ikk inhibitor Search Results


achp  (MedChemExpress)
92
MedChemExpress achp
NLRP3 inflammasome inhibitor hits validation in the speck assay. ( a ) Schematic of the priming protocol. ( b ) Schematic of the activation protocol. ASC-mCherry iBMDM cells were treated with indicated concentrations of ( c ) PU H71, ( d ) MPC-3100, ( e ) momelotinib, ( f ) CEP-33779, ( g ) <t>ACHP</t> or ( h <t>)</t> <t>MLN120B</t> with LPS (1 µg/ml) for 2 h followed by nigericin treatment (10 µM, 2 h) after which PFA was added (priming—blue trace) and specks counted. In a parallel experiment the compounds were added after LPS treatment just prior to nigericin (activation—red trace). The images are representative of the nuclei and speck formation for each compound at 10 µM in both priming and activation protocols. Data are presented as mean ± SEM, n = 3 independent experiments. Data in ( c – h ) was analyzed using GraphPad Prism version 7 software ( https://www.graphpad.com/scientific-software/prism/ ).
Achp, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ikk+inhibitor/ACHP+hydrochloride/pmc08319173-170-40-47
Average 92 stars, based on 1 article reviews
achp - by Bioz Stars, 2026-09
92/100 stars
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ikk2 compound iv  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology ikk2 compound iv
A) U87MGs were untreated, DMSO treated or pretreated with IKK inhibitors (1 µM) for 2 hours and 24 hours later cell viability was measured using the Cell-Titer-Glo Luminescent Cell Viability Assay. B) U87MG cells were pretreated with IKK inhibitors (1 µM), BAY-11-7082, BAY-11-7085 and <t>IKK2-IV</t> and non-IKK specific inhibitors (1 µM), O-Phe and DMC for 2 hours. The conditioned media (media containing inhibitor) was removed and viral infections proceeded (MOI: 0.1) for 1 hour. The viral inoculum was removed and replaced with the conditioned media. The cells were incubated for an additional 24 hours. The supernatants were collected from infected and inhibitor treated cells. Infectious viral titers were determined by plaque assay. O-phe and DMC served as positive control inhibitors. C) Supernatants from B) were subjected to q-RT-PCR analysis to determine viral RNA copies using VEEV specific primers. D) U87MGs were infected at MOI: 0.1 for 1 hour and then treated with BAY-11-7082 (1 µM), BAY-11-7085 (1 µM) and IKK2-IV (1 µM) 4 hours post-infection. Supernatants were collected 24 hours post-infection and viral titers were determined by plaque assay. E) U87MGs were pretreated with IKK inhibitors (1 µM) and non-IKK inhibitors (1 µM) for 2 hours and followed by a 1 hour infection. Conditioned media was replaced and cell viability assay was performed 72 hours later using the Cell-Titer-Glo Luminescent Cell Viability Assay. The red line is representative of the base line for luminescence units, where luminescence units above this value are indicative of increased cell viability. F) U87MGs seeded in an 8-well chambered glass slide were either pre-treated with DMSO or BAY-11-7082 (1 µM) for 2 hours and then infected with UV-TC-83 or TC-83 (MOI: 0.1) for 1 hour. The conditioned media was replaced after the infection. One hour post-infection the cells were fixed and probed for p65 with subsequent incubation with Alexa Fluor 568. The cells were stained with DAPI to observe the nuclei. Images were taken using Nikon Eclipse TE2000-U at 60× magnification and are representative of 2 replicate samples within the same experiment. The graphs represent an average of 3 independent experiments. Error bars for the 3 independent experiments were calculated and are represented thusly. **** p≤0.0001, *** p≤0.005, ** p≤0.01 and * p≤0.05.
Ikk2 Compound Iv, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ikk+inhibitor/IKK-2+Inhibitor+IV/pmc03929299-79-19-22
Average 93 stars, based on 1 article reviews
ikk2 compound iv - by Bioz Stars, 2026-09
93/100 stars
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u0126  (Thermo Fisher)
86
Thermo Fisher u0126
A) U87MGs were untreated, DMSO treated or pretreated with IKK inhibitors (1 µM) for 2 hours and 24 hours later cell viability was measured using the Cell-Titer-Glo Luminescent Cell Viability Assay. B) U87MG cells were pretreated with IKK inhibitors (1 µM), BAY-11-7082, BAY-11-7085 and <t>IKK2-IV</t> and non-IKK specific inhibitors (1 µM), O-Phe and DMC for 2 hours. The conditioned media (media containing inhibitor) was removed and viral infections proceeded (MOI: 0.1) for 1 hour. The viral inoculum was removed and replaced with the conditioned media. The cells were incubated for an additional 24 hours. The supernatants were collected from infected and inhibitor treated cells. Infectious viral titers were determined by plaque assay. O-phe and DMC served as positive control inhibitors. C) Supernatants from B) were subjected to q-RT-PCR analysis to determine viral RNA copies using VEEV specific primers. D) U87MGs were infected at MOI: 0.1 for 1 hour and then treated with BAY-11-7082 (1 µM), BAY-11-7085 (1 µM) and IKK2-IV (1 µM) 4 hours post-infection. Supernatants were collected 24 hours post-infection and viral titers were determined by plaque assay. E) U87MGs were pretreated with IKK inhibitors (1 µM) and non-IKK inhibitors (1 µM) for 2 hours and followed by a 1 hour infection. Conditioned media was replaced and cell viability assay was performed 72 hours later using the Cell-Titer-Glo Luminescent Cell Viability Assay. The red line is representative of the base line for luminescence units, where luminescence units above this value are indicative of increased cell viability. F) U87MGs seeded in an 8-well chambered glass slide were either pre-treated with DMSO or BAY-11-7082 (1 µM) for 2 hours and then infected with UV-TC-83 or TC-83 (MOI: 0.1) for 1 hour. The conditioned media was replaced after the infection. One hour post-infection the cells were fixed and probed for p65 with subsequent incubation with Alexa Fluor 568. The cells were stained with DAPI to observe the nuclei. Images were taken using Nikon Eclipse TE2000-U at 60× magnification and are representative of 2 replicate samples within the same experiment. The graphs represent an average of 3 independent experiments. Error bars for the 3 independent experiments were calculated and are represented thusly. **** p≤0.0001, *** p≤0.005, ** p≤0.01 and * p≤0.05.
U0126, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ikk+inhibitor/IKK-2+Inhibitor+V/pmc03126544-68-12-33
Average 86 stars, based on 1 article reviews
u0126 - by Bioz Stars, 2026-09
86/100 stars
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iκb kinase 2 ikk 2 inhibitor vi  (Santa Cruz Biotechnology)
92
Santa Cruz Biotechnology iκb kinase 2 ikk 2 inhibitor vi
