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ampk activator gsk621 (MedChemExpress)

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MedChemExpress ampk activator gsk621
Rescue assay with AMPK activator <t>GSK621.</t> A Western blot analysis of autophagy-related proteins under treatment conditions. B LC3B immunofluorescence and semi-quantitative analysis. Data as mean ± SD ( n = 3). * indicates results from one-way ANOVA; # indicates results from two-way ANOVA, * p < 0.05, ** p < 0.01, *** p < 0.001. ## p < 0.01

Rescue assay with AMPK activator <t>GSK621.</t> A Western blot analysis of autophagy-related proteins under treatment conditions. B LC3B immunofluorescence and semi-quantitative analysis. Data as mean ± SD ( n = 3). * indicates results from one-way ANOVA; # indicates results from two-way ANOVA, * p < 0.05, ** p < 0.01, *** p < 0.001. ## p < 0.01

Ampk Activator Gsk621, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ampk+activator+gsk621/GSK621/pmc13107912-60-1-7
Average 94 stars, based on 11 article reviews

ampk activator gsk621 - by Bioz Stars, 2026-10

94/100 stars

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1) Product Images from "Integrating network pharmacology and experimental validation to elucidate the mechanism by which 2-Dihydroailanthone induces HCT116 cell death through suppressing autophagy via the AMPK/mTOR pathway"

Journal: BMC Cancer

doi: 10.1186/s12885-026-15863-0

Rescue assay with AMPK activator GSK621. A Western blot analysis of autophagy-related proteins under treatment conditions. B LC3B immunofluorescence and semi-quantitative analysis. Data as mean ± SD ( n = 3). * indicates results from one-way ANOVA; # indicates results from two-way ANOVA, * p < 0.05, ** p < 0.01, *** p < 0.001. ## p < 0.01

Figure Legend Snippet: Rescue assay with AMPK activator GSK621. A Western blot analysis of autophagy-related proteins under treatment conditions. B LC3B immunofluorescence and semi-quantitative analysis. Data as mean ± SD ( n = 3). * indicates results from one-way ANOVA; # indicates results from two-way ANOVA, * p < 0.05, ** p < 0.01, *** p < 0.001. ## p < 0.01

Techniques Used: Rescue Assay, Western Blot, Immunofluorescence

Rescue Assay:

Article Title: Integrating network pharmacology and experimental validation to elucidate the mechanism by which 2-Dihydroailanthone induces HCT116 cell death through suppressing autophagy via the AMPK/mTOR pathway
Article Snippet: RIPA lysis buffer, BCA protein assay kit, and SDS-PAGE loading buffer were procured from Solarbio Science & Technology Co., Ltd. (Beijing, China).RIPA lysis buffer, BCA protein assay kit, and SDS-PAGE loading buffer were procured from Solarbio Science & Technology Co., Ltd. (Beijing, China).. The AMPK activator GSK621 was obtained from MedChemExpress (Monmouth Junction, NJ, USA).. Staurosporine (Cat# T6680) was sourced from TargetMol Chemicals Inc. (Boston, MA, USA) as a positive apoptosis control.Staurosporine (Cat# T6680) was sourced from TargetMol Chemicals Inc. (Boston, MA, USA) as a positive apoptosis control.

Article Title: Integrating network pharmacology and experimental validation to elucidate the mechanism by which 2-Dihydroailanthone induces HCT116 cell death through suppressing autophagy via the AMPK/mTOR pathway.
Article Snippet: RIPA lysis buffer, BCA protein assay kit, and AR TIC LE IN PR ES S SDS-PAGE loading buffer were procured from Solarbio Science & Technology Co., Ltd. (Beijing, China).RIPA lysis buffer, BCA protein assay kit, and AR TIC LE IN PR ES S SDS-PAGE loading buffer were procured from Solarbio Science & Technology Co., Ltd. (Beijing, China).. The AMPK activator GSK621 was obtained from MedChemExpress (Monmouth Junction, NJ, USA).. Staurosporine (Cat# T6680) was sourced from TargetMol Chemicals Inc. (Boston, MA, USA) as a positive apoptosis control.Staurosporine (Cat# T6680) was sourced from TargetMol Chemicals Inc. (Boston, MA, USA) as a positive apoptosis control.

