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Bucladesine (Dibutyryl cAMP; DBcAMP) sodium is a membrane-permeable 3′, 5′-cyclic adenosine monophosphate (cAMP) analog. Bucladesine selectively activates cAMP dependentproteinkinase (PKA) by increasing the intracellular level of cAMP. Bucladesine significantly attenuates MDMA-induced increases in hippocampal mitochondrial ROS formation, mitochondrial outer membrane damage, cytochrome c release, and hippocampal ADP/ATP ratio, thereby improving spatial learning and memory impairments. Bucladesine exhibit anti-nociceptive and anti-inflammation effect. Bucladesine can inhibit cancer cells proliferation, induce apoptosis. Bucladesine can be used for the researches of neurological disease, cancer, inflammation .
Bucladesine (Dibutyryl cAMP; DBcAMP) hemicalcium is a membrane-permeable 3′, 5′-cyclic adenosine monophosphate (cAMP) analog. Bucladesine selectively activates cAMP dependentproteinkinase (PKA) by increasing the intracellular level of cAMP. Bucladesine significantly attenuates MDMA-induced increases in hippocampal mitochondrial ROS formation, mitochondrial outer membrane damage, cytochrome c release, and hippocampal ADP/ATP ratio, thereby improving spatial learning and memory impairments. Bucladesine exhibit anti-nociceptive and anti-inflammation effect. Bucladesine can inhibit cancer cells proliferation, induce apoptosis. Bucladesine can be used for the researches of neurological disease, cancer, inflammation .
H-8 dihydrochloride is a selective Cyclic nucleotide-dependentproteinkinase inhibitor. H-8 dihydrochloride potently inhibits cGMP- and cAMP-dependentprotein phosphorylation. H-8 dihydrochloride enhances the vasodilatory effect induced by 8-bromo-cAMP (HY-12306A). H-8 dihydrochloride fails to attenuate the vasodilatory effects induced by 8-bromo-cGMP (HY-101379A), atrial natriuretic peptide II, or Sodium nitroprusside (HY-B0564) in rat aorta .
PKI(5-24) is a potent, competitive, and synthetic peptide inhibitor of PKA (cAMP-dependentproteinkinase), with a Ki of 2.3 nM. PKI(5-24) corresponds to residues 5-24 in the naturally occurring heat-stable proteinkinase inhibitor .
PKA Inhibitor Fragment (6-22) amide is a highly potent and specific competitive inhibitor of PKA, with Ki values of 1.7 nM and 1.6 nM against human and bovine PKA catalytic subunits, respectively. The IC50 of PKA Inhibitor Fragment (6-22) amide targeting bovine PKA is 8.6 nM. PKA Inhibitor Fragment (6-22) amide effectively abolishes PKA activity in mouse brain and spinal cord, and exerts in vivo efficacy via intracerebroventricular administration. PKA Inhibitor Fragment (6-22) amide significantly reverses low-dose morphine analgesic tolerance in mice and blocks photoaffinity labeling of cAMP-dependent proteinkinase. PKA Inhibitor Fragment (6-22) amide can be applied to research in fields related to the mechanism of morphine analgesic tolerance and skin wound healing .
HA-100 is a potent proteinkinase inhibitor, with IC50s of 4 μM, 8 μM, 12 μM and 240 μM for cGMP-dependentproteinkinase (PKG), cAMP-dependentproteinkinase (PKA), proteinkinase C (PKC) and MLC-kinase, respectively. HA-100 also used as a ROCK inhibitor .
PKA Inhibitor Fragment (6-22) amide TFA is an inhibitor of cAMP-dependentproteinkinase A (PKA), with a Ki of 2.8 nM. PKA Inhibitor Fragment (6-22) amide TFA can significantly reverse antinociceptive tolerance in mice .
Proteinkinase inhibitor H-7 is a selective inhibitor of PKC and cyclic nucleotide-dependentproteinkinases, with a Ki value of 6.0 μM for rabbit proteinkinase C, a Ki value of 3.0 μM for rabbit cAMP-dependent proteinkinase, and a Ki value of 5.8 μM for porcine cGMP-dependent proteinkinase. Proteinkinase inhibitor H-7 has no effect on Ca 2+-calmodulin-dependent enzymes. Proteinkinase inhibitor H-7 regulates the Actin cytoskeleton, inhibits contractility, disrupts stress fibers, induces protrusive activity, stabilizes intercellular junctions, and triggers rapid and reversible cytoskeletal reorganization. Proteinkinase inhibitor H-7 serves as a research tool for elucidating the functions of proteinkinase C-mediated signaling systems .
