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Cellgro elispot assay medium
HIV- and CMV-specific CMI in HIV- infected children on HAART. Data represent results of assays performed with PBMC from 12 HIV-seropositive pediatric patients, 9 of whom were also CMV seropositive. Results for each patient contributed 2 to 6 data points. Dotted lines indicate thresholds for positive results. Solid lines indicate medians. (A) HIV LPA responses were significantly lower than those for CMV with respect to proportion of positive results ( P = 0.02) and amplitude of response ( P = 0.006). (B) The difference in the proportions of positive <t>ELISPOT</t> assay results for HIV and CMV did not reach statistical significance ( P = 0.06), but the magnitude of the response was significantly lower for HIV than for CMV ( P = 0.007).(C) ICCK responses were similar for HIV- and CMV-seropositive patients with respect to proportion of positive results ( P = 0.16) and magnitude of the response ( P = 0.3).
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Images

1) Product Images from "Immunity to Human Immunodeficiency Virus (HIV) in Children with Chronic HIV Infection Receiving Highly Active Antiretroviral Therapy"

Article Title: Immunity to Human Immunodeficiency Virus (HIV) in Children with Chronic HIV Infection Receiving Highly Active Antiretroviral Therapy

Journal: Clinical and Diagnostic Laboratory Immunology

doi: 10.1128/CDLI.10.5.821-825.2003

HIV- and CMV-specific CMI in HIV- infected children on HAART. Data represent results of assays performed with PBMC from 12 HIV-seropositive pediatric patients, 9 of whom were also CMV seropositive. Results for each patient contributed 2 to 6 data points. Dotted lines indicate thresholds for positive results. Solid lines indicate medians. (A) HIV LPA responses were significantly lower than those for CMV with respect to proportion of positive results ( P = 0.02) and amplitude of response ( P = 0.006). (B) The difference in the proportions of positive ELISPOT assay results for HIV and CMV did not reach statistical significance ( P = 0.06), but the magnitude of the response was significantly lower for HIV than for CMV ( P = 0.007).(C) ICCK responses were similar for HIV- and CMV-seropositive patients with respect to proportion of positive results ( P = 0.16) and magnitude of the response ( P = 0.3).
Figure Legend Snippet: HIV- and CMV-specific CMI in HIV- infected children on HAART. Data represent results of assays performed with PBMC from 12 HIV-seropositive pediatric patients, 9 of whom were also CMV seropositive. Results for each patient contributed 2 to 6 data points. Dotted lines indicate thresholds for positive results. Solid lines indicate medians. (A) HIV LPA responses were significantly lower than those for CMV with respect to proportion of positive results ( P = 0.02) and amplitude of response ( P = 0.006). (B) The difference in the proportions of positive ELISPOT assay results for HIV and CMV did not reach statistical significance ( P = 0.06), but the magnitude of the response was significantly lower for HIV than for CMV ( P = 0.007).(C) ICCK responses were similar for HIV- and CMV-seropositive patients with respect to proportion of positive results ( P = 0.16) and magnitude of the response ( P = 0.3).

Techniques Used: Infection, Enzyme-linked Immunospot

2) Product Images from "EFFICACY OF PANOBINOSTAT AND MARIZOMIB IN ACUTE MYELOID LEUKEMIA AND BORTEZOMIB-RESISTANT MODELS"

Article Title: EFFICACY OF PANOBINOSTAT AND MARIZOMIB IN ACUTE MYELOID LEUKEMIA AND BORTEZOMIB-RESISTANT MODELS

Journal: Leukemia research

doi: 10.1016/j.leukres.2014.12.014

Panobinostat induces higher DNA fragmentation and caspase-3 activation than vorinostat in AML and bortezomib-resistant MM cells A) AML3, ML-1, and RPMI-8226vr10 cells were exposed to increasing concentrations of panobinostat and vorinostat for 24 hours, followed by PI staining for analysis of DNA fragmentation. B) ML-1 and RPMI-8226vr10 cells were treated for 24 hours with equimolar doses (1μM) of panobinostat and vorinostat. Caspase-3/7 activity was measured using the DEVD-amc fluorogenic substrate. C) ML-1 cells well treated with panobinostat or vorinostat for 24 hours, followed by Western blotting for cleaved caspase-3 (**p
Figure Legend Snippet: Panobinostat induces higher DNA fragmentation and caspase-3 activation than vorinostat in AML and bortezomib-resistant MM cells A) AML3, ML-1, and RPMI-8226vr10 cells were exposed to increasing concentrations of panobinostat and vorinostat for 24 hours, followed by PI staining for analysis of DNA fragmentation. B) ML-1 and RPMI-8226vr10 cells were treated for 24 hours with equimolar doses (1μM) of panobinostat and vorinostat. Caspase-3/7 activity was measured using the DEVD-amc fluorogenic substrate. C) ML-1 cells well treated with panobinostat or vorinostat for 24 hours, followed by Western blotting for cleaved caspase-3 (**p