A) U87MGs were untreated, DMSO treated or pretreated with IKK inhibitors (1 µM) for 2 hours and 24 hours later cell viability was measured using the Cell-Titer-Glo Luminescent Cell Viability Assay. B) U87MG cells were pretreated with IKK inhibitors (1 µM), BAY-11-7082, BAY-11-7085 and <t>IKK2-IV</t> and non-IKK specific inhibitors (1 µM), O-Phe and DMC for 2 hours. The conditioned media (media containing inhibitor) was removed and viral infections proceeded (MOI: 0.1) for 1 hour. The viral inoculum was removed and replaced with the conditioned media. The cells were incubated for an additional 24 hours. The supernatants were collected from infected and inhibitor treated cells. Infectious viral titers were determined by plaque assay. O-phe and DMC served as positive control inhibitors. C) Supernatants from B) were subjected to q-RT-PCR analysis to determine viral RNA copies using VEEV specific primers. D) U87MGs were infected at MOI: 0.1 for 1 hour and then treated with BAY-11-7082 (1 µM), BAY-11-7085 (1 µM) and IKK2-IV (1 µM) 4 hours post-infection. Supernatants were collected 24 hours post-infection and viral titers were determined by plaque assay. E) U87MGs were pretreated with IKK inhibitors (1 µM) and non-IKK inhibitors (1 µM) for 2 hours and followed by a 1 hour infection. Conditioned media was replaced and cell viability assay was performed 72 hours later using the Cell-Titer-Glo Luminescent Cell Viability Assay. The red line is representative of the base line for luminescence units, where luminescence units above this value are indicative of increased cell viability. F) U87MGs seeded in an 8-well chambered glass slide were either pre-treated with DMSO or BAY-11-7082 (1 µM) for 2 hours and then infected with UV-TC-83 or TC-83 (MOI: 0.1) for 1 hour. The conditioned media was replaced after the infection. One hour post-infection the cells were fixed and probed for p65 with subsequent incubation with Alexa Fluor 568. The cells were stained with DAPI to observe the nuclei. Images were taken using Nikon Eclipse TE2000-U at 60× magnification and are representative of 2 replicate samples within the same experiment. The graphs represent an average of 3 independent experiments. Error bars for the 3 independent experiments were calculated and are represented thusly. **** p≤0.0001, *** p≤0.005, ** p≤0.01 and * p≤0.05.
Iκb Kinase 2 Ikk 2 Inhibitor Vi, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ikk+inhibitor/IKK-2+Inhibitor+VI/pm38494067-65-6-11
Average 92 stars, based on 1 article reviews
iκb kinase 2 ikk 2 inhibitor vi - by Bioz Stars, 2026-09
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anti ikkb  (ProSci Incorporated)
90
ProSci Incorporated anti ikkb
A) U87MGs were untreated, DMSO treated or pretreated with IKK inhibitors (1 µM) for 2 hours and 24 hours later cell viability was measured using the Cell-Titer-Glo Luminescent Cell Viability Assay. B) U87MG cells were pretreated with IKK inhibitors (1 µM), BAY-11-7082, BAY-11-7085 and <t>IKK2-IV</t> and non-IKK specific inhibitors (1 µM), O-Phe and DMC for 2 hours. The conditioned media (media containing inhibitor) was removed and viral infections proceeded (MOI: 0.1) for 1 hour. The viral inoculum was removed and replaced with the conditioned media. The cells were incubated for an additional 24 hours. The supernatants were collected from infected and inhibitor treated cells. Infectious viral titers were determined by plaque assay. O-phe and DMC served as positive control inhibitors. C) Supernatants from B) were subjected to q-RT-PCR analysis to determine viral RNA copies using VEEV specific primers. D) U87MGs were infected at MOI: 0.1 for 1 hour and then treated with BAY-11-7082 (1 µM), BAY-11-7085 (1 µM) and IKK2-IV (1 µM) 4 hours post-infection. Supernatants were collected 24 hours post-infection and viral titers were determined by plaque assay. E) U87MGs were pretreated with IKK inhibitors (1 µM) and non-IKK inhibitors (1 µM) for 2 hours and followed by a 1 hour infection. Conditioned media was replaced and cell viability assay was performed 72 hours later using the Cell-Titer-Glo Luminescent Cell Viability Assay. The red line is representative of the base line for luminescence units, where luminescence units above this value are indicative of increased cell viability. F) U87MGs seeded in an 8-well chambered glass slide were either pre-treated with DMSO or BAY-11-7082 (1 µM) for 2 hours and then infected with UV-TC-83 or TC-83 (MOI: 0.1) for 1 hour. The conditioned media was replaced after the infection. One hour post-infection the cells were fixed and probed for p65 with subsequent incubation with Alexa Fluor 568. The cells were stained with DAPI to observe the nuclei. Images were taken using Nikon Eclipse TE2000-U at 60× magnification and are representative of 2 replicate samples within the same experiment. The graphs represent an average of 3 independent experiments. Error bars for the 3 independent experiments were calculated and are represented thusly. **** p≤0.0001, *** p≤0.005, ** p≤0.01 and * p≤0.05.
Anti Ikkb, supplied by ProSci Incorporated, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ikk+inhibitor/IKKb+Antibody/pm23084358-246-36-35
Average 90 stars, based on 1 article reviews
anti ikkb - by Bioz Stars, 2026-09
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ikk inhibitor x  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology ikk inhibitor x
A) U87MGs were untreated, DMSO treated or pretreated with IKK inhibitors (1 µM) for 2 hours and 24 hours later cell viability was measured using the Cell-Titer-Glo Luminescent Cell Viability Assay. B) U87MG cells were pretreated with IKK inhibitors (1 µM), BAY-11-7082, BAY-11-7085 and <t>IKK2-IV</t> and non-IKK specific inhibitors (1 µM), O-Phe and DMC for 2 hours. The conditioned media (media containing inhibitor) was removed and viral infections proceeded (MOI: 0.1) for 1 hour. The viral inoculum was removed and replaced with the conditioned media. The cells were incubated for an additional 24 hours. The supernatants were collected from infected and inhibitor treated cells. Infectious viral titers were determined by plaque assay. O-phe and DMC served as positive control inhibitors. C) Supernatants from B) were subjected to q-RT-PCR analysis to determine viral RNA copies using VEEV specific primers. D) U87MGs were infected at MOI: 0.1 for 1 hour and then treated with BAY-11-7082 (1 µM), BAY-11-7085 (1 µM) and IKK2-IV (1 µM) 4 hours post-infection. Supernatants were collected 24 hours post-infection and viral titers were determined by plaque assay. E) U87MGs were pretreated with IKK inhibitors (1 µM) and non-IKK inhibitors (1 µM) for 2 hours and followed by a 1 hour infection. Conditioned media was replaced and cell viability assay was performed 72 hours later using the Cell-Titer-Glo Luminescent Cell Viability Assay. The red line is representative of the base line for luminescence units, where luminescence units above this value are indicative of increased cell viability. F) U87MGs seeded in an 8-well chambered glass slide were either pre-treated with DMSO or BAY-11-7082 (1 µM) for 2 hours and then infected with UV-TC-83 or TC-83 (MOI: 0.1) for 1 hour. The conditioned media was replaced after the infection. One hour post-infection the cells were fixed and probed for p65 with subsequent incubation with Alexa Fluor 568. The cells were stained with DAPI to observe the nuclei. Images were taken using Nikon Eclipse TE2000-U at 60× magnification and are representative of 2 replicate samples within the same experiment. The graphs represent an average of 3 independent experiments. Error bars for the 3 independent experiments were calculated and are represented thusly. **** p≤0.0001, *** p≤0.005, ** p≤0.01 and * p≤0.05.