Bucladesine (Dibutyryl cAMP; DBcAMP) is a membrane-permeable 3′, 5′-cyclic adenosine monophosphate (cAMP) analog. Bucladesine selectively activates cAMP dependentproteinkinase (PKA) by increasing the intracellular level of cAMP. Bucladesine significantly attenuates MDMA-induced increases in hippocampal mitochondrial ROS formation, mitochondrial outer membrane damage, cytochrome c release, and hippocampal ADP/ATP ratio, thereby improving spatial learning and memory impairments. Bucladesine exhibit anti-nociceptive and anti-inflammation effect. Bucladesine can inhibit cancer cells proliferation, induce apoptosis. Bucladesine can be used for the researches of neurological disease, cancer, inflammation .
Malantide is a synthetic dodecapeptide derived from the site phosphorylated by cAMP-dependentproteinkinase (PKA) on the β-subunit of phosphorylase kinase. Malantide is a highly specific substrate for PKA with a Km of 15 μM and shows protein inhibitor (PKI) inhibition >90% substrate phosphorylation in various rat tissue extracts . Malantide is also an efficient substrate for PKC with a Km of 16 μM .
Bucladesine (Dibutyryl cAMP; DBcAMP) sodium (GMP) is a Bucladesine sodium (HY-B0764) produced by using GMP guidelines. Bucladesine (Dibutyryl cAMP; DBcAMP) is a membrane-permeable 3′, 5′-cyclic adenosine monophosphate (cAMP) analog. Bucladesine selectively activates cAMP dependentproteinkinase (PKA) by increasing the intracellular level of cAMP. Bucladesine significantly attenuates MDMA-induced increases in hippocampal mitochondrial ROS formation, mitochondrial outer membrane damage, cytochrome c release, and hippocampal ADP/ATP ratio, thereby improving spatial learning and memory impairments. Bucladesine exhibit anti-nociceptive and anti-inflammation effect. Bucladesine can inhibit cancer cells proliferation, induce apoptosis. Bucladesine can be used for the researches of neurological disease, cancer, inflammation .
Bucladesine (Dibutyryl cAMP; DBcAMP) sodium (Standard) is the analytical standard of Bucladesine sodiumn (HY-B0764). This product is intended for research and analytical applications. Bucladesine is a membrane-permeable 3′, 5′-cyclic adenosine monophosphate (cAMP) analog. Bucladesine selectively activates cAMP dependentproteinkinase (PKA) by increasing the intracellular level of cAMP. Bucladesine significantly attenuates MDMA-induced increases in hippocampal mitochondrial ROS formation, mitochondrial outer membrane damage, cytochrome c release, and hippocampal ADP/ATP ratio, thereby improving spatial learning and memory impairments. Bucladesine exhibit anti-nociceptive and anti-inflammation effect. Bucladesine can inhibit cancer cells proliferation, induce apoptosis. Bucladesine can be used for the researches of neurological disease, cancer, inflammation .
PKI (5-24),amide (IP20-amide) is a 20-residue peptide that corresponds to the active portion of the heat-stable inhibitor protein of cAMP-dependentproteinkinase. PKI (5-24),amide is a potent cAMP-dependentproteinkinase (PKA) (PKA) inhibitor with a Ki of 2.3 nM .
HA-100 dihydrochloride is a potent proteinkinase inhibitor, with IC50s of 4 μM, 8 μM, 12 μM and 240 μM for cGMP-dependentproteinkinase (PKG), cAMP-dependentproteinkinase (PKA), proteinkinase C (PKC) and MLC-kinase, respectively. HA-100 dihydrochloride also used as a ROCK inhibitor .
8-HA-cAMP is a membrane-permeable cAMP analogue and an activator of cAMP-dependentproteinkinase and PKA I. 8-HA-cAMP exerts metabolic stability towards mammalian cyclic nucleotide-responsive phosphodiesterases .