Techniques Used: Activation Assay, Staining, Activity Assay, Western Blot

Panobinostat is able to overcome β5 proteasome subunit overexpression associated with proteasome inhibitor resistance A) Top panels: AML3 and ML-1 cells were exposed to increasing concentrations of bortezomib or marizomib for 24 hours. After treatment, cell viability was assessed by trypan blue exclusion. Bottom panels: Cells were treated with equimolar drug concentrations (500 nM for AML3 and 1 μM for ML-1) for 24 hours, then stained with PI and analyzed for DNA fragmentation (NS = not significant). B) AML3 and ML-1 cell lysates were probed for the proteasome subunit β5. C) ML-1 cells treated 24 hours with equimolar (1 μM) panobinostat or vorinostat were analyzed for expression of the proteasome subunit β5. D) Lysates from parental RPMI-8226 and RMPMI-8226vr10 cells were examined for expression of the proteasome subunit β5. E) RPMI-8226vr10 cells treated for 24 hours with 1 μM panobinostat, 1 μM vorinostat, and 10 nM bortezomib alone and in combination were analyzed for protein expression of the proteasome subunit β5.
Figure Legend Snippet: Panobinostat is able to overcome β5 proteasome subunit overexpression associated with proteasome inhibitor resistance A) Top panels: AML3 and ML-1 cells were exposed to increasing concentrations of bortezomib or marizomib for 24 hours. After treatment, cell viability was assessed by trypan blue exclusion. Bottom panels: Cells were treated with equimolar drug concentrations (500 nM for AML3 and 1 μM for ML-1) for 24 hours, then stained with PI and analyzed for DNA fragmentation (NS = not significant). B) AML3 and ML-1 cell lysates were probed for the proteasome subunit β5. C) ML-1 cells treated 24 hours with equimolar (1 μM) panobinostat or vorinostat were analyzed for expression of the proteasome subunit β5. D) Lysates from parental RPMI-8226 and RMPMI-8226vr10 cells were examined for expression of the proteasome subunit β5. E) RPMI-8226vr10 cells treated for 24 hours with 1 μM panobinostat, 1 μM vorinostat, and 10 nM bortezomib alone and in combination were analyzed for protein expression of the proteasome subunit β5.

Techniques Used: Over Expression, Staining, Expressing

3) Product Images from "Dual Targeting of CDK4 and ARK5 Using a Novel Kinase Inhibitor ON123300 Exerts Potent Anticancer Activity against Multiple Myeloma"

Article Title: Dual Targeting of CDK4 and ARK5 Using a Novel Kinase Inhibitor ON123300 Exerts Potent Anticancer Activity against Multiple Myeloma

Journal: Cancer research

doi: 10.1158/0008-5472.CAN-15-2934

Anti–multiple myeloma activity of ON123300, a multitargeted kinase inhibitor. A, structure of ON123300-8-Cyclopentyl-2-[4-(4-methylpiperazin-1-yl)-phenylamino]-7-oxo-7,8-dihydro-pyrido[2,3-d]pyrimidine-6-carbonitrile. B, ARK5 protein expression was confirmed by Western blot in multiple myeloma (MM) cell lines and primary cells. ARK5 level was significantly higher in the cell lines MM1.S, NCI-H929, JJN3, EJM, and in primary samples with 1q21 deletion and cMAF translocation. The numerical values indicate densitometric analysis of band intensity using ImageJ. C, ON123300 decreased cell viability by approximately 30% to 70% (IC 50 , 50–200 nmol/L) in 8/8 multiple myeloma cell lines examined. On the basis of IC 50 of 50 nmol/L, we could separate the cell lines into two groups: four cell lines (MM.1R, KMS11, RPMI-8226, and ARP1) had IC 50 of 50–150 nmol/L, and four cell lines (MM1.S, EJM, JJN3, and NCI-H929) were very sensitive (IC 50
Figure Legend Snippet: Anti–multiple myeloma activity of ON123300, a multitargeted kinase inhibitor. A, structure of ON123300-8-Cyclopentyl-2-[4-(4-methylpiperazin-1-yl)-phenylamino]-7-oxo-7,8-dihydro-pyrido[2,3-d]pyrimidine-6-carbonitrile. B, ARK5 protein expression was confirmed by Western blot in multiple myeloma (MM) cell lines and primary cells. ARK5 level was significantly higher in the cell lines MM1.S, NCI-H929, JJN3, EJM, and in primary samples with 1q21 deletion and cMAF translocation. The numerical values indicate densitometric analysis of band intensity using ImageJ. C, ON123300 decreased cell viability by approximately 30% to 70% (IC 50 , 50–200 nmol/L) in 8/8 multiple myeloma cell lines examined. On the basis of IC 50 of 50 nmol/L, we could separate the cell lines into two groups: four cell lines (MM.1R, KMS11, RPMI-8226, and ARP1) had IC 50 of 50–150 nmol/L, and four cell lines (MM1.S, EJM, JJN3, and NCI-H929) were very sensitive (IC 50

Techniques Used: Activity Assay, Expressing, Western Blot, Translocation Assay

4) Product Images from "Genome-Wide Detection of Genes Targeted by Non-Ig Somatic Hypermutation in Lymphoma"

Article Title: Genome-Wide Detection of Genes Targeted by Non-Ig Somatic Hypermutation in Lymphoma

Journal: PLoS ONE

doi: 10.1371/journal.pone.0040332

Novel promoter SNVs target important B cell genes in DLBCL. iPAGE analysis using Gene Ontology database (#) [43] or a lymphoid specific gene set database (*) [44] showing strong enrichment of genes that are important for germinal center B cells and DLBCLs contain novel promoter SNVs in OCI-Ly1 and OCI-Ly8 cells.
Figure Legend Snippet: Novel promoter SNVs target important B cell genes in DLBCL. iPAGE analysis using Gene Ontology database (#) [43] or a lymphoid specific gene set database (*) [44] showing strong enrichment of genes that are important for germinal center B cells and DLBCLs contain novel promoter SNVs in OCI-Ly1 and OCI-Ly8 cells.