Ikk Inhibitor X, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ikk+inhibitor/IKK+Inhibitor+X/pm26213325-33-0-8
Average 93 stars, based on 1 article reviews
ikk inhibitor x - by Bioz Stars, 2026-09
93/100 stars
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fluorophenyl 2 ureidothiophene 3 carboxylic acid amide utc toronto research chemicals inc ontario canada  (Toronto Research Chemicals)
91
Toronto Research Chemicals fluorophenyl 2 ureidothiophene 3 carboxylic acid amide utc toronto research chemicals inc ontario canada
A) U87MGs were untreated, DMSO treated or pretreated with IKK inhibitors (1 µM) for 2 hours and 24 hours later cell viability was measured using the Cell-Titer-Glo Luminescent Cell Viability Assay. B) U87MG cells were pretreated with IKK inhibitors (1 µM), BAY-11-7082, BAY-11-7085 and <t>IKK2-IV</t> and non-IKK specific inhibitors (1 µM), O-Phe and DMC for 2 hours. The conditioned media (media containing inhibitor) was removed and viral infections proceeded (MOI: 0.1) for 1 hour. The viral inoculum was removed and replaced with the conditioned media. The cells were incubated for an additional 24 hours. The supernatants were collected from infected and inhibitor treated cells. Infectious viral titers were determined by plaque assay. O-phe and DMC served as positive control inhibitors. C) Supernatants from B) were subjected to q-RT-PCR analysis to determine viral RNA copies using VEEV specific primers. D) U87MGs were infected at MOI: 0.1 for 1 hour and then treated with BAY-11-7082 (1 µM), BAY-11-7085 (1 µM) and IKK2-IV (1 µM) 4 hours post-infection. Supernatants were collected 24 hours post-infection and viral titers were determined by plaque assay. E) U87MGs were pretreated with IKK inhibitors (1 µM) and non-IKK inhibitors (1 µM) for 2 hours and followed by a 1 hour infection. Conditioned media was replaced and cell viability assay was performed 72 hours later using the Cell-Titer-Glo Luminescent Cell Viability Assay. The red line is representative of the base line for luminescence units, where luminescence units above this value are indicative of increased cell viability. F) U87MGs seeded in an 8-well chambered glass slide were either pre-treated with DMSO or BAY-11-7082 (1 µM) for 2 hours and then infected with UV-TC-83 or TC-83 (MOI: 0.1) for 1 hour. The conditioned media was replaced after the infection. One hour post-infection the cells were fixed and probed for p65 with subsequent incubation with Alexa Fluor 568. The cells were stained with DAPI to observe the nuclei. Images were taken using Nikon Eclipse TE2000-U at 60× magnification and are representative of 2 replicate samples within the same experiment. The graphs represent an average of 3 independent experiments. Error bars for the 3 independent experiments were calculated and are represented thusly. **** p≤0.0001, *** p≤0.005, ** p≤0.01 and * p≤0.05.
Fluorophenyl 2 Ureidothiophene 3 Carboxylic Acid Amide Utc Toronto Research Chemicals Inc Ontario Canada, supplied by Toronto Research Chemicals, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ikk+inhibitor/TPCA-1/pmc07773657-66-31-36
Average 91 stars, based on 1 article reviews
fluorophenyl 2 ureidothiophene 3 carboxylic acid amide utc toronto research chemicals inc ontario canada - by Bioz Stars, 2026-09
91/100 stars
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ikkα  (Boster Bio)
90
Boster Bio ikkα
A) U87MGs were untreated, DMSO treated or pretreated with IKK inhibitors (1 µM) for 2 hours and 24 hours later cell viability was measured using the Cell-Titer-Glo Luminescent Cell Viability Assay. B) U87MG cells were pretreated with IKK inhibitors (1 µM), BAY-11-7082, BAY-11-7085 and <t>IKK2-IV</t> and non-IKK specific inhibitors (1 µM), O-Phe and DMC for 2 hours. The conditioned media (media containing inhibitor) was removed and viral infections proceeded (MOI: 0.1) for 1 hour. The viral inoculum was removed and replaced with the conditioned media. The cells were incubated for an additional 24 hours. The supernatants were collected from infected and inhibitor treated cells. Infectious viral titers were determined by plaque assay. O-phe and DMC served as positive control inhibitors. C) Supernatants from B) were subjected to q-RT-PCR analysis to determine viral RNA copies using VEEV specific primers. D) U87MGs were infected at MOI: 0.1 for 1 hour and then treated with BAY-11-7082 (1 µM), BAY-11-7085 (1 µM) and IKK2-IV (1 µM) 4 hours post-infection. Supernatants were collected 24 hours post-infection and viral titers were determined by plaque assay. E) U87MGs were pretreated with IKK inhibitors (1 µM) and non-IKK inhibitors (1 µM) for 2 hours and followed by a 1 hour infection. Conditioned media was replaced and cell viability assay was performed 72 hours later using the Cell-Titer-Glo Luminescent Cell Viability Assay. The red line is representative of the base line for luminescence units, where luminescence units above this value are indicative of increased cell viability. F) U87MGs seeded in an 8-well chambered glass slide were either pre-treated with DMSO or BAY-11-7082 (1 µM) for 2 hours and then infected with UV-TC-83 or TC-83 (MOI: 0.1) for 1 hour. The conditioned media was replaced after the infection. One hour post-infection the cells were fixed and probed for p65 with subsequent incubation with Alexa Fluor 568. The cells were stained with DAPI to observe the nuclei. Images were taken using Nikon Eclipse TE2000-U at 60× magnification and are representative of 2 replicate samples within the same experiment. The graphs represent an average of 3 independent experiments. Error bars for the 3 independent experiments were calculated and are represented thusly. **** p≤0.0001, *** p≤0.005, ** p≤0.01 and * p≤0.05.
Ikkα, supplied by Boster Bio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ikk+inhibitor/Anti-IKK+alpha+CHUK+Antibody/pmc12442614-258-6-16
Average 90 stars, based on 1 article reviews
ikkα - by Bioz Stars, 2026-09
90/100 stars
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ikk 2 inhibitor  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology ikk 2 inhibitor