FSBA (5'-p-Fluorosulfonylbenzoyladenosine) hydrochloride is a covalent modifier and affinity labeling reagent for adenine nucleotide-binding proteins. FSBA hydrochloride covalently attaches to the nucleotide-binding sites of pyruvate kinase, glutamate dehydrogenase, and p56 lck, and to a lysine residue in the ATP-binding site of cAMP-dependentproteinkinase, causing loss of enzymatic activity. FSBA hydrochloride can be used for the research of T lymphoma .
HA-100 hydrochloride is a potent proteinkinase inhibitor, with IC50s of 4 μM, 8 μM, 12 μM and 240 μM for cGMP-dependentproteinkinase (PKG), cAMP-dependentproteinkinase (PKA), proteinkinase C (PKC) and MLC-kinase, respectively. HA-100 hydrochloride also used as a ROCK inhibitor .
PKI(5-24) TFA is a potent, competitive, and synthetic peptide inhibitor of PKA (cAMP-dependentproteinkinase), with a Ki of 2.3 nM. PKI(5-24) TFA corresponds to residues 5-24 in the naturally occurring heat-stable proteinkinase inhibitor .
2-Cl-cAMP is an analog of cAMP and a potent stimulator of cAMP-dependentproteinkinases such as PKA type I and II. 2-Cl-cAMP can be used as starting material for cyclic nucleotides .
2-AHA-cAMP is an analogue of natural signal molecule cAMP and an activator of cAMP-dependentproteinkinase. 2-AHA-cAMP has a free terminal primary amino group, which can be used for coupling to gels or fluorescent dyes .
6-Bn-cAMP is a site-selective activator of cAMP-dependentproteinkinase (PKA) which does not activate Epac. 6-Bn-cAMP increases hydrolytic stability against PDE, esterases, amidases and considerably higher membrane permeability compared to cAMP .
Malantide TFA is a synthetic dodecapeptide derived from the site phosphorylated by cAMP-dependentproteinkinase (PKA) on the β-subunit of phosphorylase kinase. Malantide TFA is a highly specific substrate for PKA with a Km of 15 μM and shows protein inhibitor (PKI) inhibition >90% substrate phosphorylation in various rat tissue extracts . Malantide TFA is also an efficient substrate for PKC with a Km of 16 μM .
Sp-8-PIP cAMP sodium is a non-corresponding isomer of 8-Piperidino-cAMP. 8-Piperidino-cAMP binds with high affinity to site A of the regulatory subunit of cAMP-dependentproteinkinase type I (AI). Sp-8-PIP cAMP sodium can be used as an antagonist of cAMP-induced activation .
Sp-6-Phe-cAMPS is a potent, site-selective and membrane-permeable activator of cAMP-dependentproteinkinase. Sp-6-Phe-cAMPS does not activate exchange factors directly activated by cAMP and can therefore be used as an Epac negative control. Sp-6-Phe-cAMPS can be used in the study of neurodegenerative diseases .
8-Benzylthio-cAMP is a derivative of cyclic adenosine monophosphate (cAMP). 8-Bn-cAMP is a site-selective activator of cAMP-dependentproteinkinases. Compared with cyclic adenosine monophosphate, it is more stable to phosphodiesterase (PDE) hydrolysis and has higher membrane permeability. 8-Bn-cAMP can be used to study the role of cAMP in regulating cell proliferation, differentiation and apoptosis .
Sp-5,6-DCl-cBIMPS is a potent and specific cAMP-dependentproteinkinases(cAMP-PK) activator. Sp-5,6-DCl-cBIMPS stimulates insulin release. Sp-5,6-DCl-cBIMPS inhibits U-46619 (HY-108566)-induced activation of Rho, Gq and G12/G13 in platelets .
Sp-5,6-DCl-cBIMPS sodium is a potent and specific cAMP-dependentproteinkinases(cAMP-PK) activator. Sp-5,6-DCl-cBIMPS sodium stimulates insulin release. Sp-5,6-DCl-cBIMPS sodium inhibits U-46619 (HY-108566)-induced activation of Rho, Gq and G12/G13 in platelets .