Techniques Used:

Detection of SHM. (A). A snapshot of UCSC genome browser showing H3K4me3 ChIP-seq reads density at BACH2 promoter. The top three tracks represent SHMs, novel SNVs, and known SNVs (SNP132) detected in OCI-Ly1 by applying SHMseeqer to OCI-Ly1 H3K4me3 ChIP-seq short reads. (B). OCI-Ly1 H3K4me3 ChIP-seq short reads spanning chr6 position 91062534 ( BACH2 intron 1) where a SHM was detected (shaded). (C). Sanger sequencing trace showing detection of both G (wild-type) and A (mutation) at chr6 position 91062534 in OCI-Ly1. (D). Overall validation rates of selected SNVs/SHMs within BACH2 , BCL2 , BCL6 , BTG2 , and MYO1E loci. N indicates number of SNVs/SHMs validated by Sanger sequencing in each locus.
Figure Legend Snippet: Detection of SHM. (A). A snapshot of UCSC genome browser showing H3K4me3 ChIP-seq reads density at BACH2 promoter. The top three tracks represent SHMs, novel SNVs, and known SNVs (SNP132) detected in OCI-Ly1 by applying SHMseeqer to OCI-Ly1 H3K4me3 ChIP-seq short reads. (B). OCI-Ly1 H3K4me3 ChIP-seq short reads spanning chr6 position 91062534 ( BACH2 intron 1) where a SHM was detected (shaded). (C). Sanger sequencing trace showing detection of both G (wild-type) and A (mutation) at chr6 position 91062534 in OCI-Ly1. (D). Overall validation rates of selected SNVs/SHMs within BACH2 , BCL2 , BCL6 , BTG2 , and MYO1E loci. N indicates number of SNVs/SHMs validated by Sanger sequencing in each locus.

Techniques Used: Chromatin Immunoprecipitation, Sequencing, Mutagenesis

Aberrant SHMs affect promoter activity. The effects of selected SHMs on BCL6 or BACH2 promoter activities were tested by dual luciferase assay in OCI-Ly1. Reporter activity of promoter bearing individual SHM was normalized to reporter activity of the wild-type promoter. Error bars indicate standard errors of three independent experiments.
Figure Legend Snippet: Aberrant SHMs affect promoter activity. The effects of selected SHMs on BCL6 or BACH2 promoter activities were tested by dual luciferase assay in OCI-Ly1. Reporter activity of promoter bearing individual SHM was normalized to reporter activity of the wild-type promoter. Error bars indicate standard errors of three independent experiments.

Techniques Used: Activity Assay, Luciferase

5) Product Images from "Dual Targeting of CDK4 and ARK5 Using a Novel Kinase Inhibitor ON123300 Exerts Potent Anticancer Activity against Multiple Myeloma"

Article Title: Dual Targeting of CDK4 and ARK5 Using a Novel Kinase Inhibitor ON123300 Exerts Potent Anticancer Activity against Multiple Myeloma

Journal: Cancer research

doi: 10.1158/0008-5472.CAN-15-2934

Anti–multiple myeloma activity of ON123300, a multitargeted kinase inhibitor. A, structure of ON123300-8-Cyclopentyl-2-[4-(4-methylpiperazin-1-yl)-phenylamino]-7-oxo-7,8-dihydro-pyrido[2,3-d]pyrimidine-6-carbonitrile. B, ARK5 protein expression was confirmed by Western blot in multiple myeloma (MM) cell lines and primary cells. ARK5 level was significantly higher in the cell lines MM1.S, NCI-H929, JJN3, EJM, and in primary samples with 1q21 deletion and cMAF translocation. The numerical values indicate densitometric analysis of band intensity using ImageJ. C, ON123300 decreased cell viability by approximately 30% to 70% (IC 50 , 50–200 nmol/L) in 8/8 multiple myeloma cell lines examined. On the basis of IC 50 of 50 nmol/L, we could separate the cell lines into two groups: four cell lines (MM.1R, KMS11, RPMI-8226, and ARP1) had IC 50 of 50–150 nmol/L, and four cell lines (MM1.S, EJM, JJN3, and NCI-H929) were very sensitive (IC 50
Figure Legend Snippet: Anti–multiple myeloma activity of ON123300, a multitargeted kinase inhibitor. A, structure of ON123300-8-Cyclopentyl-2-[4-(4-methylpiperazin-1-yl)-phenylamino]-7-oxo-7,8-dihydro-pyrido[2,3-d]pyrimidine-6-carbonitrile. B, ARK5 protein expression was confirmed by Western blot in multiple myeloma (MM) cell lines and primary cells. ARK5 level was significantly higher in the cell lines MM1.S, NCI-H929, JJN3, EJM, and in primary samples with 1q21 deletion and cMAF translocation. The numerical values indicate densitometric analysis of band intensity using ImageJ. C, ON123300 decreased cell viability by approximately 30% to 70% (IC 50 , 50–200 nmol/L) in 8/8 multiple myeloma cell lines examined. On the basis of IC 50 of 50 nmol/L, we could separate the cell lines into two groups: four cell lines (MM.1R, KMS11, RPMI-8226, and ARP1) had IC 50 of 50–150 nmol/L, and four cell lines (MM1.S, EJM, JJN3, and NCI-H929) were very sensitive (IC 50

Techniques Used: Activity Assay, Expressing, Western Blot, Translocation Assay

6) Product Images from "EFFICACY OF PANOBINOSTAT AND MARIZOMIB IN ACUTE MYELOID LEUKEMIA AND BORTEZOMIB-RESISTANT MODELS"