Western Blot:

Article Title: Integrating network pharmacology and experimental validation to elucidate the mechanism by which 2-Dihydroailanthone induces HCT116 cell death through suppressing autophagy via the AMPK/mTOR pathway.
Article Snippet: RIPA lysis buffer, BCA protein assay kit, and AR TIC LE IN PR ES S SDS-PAGE loading buffer were procured from Solarbio Science & Technology Co., Ltd. (Beijing, China).RIPA lysis buffer, BCA protein assay kit, and AR TIC LE IN PR ES S SDS-PAGE loading buffer were procured from Solarbio Science & Technology Co., Ltd. (Beijing, China).. The AMPK activator GSK621 was obtained from MedChemExpress (Monmouth Junction, NJ, USA).. Staurosporine (Cat# T6680) was sourced from TargetMol Chemicals Inc. (Boston, MA, USA) as a positive apoptosis control.Staurosporine (Cat# T6680) was sourced from TargetMol Chemicals Inc. (Boston, MA, USA) as a positive apoptosis control.

Immunofluorescence:

Article Title: Integrating network pharmacology and experimental validation to elucidate the mechanism by which 2-Dihydroailanthone induces HCT116 cell death through suppressing autophagy via the AMPK/mTOR pathway.
Article Snippet: RIPA lysis buffer, BCA protein assay kit, and AR TIC LE IN PR ES S SDS-PAGE loading buffer were procured from Solarbio Science & Technology Co., Ltd. (Beijing, China).RIPA lysis buffer, BCA protein assay kit, and AR TIC LE IN PR ES S SDS-PAGE loading buffer were procured from Solarbio Science & Technology Co., Ltd. (Beijing, China).. The AMPK activator GSK621 was obtained from MedChemExpress (Monmouth Junction, NJ, USA).. Staurosporine (Cat# T6680) was sourced from TargetMol Chemicals Inc. (Boston, MA, USA) as a positive apoptosis control.Staurosporine (Cat# T6680) was sourced from TargetMol Chemicals Inc. (Boston, MA, USA) as a positive apoptosis control.

Image Search Results

Journal: BMC Cancer

doi: 10.1186/s12885-026-15863-0

Figure Lengend Snippet: Rescue assay with AMPK activator GSK621. A Western blot analysis of autophagy-related proteins under treatment conditions. B LC3B immunofluorescence and semi-quantitative analysis. Data as mean ± SD ( n = 3). * indicates results from one-way ANOVA; # indicates results from two-way ANOVA, * p < 0.05, ** p < 0.01, *** p < 0.001. ## p < 0.01

Article Snippet: The AMPK activator GSK621 was obtained from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Rescue Assay, Western Blot, Immunofluorescence

Figure 1. Direct AMPK activation by GSK621 triggered the UPR in AML (A–C) MOLM-14 cells were incubated with vehicle (DMSO) or 30 mM GSK621 for 6 h. Then, RNA was extracted and gene expression was analyzed. (A) Volcano plot representation of differentially expressed genes. (B) Enrichment scores of the top 10 enriched pathways using Hallmark gene sets in vehicle compared with GSK621 conditions. (C) Gene set enrichment analysis (GSEA) using Gene Ontology (GO) datasets focusing on response to ER stress and PERK-mediated UPR gene sets. FDR, false discovery rate; NES, normalized enrichment score. (D) Schematic representation of PRKAA1 (AMPKa1) and EIF2AK3 (PERK) knockout (KO) cell lines achieved by CRISPR-Cas9 and of the doxycycline (Dox)- inducible PERK rescue in PERKKO cells (referred to as PERKKO + WT), with the color code used throughout the results. Control (CTR) cells were transduced with the same vector expressing a non-targeting sgRNA. (E) CTR or AMPKKO MOLM-14 and OCI-AML2 cells were incubated with 30 mM GSK621 for 6 h. Western blots were done using anti-AMPK, -phospho-ACC, -phospho-eIF2A, -CHOP, -ATF4, -ATF6, -XBP1s, and -b-actin antibodies. Western blots for phospho-ACC (OCI-AML2) and XBP1s (MOLM-14) were performed on separate experiments. (F) PERKKO MOLM-14 cells transduced with a Dox-inducible EIF2AK3 expression vector were cultured without (PERKKO) or with (PERKKO + WT) Dox and then incubated with 30 mM GSK621 for 6 h. Western blots were done using anti-PERK, -phospho-eIF2A, -eIF2A, -ATF4, -CHOP, and -b-actin antibodies.