GEM231 is an 18mer antisense oligonucleotide targeting the mRNA of the PKA-I (RIα regulatory subunit of cAMP dependentproteinkinase type I ). GEM231 induces cell growth arrest, apoptosis, and differentiation in a variety of cancer cell lines in vitro and in tumors in vivo.
GEM231 sodium is an 18mer antisense oligonucleotide targeting the mRNA of the PKA-I (RIα regulatory subunit of cAMP dependentproteinkinase type I ). GEM231 sodium induces cell growth arrest, apoptosis, and differentiation in a variety of cancer cell lines in vitro and in tumors in vivo.
MDL 27032 is an active site-directed inhibitor of proteinkinase C (PKC) and cAMP-dependentproteinkinase (PKA) with Ki values of 24 and 14.3μM. MDL 27032 can relaxe vascular smooth muscle and can be used as vasodilator .
HA-100 (Standard) is the analytical standard of HA-100 (HY-100984). This product is intended for research and analytical applications. HA-100 is a potent proteinkinase inhibitor, with IC50s of 4 μM, 8 μM, 12 μM and 240 μM for cGMP-dependentproteinkinase (PKG), cAMP-dependentproteinkinase (PKA), proteinkinase C (PKC) and MLC-kinase, respectively. HA-100 also used as a ROCK inhibitor .
NPC-15437 is a selective PKC inhibitor with an IC50 of 19 µM. NPC-15437 competitively inhibits phorbol ester- (Ki of 5 µM) and phosphatidylserine-induced (Ki of 12 µM) PKC activity. NPC-15437 does not inhibits cAMP-dependent or calcium/calmodulin-dependentproteinkinases. NPC-15437 augments TRAIL-induced cell death in non-small cell lung cancer and medulloblastoma cells. NPC-15437 can be used for the research of non-small cell lung cancer, medulloblastoma, and neurological disease .
PKI(5-24) is a potent, competitive, and synthetic peptide inhibitor of PKA (cAMP-dependentproteinkinase), with a Ki of 2.3 nM. PKI(5-24) corresponds to residues 5-24 in the naturally occurring heat-stable proteinkinase inhibitor .
PKA Inhibitor Fragment (6-22) amide is a highly potent and specific competitive inhibitor of PKA, with Ki values of 1.7 nM and 1.6 nM against human and bovine PKA catalytic subunits, respectively. The IC50 of PKA Inhibitor Fragment (6-22) amide targeting bovine PKA is 8.6 nM. PKA Inhibitor Fragment (6-22) amide effectively abolishes PKA activity in mouse brain and spinal cord, and exerts in vivo efficacy via intracerebroventricular administration. PKA Inhibitor Fragment (6-22) amide significantly reverses low-dose morphine analgesic tolerance in mice and blocks photoaffinity labeling of cAMP-dependent proteinkinase. PKA Inhibitor Fragment (6-22) amide can be applied to research in fields related to the mechanism of morphine analgesic tolerance and skin wound healing .
PKA Inhibitor Fragment (6-22) amide TFA is an inhibitor of cAMP-dependentproteinkinase A (PKA), with a Ki of 2.8 nM. PKA Inhibitor Fragment (6-22) amide TFA can significantly reverse antinociceptive tolerance in mice .
Malantide is a synthetic dodecapeptide derived from the site phosphorylated by cAMP-dependentproteinkinase (PKA) on the β-subunit of phosphorylase kinase. Malantide is a highly specific substrate for PKA with a Km of 15 μM and shows protein inhibitor (PKI) inhibition >90% substrate phosphorylation in various rat tissue extracts . Malantide is also an efficient substrate for PKC with a Km of 16 μM .
PKI (5-24),amide (IP20-amide) is a 20-residue peptide that corresponds to the active portion of the heat-stable inhibitor protein of cAMP-dependentproteinkinase. PKI (5-24),amide is a potent cAMP-dependentproteinkinase (PKA) (PKA) inhibitor with a Ki of 2.3 nM .
Kemptide (amide) is a heptapeptide with properties of a cytophilic substrate. Kemptide is a molecule preserving cell membrane intactness, is phosphorylated by PKI, the inhibitory protein specific for cAMP-dependentproteinkinase (PK) .