Article Title: EFFICACY OF PANOBINOSTAT AND MARIZOMIB IN ACUTE MYELOID LEUKEMIA AND BORTEZOMIB-RESISTANT MODELS

Journal: Leukemia research

doi: 10.1016/j.leukres.2014.12.014

Panobinostat induces higher DNA fragmentation and caspase-3 activation than vorinostat in AML and bortezomib-resistant MM cells A) AML3, ML-1, and RPMI-8226vr10 cells were exposed to increasing concentrations of panobinostat and vorinostat for 24 hours, followed by PI staining for analysis of DNA fragmentation. B) ML-1 and RPMI-8226vr10 cells were treated for 24 hours with equimolar doses (1μM) of panobinostat and vorinostat. Caspase-3/7 activity was measured using the DEVD-amc fluorogenic substrate. C) ML-1 cells well treated with panobinostat or vorinostat for 24 hours, followed by Western blotting for cleaved caspase-3 (**p
Figure Legend Snippet: Panobinostat induces higher DNA fragmentation and caspase-3 activation than vorinostat in AML and bortezomib-resistant MM cells A) AML3, ML-1, and RPMI-8226vr10 cells were exposed to increasing concentrations of panobinostat and vorinostat for 24 hours, followed by PI staining for analysis of DNA fragmentation. B) ML-1 and RPMI-8226vr10 cells were treated for 24 hours with equimolar doses (1μM) of panobinostat and vorinostat. Caspase-3/7 activity was measured using the DEVD-amc fluorogenic substrate. C) ML-1 cells well treated with panobinostat or vorinostat for 24 hours, followed by Western blotting for cleaved caspase-3 (**p

Techniques Used: Activation Assay, Staining, Activity Assay, Western Blot

Panobinostat is able to overcome β5 proteasome subunit overexpression associated with proteasome inhibitor resistance A) Top panels: AML3 and ML-1 cells were exposed to increasing concentrations of bortezomib or marizomib for 24 hours. After treatment, cell viability was assessed by trypan blue exclusion. Bottom panels: Cells were treated with equimolar drug concentrations (500 nM for AML3 and 1 μM for ML-1) for 24 hours, then stained with PI and analyzed for DNA fragmentation (NS = not significant). B) AML3 and ML-1 cell lysates were probed for the proteasome subunit β5. C) ML-1 cells treated 24 hours with equimolar (1 μM) panobinostat or vorinostat were analyzed for expression of the proteasome subunit β5. D) Lysates from parental RPMI-8226 and RMPMI-8226vr10 cells were examined for expression of the proteasome subunit β5. E) RPMI-8226vr10 cells treated for 24 hours with 1 μM panobinostat, 1 μM vorinostat, and 10 nM bortezomib alone and in combination were analyzed for protein expression of the proteasome subunit β5.
Figure Legend Snippet: Panobinostat is able to overcome β5 proteasome subunit overexpression associated with proteasome inhibitor resistance A) Top panels: AML3 and ML-1 cells were exposed to increasing concentrations of bortezomib or marizomib for 24 hours. After treatment, cell viability was assessed by trypan blue exclusion. Bottom panels: Cells were treated with equimolar drug concentrations (500 nM for AML3 and 1 μM for ML-1) for 24 hours, then stained with PI and analyzed for DNA fragmentation (NS = not significant). B) AML3 and ML-1 cell lysates were probed for the proteasome subunit β5. C) ML-1 cells treated 24 hours with equimolar (1 μM) panobinostat or vorinostat were analyzed for expression of the proteasome subunit β5. D) Lysates from parental RPMI-8226 and RMPMI-8226vr10 cells were examined for expression of the proteasome subunit β5. E) RPMI-8226vr10 cells treated for 24 hours with 1 μM panobinostat, 1 μM vorinostat, and 10 nM bortezomib alone and in combination were analyzed for protein expression of the proteasome subunit β5.

Techniques Used: Over Expression, Staining, Expressing

7) Product Images from "EFFICACY OF PANOBINOSTAT AND MARIZOMIB IN ACUTE MYELOID LEUKEMIA AND BORTEZOMIB-RESISTANT MODELS"

Article Title: EFFICACY OF PANOBINOSTAT AND MARIZOMIB IN ACUTE MYELOID LEUKEMIA AND BORTEZOMIB-RESISTANT MODELS

Journal: Leukemia research

doi: 10.1016/j.leukres.2014.12.014

Panobinostat is able to overcome β5 proteasome subunit overexpression associated with proteasome inhibitor resistance A) Top panels: AML3 and ML-1 cells were exposed to increasing concentrations of bortezomib or marizomib for 24 hours. After treatment, cell viability was assessed by trypan blue exclusion. Bottom panels: Cells were treated with equimolar drug concentrations (500 nM for AML3 and 1 μM for ML-1) for 24 hours, then stained with PI and analyzed for DNA fragmentation (NS = not significant). B) AML3 and ML-1 cell lysates were probed for the proteasome subunit β5. C) ML-1 cells treated 24 hours with equimolar (1 μM) panobinostat or vorinostat were analyzed for expression of the proteasome subunit β5. D) Lysates from parental RPMI-8226 and RMPMI-8226vr10 cells were examined for expression of the proteasome subunit β5. E) RPMI-8226vr10 cells treated for 24 hours with 1 μM panobinostat, 1 μM vorinostat, and 10 nM bortezomib alone and in combination were analyzed for protein expression of the proteasome subunit β5.
Figure Legend Snippet: Panobinostat is able to overcome β5 proteasome subunit overexpression associated with proteasome inhibitor resistance A) Top panels: AML3 and ML-1 cells were exposed to increasing concentrations of bortezomib or marizomib for 24 hours. After treatment, cell viability was assessed by trypan blue exclusion. Bottom panels: Cells were treated with equimolar drug concentrations (500 nM for AML3 and 1 μM for ML-1) for 24 hours, then stained with PI and analyzed for DNA fragmentation (NS = not significant). B) AML3 and ML-1 cell lysates were probed for the proteasome subunit β5. C) ML-1 cells treated 24 hours with equimolar (1 μM) panobinostat or vorinostat were analyzed for expression of the proteasome subunit β5. D) Lysates from parental RPMI-8226 and RMPMI-8226vr10 cells were examined for expression of the proteasome subunit β5. E) RPMI-8226vr10 cells treated for 24 hours with 1 μM panobinostat, 1 μM vorinostat, and 10 nM bortezomib alone and in combination were analyzed for protein expression of the proteasome subunit β5.