Journal: Cell reports

Article Title: AMPK-PERK axis represses oxidative metabolism and enhances apoptotic priming of mitochondria in acute myeloid leukemia.

doi: 10.1016/j.celrep.2021.110197

Figure Lengend Snippet: Figure 1. Direct AMPK activation by GSK621 triggered the UPR in AML (A–C) MOLM-14 cells were incubated with vehicle (DMSO) or 30 mM GSK621 for 6 h. Then, RNA was extracted and gene expression was analyzed. (A) Volcano plot representation of differentially expressed genes. (B) Enrichment scores of the top 10 enriched pathways using Hallmark gene sets in vehicle compared with GSK621 conditions. (C) Gene set enrichment analysis (GSEA) using Gene Ontology (GO) datasets focusing on response to ER stress and PERK-mediated UPR gene sets. FDR, false discovery rate; NES, normalized enrichment score. (D) Schematic representation of PRKAA1 (AMPKa1) and EIF2AK3 (PERK) knockout (KO) cell lines achieved by CRISPR-Cas9 and of the doxycycline (Dox)- inducible PERK rescue in PERKKO cells (referred to as PERKKO + WT), with the color code used throughout the results. Control (CTR) cells were transduced with the same vector expressing a non-targeting sgRNA. (E) CTR or AMPKKO MOLM-14 and OCI-AML2 cells were incubated with 30 mM GSK621 for 6 h. Western blots were done using anti-AMPK, -phospho-ACC, -phospho-eIF2A, -CHOP, -ATF4, -ATF6, -XBP1s, and -b-actin antibodies. Western blots for phospho-ACC (OCI-AML2) and XBP1s (MOLM-14) were performed on separate experiments. (F) PERKKO MOLM-14 cells transduced with a Dox-inducible EIF2AK3 expression vector were cultured without (PERKKO) or with (PERKKO + WT) Dox and then incubated with 30 mM GSK621 for 6 h. Western blots were done using anti-PERK, -phospho-eIF2A, -eIF2A, -ATF4, -CHOP, and -b-actin antibodies.

Article Snippet: 2015-08-11-DC Primary Human bone marrow CD34+ normal hematopoietic cells StemCell Technologies 70002.2 Chemicals, peptides, and recombinant proteins AMPK activator GSK621 Selleck chemicals S7898, CAS 1346607-05-3 AMPK activator MK8722 Aobious AOB33226, CAS 1394371-71-1 AMPK activator PF739 Aobious AOB33584, CAS 1852452-14-2 ER stress inducer Thapsigargin Sigma-Aldrich T9033, CAS 67526-95-8 AMPK inhibitor Compound C Selleck chemicals S7306, CAS 1219168-18-9 Bcl2 inhibitor Venetoclax Selleck chemicals S8048, CAS 1257044-40-8 6-Bn-ATP-g-S Biolog Life Science Institute B072, CAS 944834-42-8 p- Nitrobenzyl Mesylate Abcam ab138910, CAS 39628-94-9 GST-tagged human recombinant PERK Thermo-Fischer Scientifc PV5106 GST-tagged human recombinant ULK-1 Thermo-Fischer Scientifc PV6430 GST-tagged human recombinant RSK-2 Thermo-Fischer Scientifc PV3323 PUMA2A New England Peptide EQWAREIGAQARRMAADLNA BAD New England Peptide LWAAQRYGRELRRMSDEFEGSFKGL W-HRK New England Peptide WSSAAQLTAARLKALGDELHQ BIM New England Peptide MRPEIWIAQELRRIGDEFNA PUMA New England Peptide EQWAREIGAQLRRMADDLNA NOXAA New England Peptide AELPPEFAAQLRKIGDKVYC (Continued on next page) e2 Cell Reports 38, 110197, January 4, 2022