PKI(5-24) TFA is a potent, competitive, and synthetic peptide inhibitor of PKA (cAMP-dependentproteinkinase), with a Ki of 2.3 nM. PKI(5-24) TFA corresponds to residues 5-24 in the naturally occurring heat-stable proteinkinase inhibitor .
Malantide TFA is a synthetic dodecapeptide derived from the site phosphorylated by cAMP-dependentproteinkinase (PKA) on the β-subunit of phosphorylase kinase. Malantide TFA is a highly specific substrate for PKA with a Km of 15 μM and shows protein inhibitor (PKI) inhibition >90% substrate phosphorylation in various rat tissue extracts . Malantide TFA is also an efficient substrate for PKC with a Km of 16 μM .
The PKI-β protein emerged as an extremely potent competitive inhibitor of cAMP-dependent protein kinase activity. This protein operates at the molecular level, binding to the catalytic subunit of the enzyme after cAMP induces dissociation of its regulatory chain. PKI-beta Protein, Human (His) is the recombinant human-derived PKI-beta protein, expressed by E. coli , with N-6*His labeled tag.
PKACα protein is a key kinase that phosphorylates a variety of substrates, including CDC25B, ABL1, NFKB1, and VASP, affecting a variety of cellular processes, such as cell cycle progression, platelet regulation, and adipogenic differentiation. It also negatively regulates mTORC1 through RPTOR phosphorylation, thereby modulating signaling networks. PKA/PRKACA Protein, Human (sf9, GST) is the recombinant human-derived PKACα protein, expressed by sf9 insect cells , with GST tagged.
PRKX is an important serine/threonine kinase that mediates cAMP signaling and phosphorylates targets such as CREB, SMAD6, and PKD1. It regulates myeloid cell differentiation through SMAD6 phosphorylation, promotes nephrogenesis by enhancing renal epithelial cell migration and tubulogenesis, and actively promotes angiogenesis by affecting endothelial cell proliferation and migration. PRKX Protein, Human (sf9, GST) is the recombinant human-derived PRKX protein, expressed by sf9 insect cells , with N-GST labeled tag.
PRKAR1A protein is a regulatory subunit of cAMP-dependent protein kinase that mediates cellular responses to cAMP signaling.The inactive holoenzyme has two regulatory chains and two catalytic chains.PRKAR1A Protein, Mouse (sf9, His) is the recombinant mouse-derived PRKAR1A protein, expressed by Sf9 insect cells , with C-His labeled tag.
phospho-PKA C alpha/beta/gamma (T197) Antibody (YA7673) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to phospho-PKA C alpha/beta/gamma (T197).
GEM231 is an 18mer antisense oligonucleotide targeting the mRNA of the PKA-I (RIα regulatory subunit of cAMP dependentproteinkinase type I ). GEM231 induces cell growth arrest, apoptosis, and differentiation in a variety of cancer cell lines in vitro and in tumors in vivo.
GEM231 sodium is an 18mer antisense oligonucleotide targeting the mRNA of the PKA-I (RIα regulatory subunit of cAMP dependentproteinkinase type I ). GEM231 sodium induces cell growth arrest, apoptosis, and differentiation in a variety of cancer cell lines in vitro and in tumors in vivo.
Bucladesine (Dibutyryl cAMP; DBcAMP) sodium (GMP) is a Bucladesine sodium (HY-B0764) produced by using GMP guidelines. Bucladesine (Dibutyryl cAMP; DBcAMP) is a membrane-permeable 3′, 5′-cyclic adenosine monophosphate (cAMP) analog. Bucladesine selectively activates cAMP dependentproteinkinase (PKA) by increasing the intracellular level of cAMP. Bucladesine significantly attenuates MDMA-induced increases in hippocampal mitochondrial ROS formation, mitochondrial outer membrane damage, cytochrome c release, and hippocampal ADP/ATP ratio, thereby improving spatial learning and memory impairments. Bucladesine exhibit anti-nociceptive and anti-inflammation effect. Bucladesine can inhibit cancer cells proliferation, induce apoptosis. Bucladesine can be used for the researches of neurological disease, cancer, inflammation .
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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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