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Succinyl CoA (Succinyl-coenzyme A) sodium is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA sodium is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA sodium acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA sodium insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl CoA sodium can be used in research on metabolic, neurological, and hematological abnormalities (such as porphyria) caused by nutritional vitamin B12 deficiency (leading to a lack of Succinyl-Coenzyme A synthesis) .
Succinyl phosphonate trisodium salt is a α-Ketoglutarate Dehydrogenase Complex (KGDHC) modulator with neuroprotective activity. Succinyl phosphonate trisodium salt protects this complex, reduces cellular succinyl-CoA concentration, downregulates protein succinylation levels, and inhibits the activity of the α-ketoglutarate dehydrogenase complex. Succinyl phosphonate trisodium salt corrects hypoxic or ethanol-induced behavioral impairments, modulates exploratory behavior and emotional stress responses, and improves hypoxia tolerance. Succinyl phosphonate trisodium salt reduces glutamate excitotoxicity, restores the activity of the α-ketoglutarate dehydrogenase complex, reverses the changes in glutamate dehydrogenase and glutamine synthetase activities induced by β-amyloid (Amyloid-β), modulates cognitive function, and prevents β-amyloid-induced neuronal damage. Succinyl phosphonate trisodium salt improves microglial senescence, alleviates neuroinflammation, reactive oxygen species (ROS) production, lipid peroxidation, and the expression of proinflammatory cytokines. Succinyl phosphonate trisodium salt can be used in the research of Alzheimer's disease, aging-related neuroinflammation, and Parkinson's disease .
Succinyladenosine, the metabolic product of dephosphorylation of intracellular adenylosuccinic acid (S-AMP) by cytosolic 5-nucleotidase, is a biochemical marker of adenylosuccinase (ASL) deficiency .
Succinyl CoA (Succinyl-coenzyme A) is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl CoA can be used in research on metabolic, neurological, and hematological abnormalities (such as porphyria) caused by nutritional vitamin B12 deficiency (leading to a lack of Succinyl-Coenzyme A synthesis) .
PSSI-51 is an orally active, peripherally selective inhibitor of succinyl-CoA:3-ketoacid-CoA transferase (SCOT). PSSI-51 inhibits SCOT activity in peripheral tissues (such as muscle and kidney) but does not affect SCOT activity in brain tissue. PSSI-51 reduces ketone body oxidation by inhibiting SCOT, thereby improving obesity-related hyperglycemia. PSSI-51 can be used in the study of type 2 diabetes (T2D) and has the potential to improve obesity-related metabolic disorders .
O-Succinyl-L-homoserine is a homoserine derivative. O-Succinyl-L-homoserine is an intermediate in the biosynthesis of methionine in Escherichia coli and Salmonella typhimurium .
Methylmalonyl-CoA (Methylmalonyl coenzyme A) tetralithium is a catabolite of valine, isoleucine, methionine, threonine, odd-chain fatty acids, and cholesterol. Methylmalonyl-CoA tetralithium is converted to succinyl-CoA by enzymatic reaction of methylmalonyl-CoA mutase (MCM) with coenzyme vitamin B12 .
Succinyl phosphonate is a α-Ketoglutarate Dehydrogenase Complex (KGDHC) modulator with neuroprotective activity. Succinyl phosphonate protects this complex, reduces cellular succinyl-CoA concentration, downregulates protein succinylation levels, and inhibits the activity of the α-ketoglutarate dehydrogenase complex. Succinyl phosphonate corrects hypoxic or ethanol-induced behavioral impairments, modulates exploratory behavior and emotional stress responses, and improves hypoxia tolerance. Succinyl phosphonate reduces glutamate excitotoxicity, restores the activity of the α-ketoglutarate dehydrogenase complex, reverses the changes in glutamate dehydrogenase and glutamine synthetase activities induced by β-amyloid (Amyloid-β), modulates cognitive function, and prevents β-amyloid-induced neuronal damage. Succinyl phosphonate improves microglial senescence, alleviates neuroinflammation, reactive oxygen species (ROS) production, lipid peroxidation, and the expression of proinflammatory cytokines. Succinyl phosphonate can be used in the research of Alzheimer's disease, aging-related neuroinflammation, and Parkinson's disease .