Techniques Used: Over Expression, Staining, Expressing

8) Product Images from "Dual Targeting of CDK4 and ARK5 Using a Novel Kinase Inhibitor ON123300 Exerts Potent Anticancer Activity against Multiple Myeloma"

Article Title: Dual Targeting of CDK4 and ARK5 Using a Novel Kinase Inhibitor ON123300 Exerts Potent Anticancer Activity against Multiple Myeloma

Journal: Cancer research

doi: 10.1158/0008-5472.CAN-15-2934

ON123300 inhibits multiple myeloma cell growth in vivo in multiple myeloma xenograft mouse models. A and B, ON123300 inhibits growth of MM1.S cells and NCI-H929 in NOD mice (Taconic). NCI-H929 cells and MM1.S (2 × 10 6 cells/mouse) were implanted subcutaneously in female mice. Mice were randomized to control and treatment groups and treated intraperitoneally with vehicle and ON123300 (100 mg/kg) every other day. Treatment with intraperitoneal injections of ON123300 slowed the growth of tumors compared with increase in tumors in control mice.
Figure Legend Snippet: ON123300 inhibits multiple myeloma cell growth in vivo in multiple myeloma xenograft mouse models. A and B, ON123300 inhibits growth of MM1.S cells and NCI-H929 in NOD mice (Taconic). NCI-H929 cells and MM1.S (2 × 10 6 cells/mouse) were implanted subcutaneously in female mice. Mice were randomized to control and treatment groups and treated intraperitoneally with vehicle and ON123300 (100 mg/kg) every other day. Treatment with intraperitoneal injections of ON123300 slowed the growth of tumors compared with increase in tumors in control mice.

Techniques Used: In Vivo, Mouse Assay

Dual ARK5 and CDK4 inhibitor ON123300 potently induces apoptosis and cell-cycle arrest and negatively regulates mTOR/MYC pathways in multiple myeloma cells. A, MM1.S and NCI-H929 cells were treated with ON123300 at three different concentrations (5 nmol/L, 10 nmol/L, and 50 nmol/L) for 24 hours, followed by analysis for apoptosis with Annexin V/PI double staining. ON123300 triggered a significant increase in both early (Annexin V+/PI−) and late (Annexin V+/PI−) apoptotic cell populations in both cell lines (mean ± SD; n = 3). B, MM1.S and NCI-H929 cells were treated with ON123300 (10 nmol/L and 50 nmol/L) for 24 hours, followed by analysis for cell proliferation by EdU incorporation assay with APC/PI double staining. Quantification of cell-incorporated (EdU) and total DNA content in control- and ON123300-treated cells showed a significant G 0 –G 1 cell-cycle arrest in treated cells. C, MM1.S and NCI-H929 cells were treated with ON123300 (50 nmol/L) for 4, 6, and 12 hours, followed by Western blot analysis. As seen, treatment with ON123300 increased the expression of AMPK and SIRT1, resulting in decreased acetylation of MYC and total MYC. Alternatively, ON123300 also inhibits Rb/mTOR pathway via reduction in phosphoRb and phosphoS6K in both cell lines.
Figure Legend Snippet: Dual ARK5 and CDK4 inhibitor ON123300 potently induces apoptosis and cell-cycle arrest and negatively regulates mTOR/MYC pathways in multiple myeloma cells. A, MM1.S and NCI-H929 cells were treated with ON123300 at three different concentrations (5 nmol/L, 10 nmol/L, and 50 nmol/L) for 24 hours, followed by analysis for apoptosis with Annexin V/PI double staining. ON123300 triggered a significant increase in both early (Annexin V+/PI−) and late (Annexin V+/PI−) apoptotic cell populations in both cell lines (mean ± SD; n = 3). B, MM1.S and NCI-H929 cells were treated with ON123300 (10 nmol/L and 50 nmol/L) for 24 hours, followed by analysis for cell proliferation by EdU incorporation assay with APC/PI double staining. Quantification of cell-incorporated (EdU) and total DNA content in control- and ON123300-treated cells showed a significant G 0 –G 1 cell-cycle arrest in treated cells. C, MM1.S and NCI-H929 cells were treated with ON123300 (50 nmol/L) for 4, 6, and 12 hours, followed by Western blot analysis. As seen, treatment with ON123300 increased the expression of AMPK and SIRT1, resulting in decreased acetylation of MYC and total MYC. Alternatively, ON123300 also inhibits Rb/mTOR pathway via reduction in phosphoRb and phosphoS6K in both cell lines.