Techniques: Activation Assay, Incubation, Gene Expression, Knock-Out, CRISPR, Control, Transduction, Plasmid Preparation, Expressing, Western Blot, Cell Culture

Figure 2. PERK is a critical effector of UPR after AMPK activation in AML (A) Schematic representation of the experimental design for in vitro kinase assays. After expression in HEK293T cells, AMPK heterotrimers containing AMPKa2 M93G are immunoprecipitated (IP) and then incubated with human recombinant PERK (hrPERK) in vitro without or with N6-benzyl-ATPgS. The letter P represents the detection of gS phosphates. N6 ATP, N6-benzyl-ATPgS. (B) In vitro kinase assays using three different recombinant proteins (RSK2, ULK-1, and PERK) and AMPK M93G, without or with N6-benzyl-ATPgS. The AMPK inhibitor compound C was used in AMPK M93G/PERK reactions. Western blots were done using anti-thiophosphate ester, anti-glutathione S-transferase (GST), and anti-AMPKa2 antibodies. (C) Left: schematic representation of anti-phospho-AMPK substrate immunoprecipitation experiments in MOLM-14 cells. Extracted proteins are represented by circles, including PERK (pale green) and AMPK substrates (gray), and anti-phospho-AMPK substrate antibodies are represented in pink. The abundance of PERK in the IPs is then investigated by western blot. Right: CTR or AMPKKO MOLM-14 cells were incubated with vehicle or 30 mM GSK621 for 6 h, and immuno- precipitation using anti-phospho-AMPK substrate was performed and revealed using anti-PERK western blot. Expression of PERK and AMPK was also evaluated in the input. (D) HEK293T cells transduced with a vector allowing the expression of MYC-tagged PERK were incubated with vehicle or 30 mM GSK621 for 6 h. Then, PERK was puriﬁed by immunoprecipitation using anti-MYC beads and submitted to mass spectrometry (MS) analysis. The blue and pink circles represent vehicle and GSK621 conditions, respectively, and the number of phospho-sites identiﬁed exclusively in each condition or commonly to both conditions is indicated. The percentage of identiﬁcation of PERK amino acid sequence by MS is provided for each condition. The bottom is a schematic representation of PERK, highlighting the serine phosphorylations detected in the GSK621 condition (purple) or in both conditions (orange). The dashed purple line indicates that this phosphorylation was detected in the GSK621 condition, but not covered by the analysis in the vehicle condition.

Journal: Cell reports

Article Title: AMPK-PERK axis represses oxidative metabolism and enhances apoptotic priming of mitochondria in acute myeloid leukemia.