Succinyl-CoA synthetase catalyzes the only substrate-level phosphoryl-ation step in the tricarboxylic acid cycle. Succinyl-CoA synthetase is a phosphate target for the activation of mitochondrial metabolism .
2'-O-Succinyl-cAMP is a cAMP analog that can be covalently coupled to acetylcholinesterase. 2'-O-Succinyl-cAMP conjugate has been used as tracers in a classical heterogeneous competitive enzyme immunoassay allowing the determination of cAMP .
Suc-Ala-Ala-Pro-Leu-pNA (N-Succinyl-AAPL-p-nitroanilide) is a tripeptidyl p-nitroanilide substrate that can be catalytically hydrolyzed by acyl amidase-like leucine aminopeptidase in seminal plasma. Amastatin (HY-129298) and Actinonin (HY-113952) exert potent inhibitory effects on this hydrolytic activity. Suc-Ala-Ala-Pro-Leu-pNA can be used for the research of diseases such as azoospermia .
Glucosamine Cholesterol (N-Cholesteryl succinyl glucosamine) is a glucosamine-based lipid conjugate, and can be used in the formation of lipid nanoparticles (LNPs) .
LY-266500 is a succinyl CoA synthetase (SCS) specific inhibitor. LY-266500 has inhibitory effects on various parasites, such as Trypanosoma brucei brucei (IC50 =0.6 μM) and Leishmania donovani (IC50 =2.86 μM). LY-266500 can be used for research on parasitic infections .
1-Palmitoyl-2-succinyl-sn-glycerophosphorylcholine is a glycerophosphorylcholine, consisting of glycerol phosphate, choline and palmitic acid. It accumulates in vivo at sites of oxidative stress. 1-Palmitoyl-2-succinyl-sn-glycerophosphorylcholine may be a ligand of scavenger receptors class B, while oxidized phospholipids oxPC(CD36) are potent ligands of scavenger receptors class B (CD36 and SR-BI). Oxidized phospholipids (oxPLs) also play an important role in tumor apoptosis, may be elevated in malignant biliary strictures .
Paclitaxel succinate sulfo-NHS ester is a derivative of Paclitaxel (HY-B0015). Paclitaxel succinate sulfo-NHS ester can be used for the research of cancer .
Succinyl CoA (Succinyl-coenzyme A) disodium is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA disodium is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA disodium acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA disodium insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl-Coenzyme A sodium can be used in research on metabolic, neurological, and hematological abnormalities (such as porphyria) caused by nutritional vitamin B12 deficiency (leading to a lack of Succinyl-Coenzyme A synthesis) .
Succinyl-β-cycloaltrin is a modified cyclodextrin with unique chemical properties that make it an effective solubilizer and stabilizer for various compounds, especially in the pharmaceutical industry. Succinyl-β-cycloaltrin has a hydrophobic interior and a hydrophilic exterior, enabling it to form stable clathrates with hydrophobic molecules such as drugs and nutrients. This increases their solubility and bioavailability, making them more effective for recreational or nutritional purposes.
Succinyl-(Pro58,D-Glu65)-Hirudin (56-65) (sulfated) is a hirugen-like peptide, and has high affnity for thrombin than Hirugen, with a KD < 100 nM. Succinyl-(Pro58,D-Glu65)-Hirudin (56-65) (sulfated) is an antithrombotic agent. Succinyl-(Pro58,D-Glu65)-Hirudin (56-65) (sulfated) inhibits the thrombin-induced fibrin clot formation with an IC50 value of 0.087 μM .
Succinyladenosine- 13C4 (N6-Succinyl adenosine- 13C4) is the 13C-labeled Succinyladenosine (HY-113284). Succinyladenosine, the metabolic product of dephosphorylation of intracellular adenylosuccinic acid (S-AMP) by cytosolic 5-nucleotidase, is a biochemical marker of adenylosuccinase (ASL) deficiency .
IMP 243 is a symmetric di-HSG (histamine-succinyl-glycine) bivalent hapten containing a Tscg-Cys ligand and two HSG groups. IMP 243 can be radiolabeled with 99mTc-pertechnetate. IMP 243 can be conjugated to other peptides to design bispecific antibodies (bsMAbs) for cancer research .