Techniques Used: Double Staining, Western Blot, Expressing

ARK5 depletion inhibits multiple myeloma cell growth via Rb/mTOR/MYC pathways and induces apoptosis and cell-cycle arrest. A, ARK5 repression significantly attenuated phosphoS6K, phosphoRb, MYC, and acetyl MYC activities in multiple myeloma. Conversely, depletion of ARK5 increased AMPK and SIRT1. Western blot analysis showing the levels of ARK5, SIRT1, MYC, acetyl MYC, total S6K, Rb, phosphoS6K, and phosphoRb proteins after 24-hour transfection in MM1.S and NCI-H929 siRNA–transfected cells. There was no difference in total Rb and total S6K between the groups. B and C, MM1.S and NCI-H929 cells were subjected to SIRT1 depletion by siRNA and SIRT1 activation with SRT1720. Western blotting confirmed that depletion of SIRT1 increased the acetylation activities of MYC, whereas the activation with SRT1720 resulted in decreased acetylation of MYC in a dose- and time-dependent manner. D, transfection in MM1.S and NCI-H929 cells induced apoptosis in ARK5-depleted cells as compared with nontransfected cells after 24-hour transfection confirmed with Annexin V/PI double staining. E, transfection in MM1.S and NCI-H929 cells also induced cell-cycle arrest in ARK5-depleted cells confirmed by EdU cell proliferation assay. Forty percent of MM1.S cells transfected with scrambled control siRNA showed EdU incorporation. EdU incorporation in cells transfected with ARK5 siRNA was approximately half that of the negative control. In NCI-H929 cells, 50% of cells transfected with negative control siRNA showed EdU incorporation, and EdU incorporation in cells transfected with ARK5 siRNA was less than half that.
Figure Legend Snippet: ARK5 depletion inhibits multiple myeloma cell growth via Rb/mTOR/MYC pathways and induces apoptosis and cell-cycle arrest. A, ARK5 repression significantly attenuated phosphoS6K, phosphoRb, MYC, and acetyl MYC activities in multiple myeloma. Conversely, depletion of ARK5 increased AMPK and SIRT1. Western blot analysis showing the levels of ARK5, SIRT1, MYC, acetyl MYC, total S6K, Rb, phosphoS6K, and phosphoRb proteins after 24-hour transfection in MM1.S and NCI-H929 siRNA–transfected cells. There was no difference in total Rb and total S6K between the groups. B and C, MM1.S and NCI-H929 cells were subjected to SIRT1 depletion by siRNA and SIRT1 activation with SRT1720. Western blotting confirmed that depletion of SIRT1 increased the acetylation activities of MYC, whereas the activation with SRT1720 resulted in decreased acetylation of MYC in a dose- and time-dependent manner. D, transfection in MM1.S and NCI-H929 cells induced apoptosis in ARK5-depleted cells as compared with nontransfected cells after 24-hour transfection confirmed with Annexin V/PI double staining. E, transfection in MM1.S and NCI-H929 cells also induced cell-cycle arrest in ARK5-depleted cells confirmed by EdU cell proliferation assay. Forty percent of MM1.S cells transfected with scrambled control siRNA showed EdU incorporation. EdU incorporation in cells transfected with ARK5 siRNA was approximately half that of the negative control. In NCI-H929 cells, 50% of cells transfected with negative control siRNA showed EdU incorporation, and EdU incorporation in cells transfected with ARK5 siRNA was less than half that.

Techniques Used: Western Blot, Transfection, Activation Assay, Double Staining, Proliferation Assay, Negative Control

ON123300 overcomes bone marrow stromal protection. A, ON123300 overcomes the cytoprotective effects of the multiple myeloma–host bone marrow microenvironment as observed in MM1.S and NCI-H929 cells. MM1.S cells were cultured alone or with BMSCs for 48 hours in the presence or absence of ON123300 (50 nmol/L) and confirmed with Annexin V/PI double staining. As shown, there was significant inhibition of BMSC-induced proliferation of multiple myeloma cells in response to ON123300 treatment. B, MM1.S and NCI-H929 cells were treated with proteasome inhibitor bortezomib at different concentrations (1–6 nmol/L) in the presence or absence of BMSCs for 48 hours and then analyzed for cytotoxicity by CellTiter-Blue assay. As shown, there was no significant inhibition of BMSC-induced proliferation of multiple myeloma cells in response to bortezomib treatment.
Figure Legend Snippet: ON123300 overcomes bone marrow stromal protection. A, ON123300 overcomes the cytoprotective effects of the multiple myeloma–host bone marrow microenvironment as observed in MM1.S and NCI-H929 cells. MM1.S cells were cultured alone or with BMSCs for 48 hours in the presence or absence of ON123300 (50 nmol/L) and confirmed with Annexin V/PI double staining. As shown, there was significant inhibition of BMSC-induced proliferation of multiple myeloma cells in response to ON123300 treatment. B, MM1.S and NCI-H929 cells were treated with proteasome inhibitor bortezomib at different concentrations (1–6 nmol/L) in the presence or absence of BMSCs for 48 hours and then analyzed for cytotoxicity by CellTiter-Blue assay. As shown, there was no significant inhibition of BMSC-induced proliferation of multiple myeloma cells in response to bortezomib treatment.