A) U87MGs were untreated, DMSO treated or pretreated with IKK inhibitors (1 µM) for 2 hours and 24 hours later cell viability was measured using the Cell-Titer-Glo Luminescent Cell Viability Assay. B) U87MG cells were pretreated with IKK inhibitors (1 µM), BAY-11-7082, BAY-11-7085 and <t>IKK2-IV</t> and non-IKK specific inhibitors (1 µM), O-Phe and DMC for 2 hours. The conditioned media (media containing inhibitor) was removed and viral infections proceeded (MOI: 0.1) for 1 hour. The viral inoculum was removed and replaced with the conditioned media. The cells were incubated for an additional 24 hours. The supernatants were collected from infected and inhibitor treated cells. Infectious viral titers were determined by plaque assay. O-phe and DMC served as positive control inhibitors. C) Supernatants from B) were subjected to q-RT-PCR analysis to determine viral RNA copies using VEEV specific primers. D) U87MGs were infected at MOI: 0.1 for 1 hour and then treated with BAY-11-7082 (1 µM), BAY-11-7085 (1 µM) and IKK2-IV (1 µM) 4 hours post-infection. Supernatants were collected 24 hours post-infection and viral titers were determined by plaque assay. E) U87MGs were pretreated with IKK inhibitors (1 µM) and non-IKK inhibitors (1 µM) for 2 hours and followed by a 1 hour infection. Conditioned media was replaced and cell viability assay was performed 72 hours later using the Cell-Titer-Glo Luminescent Cell Viability Assay. The red line is representative of the base line for luminescence units, where luminescence units above this value are indicative of increased cell viability. F) U87MGs seeded in an 8-well chambered glass slide were either pre-treated with DMSO or BAY-11-7082 (1 µM) for 2 hours and then infected with UV-TC-83 or TC-83 (MOI: 0.1) for 1 hour. The conditioned media was replaced after the infection. One hour post-infection the cells were fixed and probed for p65 with subsequent incubation with Alexa Fluor 568. The cells were stained with DAPI to observe the nuclei. Images were taken using Nikon Eclipse TE2000-U at 60× magnification and are representative of 2 replicate samples within the same experiment. The graphs represent an average of 3 independent experiments. Error bars for the 3 independent experiments were calculated and are represented thusly. **** p≤0.0001, *** p≤0.005, ** p≤0.01 and * p≤0.05.
Ikk 2 Inhibitor, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ikk+inhibitor/IKK-2+Inhibitor+XI/pmc06289618-122-6-13
Average 93 stars, based on 1 article reviews
ikk 2 inhibitor - by Bioz Stars, 2026-09
93/100 stars
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ikkβ  (Boster Bio)
93
Boster Bio ikkβ
SHPL-49 exerts anti-inflammatory effects by suppressing the NF-κB signaling pathway. ( A ) Immunohistochemical staining images of NF-κB and IL-6 in brain tissue sections from rats subjected to pMCAO and treated with SHPL-49 (15 mg/kg) and ED (7.5 mg/kg) for three days, Scale = 100 μm. ( B ) The IODs for NF-κB and IL-6 immunohistochemistry in brain tissue sections for each treatment group. ( C ) Representative Western blot of NF-κB in the nucleus and cytoplasm of OGD-BV2 cells after treatment with SHPL-49 (200 μM). ( D ) Quantification of the Western blot results. ( E ) Immunofluorescence staining pattern of NF-κB in OGD-BV2 cells following treatment with SHPL-49 (200 μM); Scale = 10 μm. ( F ) Quantification of the average fluorescence intensity of NF-κB in the nucleus of BV2 cells. ( G ) Representative Western blot of <t>p-IKKβ,</t> <t>IKKβ,</t> <t>p-IκBα,</t> and IκBα proteins in OGD-BV2 cells after treatment with SHPL-49 (200 μM). ( H ) Quantification of the Western blot results. ( I ) The protein expression levels of inflammatory factors IL-6, IL-1β, and iNOS in the supernatant of OGD-BV2 cells following treatment with SHPL-49 (200 μM). Data are presented as means ± SD with n = 6 per group. *** p < 0.001 vs. Ctrl; ## p < 0.01, ### p < 0.001 vs. OGD.
Ikkβ, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ikk+inhibitor/Anti-IKK+Beta+(phospho-Y188)+IKBKB+Antibody/pmc11941147-108-44-46
Average 93 stars, based on 1 article reviews
ikkβ - by Bioz Stars, 2026-09
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phospho ikkα β ser176 180 antibodies  (Boster Bio)
90
Boster Bio phospho ikkα β ser176 180 antibodies
SHPL-49 exerts anti-inflammatory effects by suppressing the NF-κB signaling pathway. ( A ) Immunohistochemical staining images of NF-κB and IL-6 in brain tissue sections from rats subjected to pMCAO and treated with SHPL-49 (15 mg/kg) and ED (7.5 mg/kg) for three days, Scale = 100 μm. ( B ) The IODs for NF-κB and IL-6 immunohistochemistry in brain tissue sections for each treatment group. ( C ) Representative Western blot of NF-κB in the nucleus and cytoplasm of OGD-BV2 cells after treatment with SHPL-49 (200 μM). ( D ) Quantification of the Western blot results. ( E ) Immunofluorescence staining pattern of NF-κB in OGD-BV2 cells following treatment with SHPL-49 (200 μM); Scale = 10 μm. ( F ) Quantification of the average fluorescence intensity of NF-κB in the nucleus of BV2 cells. ( G ) Representative Western blot of <t>p-IKKβ,</t> <t>IKKβ,</t> <t>p-IκBα,</t> and IκBα proteins in OGD-BV2 cells after treatment with SHPL-49 (200 μM). ( H ) Quantification of the Western blot results. ( I ) The protein expression levels of inflammatory factors IL-6, IL-1β, and iNOS in the supernatant of OGD-BV2 cells following treatment with SHPL-49 (200 μM). Data are presented as means ± SD with n = 6 per group. *** p < 0.001 vs. Ctrl; ## p < 0.01, ### p < 0.001 vs. OGD.
Phospho Ikkα β Ser176 180 Antibodies, supplied by Boster Bio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ikk+inhibitor/Anti-IKK+Alpha+%2F+Beta+(phospho-S176%2F177)+CHUK+Antibody/pm40548883-341-10-16
Average 90 stars, based on 1 article reviews
phospho ikkα β ser176 180 antibodies - by Bioz Stars, 2026-09
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rabbit anti ikkα antibody  (Boster Bio)
90
Boster Bio rabbit anti ikkα antibody
IL-1β increases <t>IKKα</t> nuclear translocation <t>and</t> <t>phosphorylation</t> of serine 10 on histone H3, while NAPA attenuates these signalling events. ( A ) Overlapping signals of nuclear counterstaining (DAPI) and IKKα detected via an Alexa Fluor 555 secondary antibody: the colocalized signals indicate that NAPA addition is effective in reducing nuclear translocation of IKKα. ( B ) Upper pictures: left, western blot of anti-phosphorylated serine 10 of histone H3, along with GAPDH as a loading control and right: densitometric analysis of the signal showing the different pattern of H3pSer10 accumulation in CTR (circle), IL-1β (square) or IL-1β + NAPA (triangle) conditions. Lower images: specificity of the signal obtained with the anti-H3 phosphorylated serine 10: 20x field pictures of chondrocytes grown on coverslips in the bottom of wells at time 0 in control (upper row) or IL-1β stimulated conditions (lower row): Green: IKKα detected with an Alexa Fluor 488 anti-rabbit antibody; red: H3pSer10 signal detected with an Alexa Fluor 555 anti-mouse antibody; blue: nuclear DNA stained with Hoechst 33342 and merged images.
Rabbit Anti Ikkα Antibody, supplied by Boster Bio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ikk+inhibitor/Anti-IKK+alpha+CHUK+Rabbit+Monoclonal+Antibody/pmc06753094-114-7-10
Average 90 stars, based on 1 article reviews
rabbit anti ikkα antibody - by Bioz Stars, 2026-09
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Image Search Results