doi: 10.1016/j.celrep.2021.110197

Figure Lengend Snippet: Figure 2. PERK is a critical effector of UPR after AMPK activation in AML (A) Schematic representation of the experimental design for in vitro kinase assays. After expression in HEK293T cells, AMPK heterotrimers containing AMPKa2 M93G are immunoprecipitated (IP) and then incubated with human recombinant PERK (hrPERK) in vitro without or with N6-benzyl-ATPgS. The letter P represents the detection of gS phosphates. N6 ATP, N6-benzyl-ATPgS. (B) In vitro kinase assays using three different recombinant proteins (RSK2, ULK-1, and PERK) and AMPK M93G, without or with N6-benzyl-ATPgS. The AMPK inhibitor compound C was used in AMPK M93G/PERK reactions. Western blots were done using anti-thiophosphate ester, anti-glutathione S-transferase (GST), and anti-AMPKa2 antibodies. (C) Left: schematic representation of anti-phospho-AMPK substrate immunoprecipitation experiments in MOLM-14 cells. Extracted proteins are represented by circles, including PERK (pale green) and AMPK substrates (gray), and anti-phospho-AMPK substrate antibodies are represented in pink. The abundance of PERK in the IPs is then investigated by western blot. Right: CTR or AMPKKO MOLM-14 cells were incubated with vehicle or 30 mM GSK621 for 6 h, and immuno- precipitation using anti-phospho-AMPK substrate was performed and revealed using anti-PERK western blot. Expression of PERK and AMPK was also evaluated in the input. (D) HEK293T cells transduced with a vector allowing the expression of MYC-tagged PERK were incubated with vehicle or 30 mM GSK621 for 6 h. Then, PERK was puriﬁed by immunoprecipitation using anti-MYC beads and submitted to mass spectrometry (MS) analysis. The blue and pink circles represent vehicle and GSK621 conditions, respectively, and the number of phospho-sites identiﬁed exclusively in each condition or commonly to both conditions is indicated. The percentage of identiﬁcation of PERK amino acid sequence by MS is provided for each condition. The bottom is a schematic representation of PERK, highlighting the serine phosphorylations detected in the GSK621 condition (purple) or in both conditions (orange). The dashed purple line indicates that this phosphorylation was detected in the GSK621 condition, but not covered by the analysis in the vehicle condition.

Techniques: Activation Assay, In Vitro, Expressing, Immunoprecipitation, Incubation, Recombinant, Western Blot, Transduction, Plasmid Preparation, Mass Spectrometry, Sequencing, Phospho-proteomics

Figure 3. PERK regulates mitochondrial oxidative metabolism after pharmacological AMPK activation (A) Experimental groups in transcriptomic (n = 3), metabolomic (n = 4), and bioenergetic analysis experiments (n = 4). CTR and PERKKO MOLM-14 cells were incubated with 30 mM GSK621. (B) Volcano plot representation of differentially expressed genes between PERKKO (in red) and CTR (in blue). (C) Enrichment plots using GSEA between GSK621-treated CTR and PERKKO conditions using the high OxPHOS signature (Farge et al., 2017).

Journal: Cell reports

Article Title: AMPK-PERK axis represses oxidative metabolism and enhances apoptotic priming of mitochondria in acute myeloid leukemia.

doi: 10.1016/j.celrep.2021.110197

Figure Lengend Snippet: Figure 3. PERK regulates mitochondrial oxidative metabolism after pharmacological AMPK activation (A) Experimental groups in transcriptomic (n = 3), metabolomic (n = 4), and bioenergetic analysis experiments (n = 4). CTR and PERKKO MOLM-14 cells were incubated with 30 mM GSK621. (B) Volcano plot representation of differentially expressed genes between PERKKO (in red) and CTR (in blue). (C) Enrichment plots using GSEA between GSK621-treated CTR and PERKKO conditions using the high OxPHOS signature (Farge et al., 2017).

Techniques: Activation Assay, Incubation

Figure 4. Mitochondrial depolarization and apoptosis induced by AMPK activation are mediated by PERK (A) Patient-derived AML cells (sample PDX#4) were transduced with mCherry-tagged lentiviral vectors, allowing the expression of CTR and EIF2AK3 CRISPR- Cas9 sgRNAs targeting PERK exon 2 or 4 (PERKKO#2 and PERKKO#4). One week after transduction, cells were incubated with vehicle or 30 mM GSK621 for 48 h. Then, the proportion of mCherry-positive cells was quantiﬁed by ﬂow cytometry in each condition among living cells, and results are presented as a ratio between GSK621 and vehicle conditions (n = 4). (B) Flow cytometry TMRM staining in PERKWT or PERKKO MOLM-14 cells incubated with vehicle or 30 mM GSK621 for 24 h. (C) TMRM staining in MOLM-14 AMPKWT or AMPKKO cells incubated with vehicle or GSK621 for 24 h. Results are presented as the proportion of TMRM-negative cells for each condition. (D) PERKWT, PERKKO, or PERKKO + WT MOLM-14 cells were incubated with vehicle or 30 mM GSK621 for 24 h, and TMRM staining was evaluated by ﬂow cytometry (n = 3). (E) CTR, AMPKKO, or PERKKO MOLM-14 cells were treated with GSK621 for the indicated times. Immunoblots were performed using anti-phospho-AMPK, -caspase-3, -PARP, and -b-actin antibodies (n = 3). (F) PDX#4 cells derived from an AML patient were cultured with vehicle or 30 mM GSK621 for 24 h. Immunoblots were performed using anti-caspase-3, -PARP, and -b-actin antibodies.