CH 5450 (Z-Ile-Glu-Pro-Phe-Ome) is a selective short peptide human cardiac chymase inhibitor. CH-5450 inhibits the action of rat MAB elastase 2 on substrate Ang I with an IC50 value of 49 µM and N-succinyl-Ala-Ala-Pro-Phe-p-nitroanilide with an IC50 value of 4.8 µM .
DdBIC is a pyroptosis inducer. DdBIC binds to Nur77 and triggers its translocation to mitochondria, activates SDHA to deplete succinyl-CoA, disrupts heme homeostasis, induces electron leakage, and elicits mitochondrial ROS production. DdBIC induces mitochondrial ROS that oxidatively activates OMA1, promotes OPA1 cleavage and its release into the cytoplasm, activates the integrated stress response via PERK, and ultimately activates granzyme B to cleave GSDMC. DdBIC can be used for the study of melanoma .
Succinyl-β-cycloaltrin is a modified cyclodextrin with unique chemical properties that make it an effective solubilizer and stabilizer for various compounds, especially in the pharmaceutical industry. Succinyl-β-cycloaltrin has a hydrophobic interior and a hydrophilic exterior, enabling it to form stable clathrates with hydrophobic molecules such as drugs and nutrients. This increases their solubility and bioavailability, making them more effective for recreational or nutritional purposes.
O-Succinyl-L-homoserine is a homoserine derivative. O-Succinyl-L-homoserine is an intermediate in the biosynthesis of methionine in Escherichia coli and Salmonella typhimurium .
Suc-Ala-Ala-Pro-Leu-pNA (N-Succinyl-AAPL-p-nitroanilide) is a tripeptidyl p-nitroanilide substrate that can be catalytically hydrolyzed by acyl amidase-like leucine aminopeptidase in seminal plasma. Amastatin (HY-129298) and Actinonin (HY-113952) exert potent inhibitory effects on this hydrolytic activity. Suc-Ala-Ala-Pro-Leu-pNA can be used for the research of diseases such as azoospermia .
Succinyl-(Pro58,D-Glu65)-Hirudin (56-65) (sulfated) is a hirugen-like peptide, and has high affnity for thrombin than Hirugen, with a KD < 100 nM. Succinyl-(Pro58,D-Glu65)-Hirudin (56-65) (sulfated) is an antithrombotic agent. Succinyl-(Pro58,D-Glu65)-Hirudin (56-65) (sulfated) inhibits the thrombin-induced fibrin clot formation with an IC50 value of 0.087 μM .
CH 5450 (Z-Ile-Glu-Pro-Phe-Ome) is a selective short peptide human cardiac chymase inhibitor. CH-5450 inhibits the action of rat MAB elastase 2 on substrate Ang I with an IC50 value of 49 µM and N-succinyl-Ala-Ala-Pro-Phe-p-nitroanilide with an IC50 value of 4.8 µM .
Succinyl CoA (Succinyl-coenzyme A) sodium is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA sodium is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA sodium acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA sodium insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl CoA sodium can be used in research on metabolic, neurological, and hematological abnormalities (such as porphyria) caused by nutritional vitamin B12 deficiency (leading to a lack of Succinyl-Coenzyme A synthesis) .
Succinyl phosphonate trisodium salt is a α-Ketoglutarate Dehydrogenase Complex (KGDHC) modulator with neuroprotective activity. Succinyl phosphonate trisodium salt protects this complex, reduces cellular succinyl-CoA concentration, downregulates protein succinylation levels, and inhibits the activity of the α-ketoglutarate dehydrogenase complex. Succinyl phosphonate trisodium salt corrects hypoxic or ethanol-induced behavioral impairments, modulates exploratory behavior and emotional stress responses, and improves hypoxia tolerance. Succinyl phosphonate trisodium salt reduces glutamate excitotoxicity, restores the activity of the α-ketoglutarate dehydrogenase complex, reverses the changes in glutamate dehydrogenase and glutamine synthetase activities induced by β-amyloid (Amyloid-β), modulates cognitive function, and prevents β-amyloid-induced neuronal damage. Succinyl phosphonate trisodium salt improves microglial senescence, alleviates neuroinflammation, reactive oxygen species (ROS) production, lipid peroxidation, and the expression of proinflammatory cytokines. Succinyl phosphonate trisodium salt can be used in the research of Alzheimer's disease, aging-related neuroinflammation, and Parkinson's disease .