NLRP3 inflammasome inhibitor hits validation in the speck assay. ( a ) Schematic of the priming protocol. ( b ) Schematic of the activation protocol. ASC-mCherry iBMDM cells were treated with indicated concentrations of ( c ) PU H71, ( d ) MPC-3100, ( e ) momelotinib, ( f ) CEP-33779, ( g ) ACHP or ( h ) MLN120B with LPS (1 µg/ml) for 2 h followed by nigericin treatment (10 µM, 2 h) after which PFA was added (priming—blue trace) and specks counted. In a parallel experiment the compounds were added after LPS treatment just prior to nigericin (activation—red trace). The images are representative of the nuclei and speck formation for each compound at 10 µM in both priming and activation protocols. Data are presented as mean ± SEM, n = 3 independent experiments. Data in ( c – h ) was analyzed using GraphPad Prism version 7 software ( https://www.graphpad.com/scientific-software/prism/ ).

Journal: Scientific Reports

Article Title: A phenotypic high-content, high-throughput screen identifies inhibitors of NLRP3 inflammasome activation

doi: 10.1038/s41598-021-94850-w

Figure Lengend Snippet: NLRP3 inflammasome inhibitor hits validation in the speck assay. ( a ) Schematic of the priming protocol. ( b ) Schematic of the activation protocol. ASC-mCherry iBMDM cells were treated with indicated concentrations of ( c ) PU H71, ( d ) MPC-3100, ( e ) momelotinib, ( f ) CEP-33779, ( g ) ACHP or ( h ) MLN120B with LPS (1 µg/ml) for 2 h followed by nigericin treatment (10 µM, 2 h) after which PFA was added (priming—blue trace) and specks counted. In a parallel experiment the compounds were added after LPS treatment just prior to nigericin (activation—red trace). The images are representative of the nuclei and speck formation for each compound at 10 µM in both priming and activation protocols. Data are presented as mean ± SEM, n = 3 independent experiments. Data in ( c – h ) was analyzed using GraphPad Prism version 7 software ( https://www.graphpad.com/scientific-software/prism/ ).

Article Snippet: MCC950 (CAS number: 256373-96-3) was purchased from Tocris; PU H71 (Cat. number: 1856) and momelotinib (CAS number: 1056634-68-4) were purchased from Axon Medchem; MPC-3100 (Cat. number: A4063) was purchased from ApexBio; MLN120B (CAS number: 783348-36-7), CEP-33779 (CAS number: 958025-66-6) and ACHP (CAS number: 406209-26-5) were purchased from MedChemExpress.

