in response to nutrient limitation, negatively regulates the mTORC1 complex by phosphorylating RPTOR component of the mTORC1 complex and by phosphorylating and activating TSC2 . Also phosphorylates and inhibits GATOR2 subunit WDR24 in response to nutrient limitation, leading to suppress glucose-mediated mTORC1 activation . In response to energetic stress, phosphorylates FNIP1, inactivating the non-canonical mTORC1 signaling, thereby promoting nuclear translocation of TFEB and TFE3, and inducing transcription of lysosomal or autophagy genes . In response to nutrient limitation, promotes autophagy by phosphorylating and activating ATG1/ULK1 . In that process, it also activates WDR45/WIPI4 . Phosphorylates CASP6, thereby preventing its autoprocessing and subsequent activation . In response to nutrient limitation, phosphorylates transcription factor FOXO3 promoting FOXO3 mitochondrial import . Also acts as a regulator of cellular polarity by remodeling the actin cytoskeleton; probably by indirectly activating myosin . AMPK also acts as a regulator of circadian rhythm by mediating phosphorylation of CRY1, leading to destabilize it . May regulate the Wnt signaling pathway by phosphorylating CTNNB1, leading to stabilize it . Also has tau-protein kinase activity: in response to amyloid beta A4 protein exposure, activated by CAMKK2, leading to phosphorylation of MAPT/TAU; however the relevance of such data remains unclear in vivo . Also phosphorylates CFTR, EEF2K, KLC1, NOS3 and SLC12A1 . Regulates hepatic lipogenesis. Activated via SIRT3, represses sterol regulatory element-binding protein transcriptional activities and ATP-consuming lipogenesis to restore cellular energy balance. Upon stress, regulates mitochondrial fragmentation through phosphorylation of MTFR1L .

5'-AMP-activated protein kinase catalytic subunit alpha-1 (AMPK subunit alpha-1) (EC 2.7.11.1) (Acetyl-CoA carboxylase kinase) (ACACA kinase) (Hydroxymethylglutaryl-CoA reductase kinase) (HMGCR kinase) (EC 2.7.11.31) (Tau-protein kinase PRKAA1) (EC 2.7.11.26)

q13131

Human

WB,IF,ICC

WB 1:1000-1:5000
IF 1:100-1:200
ICC 1:100-1:200

~65 kD

Rabbit

50mM Tris-Glycine(pH 7.4), 0.15M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.

Store at -20°C. Stable for 12 months from date of receipt.