Journal: Cell reports

Article Title: AMPK-PERK axis represses oxidative metabolism and enhances apoptotic priming of mitochondria in acute myeloid leukemia.

doi: 10.1016/j.celrep.2021.110197

Figure Lengend Snippet: Figure 4. Mitochondrial depolarization and apoptosis induced by AMPK activation are mediated by PERK (A) Patient-derived AML cells (sample PDX#4) were transduced with mCherry-tagged lentiviral vectors, allowing the expression of CTR and EIF2AK3 CRISPR- Cas9 sgRNAs targeting PERK exon 2 or 4 (PERKKO#2 and PERKKO#4). One week after transduction, cells were incubated with vehicle or 30 mM GSK621 for 48 h. Then, the proportion of mCherry-positive cells was quantiﬁed by ﬂow cytometry in each condition among living cells, and results are presented as a ratio between GSK621 and vehicle conditions (n = 4). (B) Flow cytometry TMRM staining in PERKWT or PERKKO MOLM-14 cells incubated with vehicle or 30 mM GSK621 for 24 h. (C) TMRM staining in MOLM-14 AMPKWT or AMPKKO cells incubated with vehicle or GSK621 for 24 h. Results are presented as the proportion of TMRM-negative cells for each condition. (D) PERKWT, PERKKO, or PERKKO + WT MOLM-14 cells were incubated with vehicle or 30 mM GSK621 for 24 h, and TMRM staining was evaluated by ﬂow cytometry (n = 3). (E) CTR, AMPKKO, or PERKKO MOLM-14 cells were treated with GSK621 for the indicated times. Immunoblots were performed using anti-phospho-AMPK, -caspase-3, -PARP, and -b-actin antibodies (n = 3). (F) PDX#4 cells derived from an AML patient were cultured with vehicle or 30 mM GSK621 for 24 h. Immunoblots were performed using anti-caspase-3, -PARP, and -b-actin antibodies.

Techniques: Activation Assay, Derivative Assay, Transduction, Expressing, CRISPR, Incubation, Cytometry, Flow Cytometry, Staining, Western Blot, Cell Culture

Figure 5. Synergy between AMPK activators and the Bcl-2 inhibitor venetoclax in AML (A) AML cell lines (n = 14) were incubated with vehicle, single-agent GSK621 or venetoclax, or the combination of these two agents at different concentrations (n = 4). After 48 h, cell viability was measured using the ATPlite luminescence assay system and results were used to calculate synergy scores with the SynergyFinder software. Blue, orange, and gray histograms represent synergy, antagonism, and neutral impact, respectively.

Journal: Cell reports

Article Title: AMPK-PERK axis represses oxidative metabolism and enhances apoptotic priming of mitochondria in acute myeloid leukemia.

doi: 10.1016/j.celrep.2021.110197

Figure Lengend Snippet: Figure 5. Synergy between AMPK activators and the Bcl-2 inhibitor venetoclax in AML (A) AML cell lines (n = 14) were incubated with vehicle, single-agent GSK621 or venetoclax, or the combination of these two agents at different concentrations (n = 4). After 48 h, cell viability was measured using the ATPlite luminescence assay system and results were used to calculate synergy scores with the SynergyFinder software. Blue, orange, and gray histograms represent synergy, antagonism, and neutral impact, respectively.

Techniques: Incubation, Luminescence Assay, Software

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ampk activator gsk621 (MedChemExpress)

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1) Product Images from "Integrating network pharmacology and experimental validation to elucidate the mechanism by which 2-Dihydroailanthone induces HCT116 cell death through suppressing autophagy via the AMPK/mTOR pathway"

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