Techniques: Biomarker Discovery, Activation Assay, Software

A) U87MGs were untreated, DMSO treated or pretreated with IKK inhibitors (1 µM) for 2 hours and 24 hours later cell viability was measured using the Cell-Titer-Glo Luminescent Cell Viability Assay. B) U87MG cells were pretreated with IKK inhibitors (1 µM), BAY-11-7082, BAY-11-7085 and IKK2-IV and non-IKK specific inhibitors (1 µM), O-Phe and DMC for 2 hours. The conditioned media (media containing inhibitor) was removed and viral infections proceeded (MOI: 0.1) for 1 hour. The viral inoculum was removed and replaced with the conditioned media. The cells were incubated for an additional 24 hours. The supernatants were collected from infected and inhibitor treated cells. Infectious viral titers were determined by plaque assay. O-phe and DMC served as positive control inhibitors. C) Supernatants from B) were subjected to q-RT-PCR analysis to determine viral RNA copies using VEEV specific primers. D) U87MGs were infected at MOI: 0.1 for 1 hour and then treated with BAY-11-7082 (1 µM), BAY-11-7085 (1 µM) and IKK2-IV (1 µM) 4 hours post-infection. Supernatants were collected 24 hours post-infection and viral titers were determined by plaque assay. E) U87MGs were pretreated with IKK inhibitors (1 µM) and non-IKK inhibitors (1 µM) for 2 hours and followed by a 1 hour infection. Conditioned media was replaced and cell viability assay was performed 72 hours later using the Cell-Titer-Glo Luminescent Cell Viability Assay. The red line is representative of the base line for luminescence units, where luminescence units above this value are indicative of increased cell viability. F) U87MGs seeded in an 8-well chambered glass slide were either pre-treated with DMSO or BAY-11-7082 (1 µM) for 2 hours and then infected with UV-TC-83 or TC-83 (MOI: 0.1) for 1 hour. The conditioned media was replaced after the infection. One hour post-infection the cells were fixed and probed for p65 with subsequent incubation with Alexa Fluor 568. The cells were stained with DAPI to observe the nuclei. Images were taken using Nikon Eclipse TE2000-U at 60× magnification and are representative of 2 replicate samples within the same experiment. The graphs represent an average of 3 independent experiments. Error bars for the 3 independent experiments were calculated and are represented thusly. **** p≤0.0001, *** p≤0.005, ** p≤0.01 and * p≤0.05.

Journal: PLoS ONE

Article Title: The Role of IKKβ in Venezuelan Equine Encephalitis Virus Infection

doi: 10.1371/journal.pone.0086745

Figure Lengend Snippet: A) U87MGs were untreated, DMSO treated or pretreated with IKK inhibitors (1 µM) for 2 hours and 24 hours later cell viability was measured using the Cell-Titer-Glo Luminescent Cell Viability Assay. B) U87MG cells were pretreated with IKK inhibitors (1 µM), BAY-11-7082, BAY-11-7085 and IKK2-IV and non-IKK specific inhibitors (1 µM), O-Phe and DMC for 2 hours. The conditioned media (media containing inhibitor) was removed and viral infections proceeded (MOI: 0.1) for 1 hour. The viral inoculum was removed and replaced with the conditioned media. The cells were incubated for an additional 24 hours. The supernatants were collected from infected and inhibitor treated cells. Infectious viral titers were determined by plaque assay. O-phe and DMC served as positive control inhibitors. C) Supernatants from B) were subjected to q-RT-PCR analysis to determine viral RNA copies using VEEV specific primers. D) U87MGs were infected at MOI: 0.1 for 1 hour and then treated with BAY-11-7082 (1 µM), BAY-11-7085 (1 µM) and IKK2-IV (1 µM) 4 hours post-infection. Supernatants were collected 24 hours post-infection and viral titers were determined by plaque assay. E) U87MGs were pretreated with IKK inhibitors (1 µM) and non-IKK inhibitors (1 µM) for 2 hours and followed by a 1 hour infection. Conditioned media was replaced and cell viability assay was performed 72 hours later using the Cell-Titer-Glo Luminescent Cell Viability Assay. The red line is representative of the base line for luminescence units, where luminescence units above this value are indicative of increased cell viability. F) U87MGs seeded in an 8-well chambered glass slide were either pre-treated with DMSO or BAY-11-7082 (1 µM) for 2 hours and then infected with UV-TC-83 or TC-83 (MOI: 0.1) for 1 hour. The conditioned media was replaced after the infection. One hour post-infection the cells were fixed and probed for p65 with subsequent incubation with Alexa Fluor 568. The cells were stained with DAPI to observe the nuclei. Images were taken using Nikon Eclipse TE2000-U at 60× magnification and are representative of 2 replicate samples within the same experiment. The graphs represent an average of 3 independent experiments. Error bars for the 3 independent experiments were calculated and are represented thusly. **** p≤0.0001, *** p≤0.005, ** p≤0.01 and * p≤0.05.

Article Snippet: The next day the cells were pretreated with inhibitors, BAY-11-7082 (Sigma, Catalogue No. B5556), BAY-11-7085 (Sigma, Catalogue No. B5681), IKK2 compound IV (Santa Cruz Biotechnology, Catalogue No. sc-203083), 5,7-dihydroxy-4-methylcoumarin (DMC) (Santa Cruz Biotechnology, Catalogue No. sc-254863), o -phenanthroline (O-Phe) (Santa Cruz Biotechnology, Catalogue No. sc-202256) for 2 hours.

Techniques: Cell Viability Assay, Incubation, Infection, Plaque Assay, Positive Control, Reverse Transcription Polymerase Chain Reaction, Viability Assay, Staining

A) Neurons were pre-treated with DMSO or with IKK inhibitors (1 µM) for 2 hours and 24 hours later cell viability was measured using the Cell-Titer-Glo Luminescent Cell Viability Assay. B) Neurons were pretreated with IKK inhibitors (1 µM), BAY-11-7082, BAY-11-7085 and IKK2-IV for 2 hours. Following the pretreatment, the conditioned media (media containing inhibitor) was removed and the cells infected at MOI: 1 for 1 hour. The viral inoculum was removed and the conditioned media replaced. Supernatants were collected 24 hours post-infection, and infectious viral titers were determined by plaque assay. C) Neurons were pretreated with IKK inhibitors (1 µM) for 2 hours and infected with TC-83 for 1 hour. Conditioned media was replaced after removal of the viral inoculum. Cell viability assay was performed 48 hours later using the Cell-Titer-Glo Luminescent Cell Viability Assay. The red line is representative of the base line for luminescence units, such that luminescence units above this are indicative of increased cell viability. The graphs are representative of 2 independent experiments. Error bars for the independent experiments were calculated and are represented thusly. *** p≤0.005, ** p≤0.01 and * p≤0.05.