Techniques Used: Cell Culture, Double Staining, Inhibition, CtB Assay

Anti–multiple myeloma activity of ON123300, a multitargeted kinase inhibitor. A, structure of ON123300-8-Cyclopentyl-2-[4-(4-methylpiperazin-1-yl)-phenylamino]-7-oxo-7,8-dihydro-pyrido[2,3-d]pyrimidine-6-carbonitrile. B, ARK5 protein expression was confirmed by Western blot in multiple myeloma (MM) cell lines and primary cells. ARK5 level was significantly higher in the cell lines MM1.S, NCI-H929, JJN3, EJM, and in primary samples with 1q21 deletion and cMAF translocation. The numerical values indicate densitometric analysis of band intensity using ImageJ. C, ON123300 decreased cell viability by approximately 30% to 70% (IC 50 , 50–200 nmol/L) in 8/8 multiple myeloma cell lines examined. On the basis of IC 50 of 50 nmol/L, we could separate the cell lines into two groups: four cell lines (MM.1R, KMS11, RPMI-8226, and ARP1) had IC 50 of 50–150 nmol/L, and four cell lines (MM1.S, EJM, JJN3, and NCI-H929) were very sensitive (IC 50
Figure Legend Snippet: Anti–multiple myeloma activity of ON123300, a multitargeted kinase inhibitor. A, structure of ON123300-8-Cyclopentyl-2-[4-(4-methylpiperazin-1-yl)-phenylamino]-7-oxo-7,8-dihydro-pyrido[2,3-d]pyrimidine-6-carbonitrile. B, ARK5 protein expression was confirmed by Western blot in multiple myeloma (MM) cell lines and primary cells. ARK5 level was significantly higher in the cell lines MM1.S, NCI-H929, JJN3, EJM, and in primary samples with 1q21 deletion and cMAF translocation. The numerical values indicate densitometric analysis of band intensity using ImageJ. C, ON123300 decreased cell viability by approximately 30% to 70% (IC 50 , 50–200 nmol/L) in 8/8 multiple myeloma cell lines examined. On the basis of IC 50 of 50 nmol/L, we could separate the cell lines into two groups: four cell lines (MM.1R, KMS11, RPMI-8226, and ARP1) had IC 50 of 50–150 nmol/L, and four cell lines (MM1.S, EJM, JJN3, and NCI-H929) were very sensitive (IC 50

Techniques Used: Activity Assay, Expressing, Western Blot, Translocation Assay

9) Product Images from "Dual Targeting of CDK4 and ARK5 Using a Novel Kinase Inhibitor ON123300 Exerts Potent Anticancer Activity against Multiple Myeloma"

Article Title: Dual Targeting of CDK4 and ARK5 Using a Novel Kinase Inhibitor ON123300 Exerts Potent Anticancer Activity against Multiple Myeloma

Journal: Cancer research

doi: 10.1158/0008-5472.CAN-15-2934

Anti–multiple myeloma activity of ON123300, a multitargeted kinase inhibitor. A, structure of ON123300-8-Cyclopentyl-2-[4-(4-methylpiperazin-1-yl)-phenylamino]-7-oxo-7,8-dihydro-pyrido[2,3-d]pyrimidine-6-carbonitrile. B, ARK5 protein expression was confirmed by Western blot in multiple myeloma (MM) cell lines and primary cells. ARK5 level was significantly higher in the cell lines MM1.S, NCI-H929, JJN3, EJM, and in primary samples with 1q21 deletion and cMAF translocation. The numerical values indicate densitometric analysis of band intensity using ImageJ. C, ON123300 decreased cell viability by approximately 30% to 70% (IC 50 , 50–200 nmol/L) in 8/8 multiple myeloma cell lines examined. On the basis of IC 50 of 50 nmol/L, we could separate the cell lines into two groups: four cell lines (MM.1R, KMS11, RPMI-8226, and ARP1) had IC 50 of 50–150 nmol/L, and four cell lines (MM1.S, EJM, JJN3, and NCI-H929) were very sensitive (IC 50
Figure Legend Snippet: Anti–multiple myeloma activity of ON123300, a multitargeted kinase inhibitor. A, structure of ON123300-8-Cyclopentyl-2-[4-(4-methylpiperazin-1-yl)-phenylamino]-7-oxo-7,8-dihydro-pyrido[2,3-d]pyrimidine-6-carbonitrile. B, ARK5 protein expression was confirmed by Western blot in multiple myeloma (MM) cell lines and primary cells. ARK5 level was significantly higher in the cell lines MM1.S, NCI-H929, JJN3, EJM, and in primary samples with 1q21 deletion and cMAF translocation. The numerical values indicate densitometric analysis of band intensity using ImageJ. C, ON123300 decreased cell viability by approximately 30% to 70% (IC 50 , 50–200 nmol/L) in 8/8 multiple myeloma cell lines examined. On the basis of IC 50 of 50 nmol/L, we could separate the cell lines into two groups: four cell lines (MM.1R, KMS11, RPMI-8226, and ARP1) had IC 50 of 50–150 nmol/L, and four cell lines (MM1.S, EJM, JJN3, and NCI-H929) were very sensitive (IC 50

Techniques Used: Activity Assay, Expressing, Western Blot, Translocation Assay

10) Product Images from "The BCL6 transcriptional program features repression of multiple oncogenes in primary B cells and is deregulated in DLBCL"

Article Title: The BCL6 transcriptional program features repression of multiple oncogenes in primary B cells and is deregulated in DLBCL

Journal: Blood

doi: 10.1182/blood-2008-12-193037

Differential BCL6 binding to specific promoters in DLBCL and GC B cells . (A) An example of BCL6-binding peaks for genes that were identified as differentially bound in GC versus DLBCL cells. The y-axis indicates enrichment versus input. The x-axis indicates the location of probes within the respective loci relative to the transcriptional start site. The dark gray and light gray tracings correspond to the different replicates. (B) A subset of genes predicted to be differentially bound by ChIP-on-chip were validated by independent quantitative ChIP experiments. The x-axis measures the fold enrichment ratio of promoters in GC cells versus OCI-Ly1 (black arrow) or OCI-Ly1 versus GC cells (red arrow). The data are from 3 independent experiments. Error bars represent the SEM for triplicates.
Figure Legend Snippet: Differential BCL6 binding to specific promoters in DLBCL and GC B cells . (A) An example of BCL6-binding peaks for genes that were identified as differentially bound in GC versus DLBCL cells. The y-axis indicates enrichment versus input. The x-axis indicates the location of probes within the respective loci relative to the transcriptional start site. The dark gray and light gray tracings correspond to the different replicates. (B) A subset of genes predicted to be differentially bound by ChIP-on-chip were validated by independent quantitative ChIP experiments. The x-axis measures the fold enrichment ratio of promoters in GC cells versus OCI-Ly1 (black arrow) or OCI-Ly1 versus GC cells (red arrow). The data are from 3 independent experiments. Error bars represent the SEM for triplicates.