Succinyl CoA (Succinyl-coenzyme A) is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl CoA can be used in research on metabolic, neurological, and hematological abnormalities (such as porphyria) caused by nutritional vitamin B12 deficiency (leading to a lack of Succinyl-Coenzyme A synthesis) .
O-Succinyl-L-homoserine is a homoserine derivative. O-Succinyl-L-homoserine is an intermediate in the biosynthesis of methionine in Escherichia coli and Salmonella typhimurium .
Methylmalonyl-CoA (Methylmalonyl coenzyme A) tetralithium is a catabolite of valine, isoleucine, methionine, threonine, odd-chain fatty acids, and cholesterol. Methylmalonyl-CoA tetralithium is converted to succinyl-CoA by enzymatic reaction of methylmalonyl-CoA mutase (MCM) with coenzyme vitamin B12 .
Succinyl phosphonate is a α-Ketoglutarate Dehydrogenase Complex (KGDHC) modulator with neuroprotective activity. Succinyl phosphonate protects this complex, reduces cellular succinyl-CoA concentration, downregulates protein succinylation levels, and inhibits the activity of the α-ketoglutarate dehydrogenase complex. Succinyl phosphonate corrects hypoxic or ethanol-induced behavioral impairments, modulates exploratory behavior and emotional stress responses, and improves hypoxia tolerance. Succinyl phosphonate reduces glutamate excitotoxicity, restores the activity of the α-ketoglutarate dehydrogenase complex, reverses the changes in glutamate dehydrogenase and glutamine synthetase activities induced by β-amyloid (Amyloid-β), modulates cognitive function, and prevents β-amyloid-induced neuronal damage. Succinyl phosphonate improves microglial senescence, alleviates neuroinflammation, reactive oxygen species (ROS) production, lipid peroxidation, and the expression of proinflammatory cytokines. Succinyl phosphonate can be used in the research of Alzheimer's disease, aging-related neuroinflammation, and Parkinson's disease .
Acetylornithine deacylase protein catalyzes the hydrolysis of N-succinyl-L,L-diaminopimelic acid (SDAP), leading to the formation of succinic acid and LL-2,6-diaminopimelic acid (DAP) , plays a key role in cellular processes. This enzyme activity is integral to the bacterial biosynthesis of lysine and mesodiaminopimelic acid, both of which contribute to the structural integrity of the bacterial cell wall. Acetylornithine Deacylase Protein, Shigella sonnei is the recombinant Acetylornithine Deacylase protein, expressed by E. coli , with tag free.
Acetylornithine deacylase protein catalyzes the hydrolysis of N-succinyl-L,L-diaminopimelic acid (SDAP), leading to the formation of succinic acid and LL-2,6-diaminopimelic acid (DAP) , plays a key role in cellular processes. This enzyme activity is integral to the bacterial biosynthesis of lysine and mesodiaminopimelic acid, both of which contribute to the structural integrity of the bacterial cell wall. Acetylornithine Deacylase Protein, Shigella sonnei (His) is the recombinant Acetylornithine Deacylase protein, expressed by E. coli , with N-6*His labeled tag.
Succinyladenosine- 13C4 (N6-Succinyl adenosine- 13C4) is the 13C-labeled Succinyladenosine (HY-113284). Succinyladenosine, the metabolic product of dephosphorylation of intracellular adenylosuccinic acid (S-AMP) by cytosolic 5-nucleotidase, is a biochemical marker of adenylosuccinase (ASL) deficiency .
Succinyladenosine, the metabolic product of dephosphorylation of intracellular adenylosuccinic acid (S-AMP) by cytosolic 5-nucleotidase, is a biochemical marker of adenylosuccinase (ASL) deficiency .
Glucosamine Cholesterol (N-Cholesteryl succinyl glucosamine) is a glucosamine-based lipid conjugate, and can be used in the formation of lipid nanoparticles (LNPs) .
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Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
MedchemExpress Validation 03
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
MedchemExpress Validation 04
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
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