Journal: PLoS ONE

Article Title: The Role of IKKβ in Venezuelan Equine Encephalitis Virus Infection

doi: 10.1371/journal.pone.0086745

Figure Lengend Snippet: A) Neurons were pre-treated with DMSO or with IKK inhibitors (1 µM) for 2 hours and 24 hours later cell viability was measured using the Cell-Titer-Glo Luminescent Cell Viability Assay. B) Neurons were pretreated with IKK inhibitors (1 µM), BAY-11-7082, BAY-11-7085 and IKK2-IV for 2 hours. Following the pretreatment, the conditioned media (media containing inhibitor) was removed and the cells infected at MOI: 1 for 1 hour. The viral inoculum was removed and the conditioned media replaced. Supernatants were collected 24 hours post-infection, and infectious viral titers were determined by plaque assay. C) Neurons were pretreated with IKK inhibitors (1 µM) for 2 hours and infected with TC-83 for 1 hour. Conditioned media was replaced after removal of the viral inoculum. Cell viability assay was performed 48 hours later using the Cell-Titer-Glo Luminescent Cell Viability Assay. The red line is representative of the base line for luminescence units, such that luminescence units above this are indicative of increased cell viability. The graphs are representative of 2 independent experiments. Error bars for the independent experiments were calculated and are represented thusly. *** p≤0.005, ** p≤0.01 and * p≤0.05.

Article Snippet: The next day the cells were pretreated with inhibitors, BAY-11-7082 (Sigma, Catalogue No. B5556), BAY-11-7085 (Sigma, Catalogue No. B5681), IKK2 compound IV (Santa Cruz Biotechnology, Catalogue No. sc-203083), 5,7-dihydroxy-4-methylcoumarin (DMC) (Santa Cruz Biotechnology, Catalogue No. sc-254863), o -phenanthroline (O-Phe) (Santa Cruz Biotechnology, Catalogue No. sc-202256) for 2 hours.

Techniques: Cell Viability Assay, Infection, Plaque Assay, Viability Assay

A) U87MG cells (A) or neuronal rat AP7 cells (B) were pretreated with 1 µM IKK inhibitors, BAY-11-7082, BAY-11-7085 and IKK2-IV for 2 hours. The cells were infected with the wild type strain of VEEV (TrD) at a MOI: 0.1 (A) or MOI: 1 (B) for 1 hour. The conditioned media (media containing inhibitor) was removed prior to the viral infections and replaced after the viral inoculum was removed. The cells were incubated for an additional 24 hours. The supernatants were collected from all samples and viral titers were determined by plaque assay. The graphs are representative of 2 independent experiments. Error bars (Standard deviations) for 3 replicates within the 2 independent experiments were calculated and are represented thusly. ** p≤0.01.

Journal: PLoS ONE

Article Title: The Role of IKKβ in Venezuelan Equine Encephalitis Virus Infection

doi: 10.1371/journal.pone.0086745

Figure Lengend Snippet: A) U87MG cells (A) or neuronal rat AP7 cells (B) were pretreated with 1 µM IKK inhibitors, BAY-11-7082, BAY-11-7085 and IKK2-IV for 2 hours. The cells were infected with the wild type strain of VEEV (TrD) at a MOI: 0.1 (A) or MOI: 1 (B) for 1 hour. The conditioned media (media containing inhibitor) was removed prior to the viral infections and replaced after the viral inoculum was removed. The cells were incubated for an additional 24 hours. The supernatants were collected from all samples and viral titers were determined by plaque assay. The graphs are representative of 2 independent experiments. Error bars (Standard deviations) for 3 replicates within the 2 independent experiments were calculated and are represented thusly. ** p≤0.01.

Article Snippet: The next day the cells were pretreated with inhibitors, BAY-11-7082 (Sigma, Catalogue No. B5556), BAY-11-7085 (Sigma, Catalogue No. B5681), IKK2 compound IV (Santa Cruz Biotechnology, Catalogue No. sc-203083), 5,7-dihydroxy-4-methylcoumarin (DMC) (Santa Cruz Biotechnology, Catalogue No. sc-254863), o -phenanthroline (O-Phe) (Santa Cruz Biotechnology, Catalogue No. sc-202256) for 2 hours.

Techniques: Infection, Incubation, Plaque Assay

SHPL-49 exerts anti-inflammatory effects by suppressing the NF-κB signaling pathway. ( A ) Immunohistochemical staining images of NF-κB and IL-6 in brain tissue sections from rats subjected to pMCAO and treated with SHPL-49 (15 mg/kg) and ED (7.5 mg/kg) for three days, Scale = 100 μm. ( B ) The IODs for NF-κB and IL-6 immunohistochemistry in brain tissue sections for each treatment group. ( C ) Representative Western blot of NF-κB in the nucleus and cytoplasm of OGD-BV2 cells after treatment with SHPL-49 (200 μM). ( D ) Quantification of the Western blot results. ( E ) Immunofluorescence staining pattern of NF-κB in OGD-BV2 cells following treatment with SHPL-49 (200 μM); Scale = 10 μm. ( F ) Quantification of the average fluorescence intensity of NF-κB in the nucleus of BV2 cells. ( G ) Representative Western blot of p-IKKβ, IKKβ, p-IκBα, and IκBα proteins in OGD-BV2 cells after treatment with SHPL-49 (200 μM). ( H ) Quantification of the Western blot results. ( I ) The protein expression levels of inflammatory factors IL-6, IL-1β, and iNOS in the supernatant of OGD-BV2 cells following treatment with SHPL-49 (200 μM). Data are presented as means ± SD with n = 6 per group. *** p < 0.001 vs. Ctrl; ## p < 0.01, ### p < 0.001 vs. OGD.

Journal: Cells

Article Title: Salidroside Derivative SHPL-49 Exerts Anti-Neuroinflammatory Effects by Modulating Excessive Autophagy in Microglia

doi: 10.3390/cells14060425

Figure Lengend Snippet: SHPL-49 exerts anti-inflammatory effects by suppressing the NF-κB signaling pathway. ( A ) Immunohistochemical staining images of NF-κB and IL-6 in brain tissue sections from rats subjected to pMCAO and treated with SHPL-49 (15 mg/kg) and ED (7.5 mg/kg) for three days, Scale = 100 μm. ( B ) The IODs for NF-κB and IL-6 immunohistochemistry in brain tissue sections for each treatment group. ( C ) Representative Western blot of NF-κB in the nucleus and cytoplasm of OGD-BV2 cells after treatment with SHPL-49 (200 μM). ( D ) Quantification of the Western blot results. ( E ) Immunofluorescence staining pattern of NF-κB in OGD-BV2 cells following treatment with SHPL-49 (200 μM); Scale = 10 μm. ( F ) Quantification of the average fluorescence intensity of NF-κB in the nucleus of BV2 cells. ( G ) Representative Western blot of p-IKKβ, IKKβ, p-IκBα, and IκBα proteins in OGD-BV2 cells after treatment with SHPL-49 (200 μM). ( H ) Quantification of the Western blot results. ( I ) The protein expression levels of inflammatory factors IL-6, IL-1β, and iNOS in the supernatant of OGD-BV2 cells following treatment with SHPL-49 (200 μM). Data are presented as means ± SD with n = 6 per group. *** p < 0.001 vs. Ctrl; ## p < 0.01, ### p < 0.001 vs. OGD.

Article Snippet: Membranes were incubated with 5% nonfat milk (Beyotime, Shanghai, China, P0216) or BSA (Beyotime, Shanghai, China, ST023) followed by overnight incubation at 4 °C with the following primary antibodies: NF-κB (1:1000, Cell Signaling Technology, MA, USA, D14E12), p-IKKβ (1:1000, UpingBio, Hangzhou, Zhejiang, China, YP-Ab-14443), IKKβ (1:1000, Boster, Wuhan, China, BM4875), p-IκBα (1:1000, UpingBio, Zhejiang, China, YP-Ab-01253), IKBα (1:1000, UpingBio, Zhejiang, China, YP-Ab-01830), P62/SQSTM1 (1:1000, Boster, Wuhan, China, BM4385), LC3B (1:200, PTMab, Zhejiang, China, PTM-6384), ATG5 (1:1000, Cell Signaling Technology, MA, USA, D5F5U), Bclin1 (1:1000, Cell Signaling Technology, MA, USA, D40C5), LAMP2 (1:200, UpingBio, Zhejiang, China, YP-Ab-14094), Bax (1:1000, Cell Signaling Technology, MA, USA, 14796), Bcl-2 (1:1000, AiFang biologic, Hunan, China, AF0060), Cleaved caspase-3 (1:1000, Cell Signaling Technology, MA, USA, 9661S), and Cleaved caspase-9 (1:1000, Cell Signaling Technology, MA, USA, 9507S).

Techniques: Immunohistochemical staining, Staining, Immunohistochemistry, Western Blot, Immunofluorescence, Fluorescence, Expressing

IL-1β increases IKKα nuclear translocation and phosphorylation of serine 10 on histone H3, while NAPA attenuates these signalling events. ( A ) Overlapping signals of nuclear counterstaining (DAPI) and IKKα detected via an Alexa Fluor 555 secondary antibody: the colocalized signals indicate that NAPA addition is effective in reducing nuclear translocation of IKKα. ( B ) Upper pictures: left, western blot of anti-phosphorylated serine 10 of histone H3, along with GAPDH as a loading control and right: densitometric analysis of the signal showing the different pattern of H3pSer10 accumulation in CTR (circle), IL-1β (square) or IL-1β + NAPA (triangle) conditions. Lower images: specificity of the signal obtained with the anti-H3 phosphorylated serine 10: 20x field pictures of chondrocytes grown on coverslips in the bottom of wells at time 0 in control (upper row) or IL-1β stimulated conditions (lower row): Green: IKKα detected with an Alexa Fluor 488 anti-rabbit antibody; red: H3pSer10 signal detected with an Alexa Fluor 555 anti-mouse antibody; blue: nuclear DNA stained with Hoechst 33342 and merged images.

Journal: Scientific Reports

Article Title: The N-Acetyl Phenylalanine Glucosamine Derivative Attenuates the Inflammatory/Catabolic Environment in a Chondrocyte-Synoviocyte Co-Culture System

doi: 10.1038/s41598-019-49188-9

Figure Lengend Snippet: IL-1β increases IKKα nuclear translocation and phosphorylation of serine 10 on histone H3, while NAPA attenuates these signalling events. ( A ) Overlapping signals of nuclear counterstaining (DAPI) and IKKα detected via an Alexa Fluor 555 secondary antibody: the colocalized signals indicate that NAPA addition is effective in reducing nuclear translocation of IKKα. ( B ) Upper pictures: left, western blot of anti-phosphorylated serine 10 of histone H3, along with GAPDH as a loading control and right: densitometric analysis of the signal showing the different pattern of H3pSer10 accumulation in CTR (circle), IL-1β (square) or IL-1β + NAPA (triangle) conditions. Lower images: specificity of the signal obtained with the anti-H3 phosphorylated serine 10: 20x field pictures of chondrocytes grown on coverslips in the bottom of wells at time 0 in control (upper row) or IL-1β stimulated conditions (lower row): Green: IKKα detected with an Alexa Fluor 488 anti-rabbit antibody; red: H3pSer10 signal detected with an Alexa Fluor 555 anti-mouse antibody; blue: nuclear DNA stained with Hoechst 33342 and merged images.

Article Snippet: IKKα staining was performed with 5 μg/ml rabbit anti-IKKα antibody (BOSTER Biological Technology, Freemont, CA, USA), while the extent of phosphorylation of serine 10 of histone H3 was evaluated with 5 μg/ml anti-phospho-histone H3, (Ser10), (mouse monoclonal, Upstate–Millipore) overnight at 4 °C.

Techniques: Translocation Assay, Phospho-proteomics, Western Blot, Control, Staining