Techniques Used: Binding Assay, Chromatin Immunoprecipitation

11) Product Images from "Dual Targeting of CDK4 and ARK5 Using a Novel Kinase Inhibitor ON123300 Exerts Potent Anticancer Activity against Multiple Myeloma"

Article Title: Dual Targeting of CDK4 and ARK5 Using a Novel Kinase Inhibitor ON123300 Exerts Potent Anticancer Activity against Multiple Myeloma

Journal: Cancer research

doi: 10.1158/0008-5472.CAN-15-2934

Transcriptomic profiling reveals ARK5 depletion results in the suppression of cell cycle regulating genes in multiple myeloma cell lines. A, RNA sequencing data from ARK5-depleted NCI-H929 cells identified 894 DEGs between ARK5 siRNA and scrambled siRNA. Cell-cycle pathway was enriched in ARK5-depleted cells with cell-cycle regulators like MYC, cyclin D and E , and CDK4 genes significantly repressed after ARK5 depletion as shown. B, enrichment score plot by GSEA showed a strong negative enrichment of MYC target genes in ARK5 depleted NCI-H929 cells. Preranked list of 894 DEGs was used for GSEA in the C6 oncogenic signatures. The distribution of MYC target genes (black lines) is presented as a function of the change in expression between ARK5 siRNA and scrambled siRNA, from highly upregulated (red) to highly downregulated (blue). Normalized enrichment score (NES) and FDR q values for MYC target gene set are shown. C, schematic representing the downstream signaling events of ARK5 is shown.
Figure Legend Snippet: Transcriptomic profiling reveals ARK5 depletion results in the suppression of cell cycle regulating genes in multiple myeloma cell lines. A, RNA sequencing data from ARK5-depleted NCI-H929 cells identified 894 DEGs between ARK5 siRNA and scrambled siRNA. Cell-cycle pathway was enriched in ARK5-depleted cells with cell-cycle regulators like MYC, cyclin D and E , and CDK4 genes significantly repressed after ARK5 depletion as shown. B, enrichment score plot by GSEA showed a strong negative enrichment of MYC target genes in ARK5 depleted NCI-H929 cells. Preranked list of 894 DEGs was used for GSEA in the C6 oncogenic signatures. The distribution of MYC target genes (black lines) is presented as a function of the change in expression between ARK5 siRNA and scrambled siRNA, from highly upregulated (red) to highly downregulated (blue). Normalized enrichment score (NES) and FDR q values for MYC target gene set are shown. C, schematic representing the downstream signaling events of ARK5 is shown.

Techniques Used: RNA Sequencing Assay, Expressing

ON123300 inhibits multiple myeloma cell growth in vivo in multiple myeloma xenograft mouse models. A and B, ON123300 inhibits growth of MM1.S cells and NCI-H929 in NOD mice (Taconic). NCI-H929 cells and MM1.S (2 × 10 6 cells/mouse) were implanted subcutaneously in female mice. Mice were randomized to control and treatment groups and treated intraperitoneally with vehicle and ON123300 (100 mg/kg) every other day. Treatment with intraperitoneal injections of ON123300 slowed the growth of tumors compared with increase in tumors in control mice.
Figure Legend Snippet: ON123300 inhibits multiple myeloma cell growth in vivo in multiple myeloma xenograft mouse models. A and B, ON123300 inhibits growth of MM1.S cells and NCI-H929 in NOD mice (Taconic). NCI-H929 cells and MM1.S (2 × 10 6 cells/mouse) were implanted subcutaneously in female mice. Mice were randomized to control and treatment groups and treated intraperitoneally with vehicle and ON123300 (100 mg/kg) every other day. Treatment with intraperitoneal injections of ON123300 slowed the growth of tumors compared with increase in tumors in control mice.

Techniques Used: In Vivo, Mouse Assay

Dual ARK5 and CDK4 inhibitor ON123300 potently induces apoptosis and cell-cycle arrest and negatively regulates mTOR/MYC pathways in multiple myeloma cells. A, MM1.S and NCI-H929 cells were treated with ON123300 at three different concentrations (5 nmol/L, 10 nmol/L, and 50 nmol/L) for 24 hours, followed by analysis for apoptosis with Annexin V/PI double staining. ON123300 triggered a significant increase in both early (Annexin V+/PI−) and late (Annexin V+/PI−) apoptotic cell populations in both cell lines (mean ± SD; n = 3). B, MM1.S and NCI-H929 cells were treated with ON123300 (10 nmol/L and 50 nmol/L) for 24 hours, followed by analysis for cell proliferation by EdU incorporation assay with APC/PI double staining. Quantification of cell-incorporated (EdU) and total DNA content in control- and ON123300-treated cells showed a significant G 0 –G 1 cell-cycle arrest in treated cells. C, MM1.S and NCI-H929 cells were treated with ON123300 (50 nmol/L) for 4, 6, and 12 hours, followed by Western blot analysis. As seen, treatment with ON123300 increased the expression of AMPK and SIRT1, resulting in decreased acetylation of MYC and total MYC. Alternatively, ON123300 also inhibits Rb/mTOR pathway via reduction in phosphoRb and phosphoS6K in both cell lines.
Figure Legend Snippet: Dual ARK5 and CDK4 inhibitor ON123300 potently induces apoptosis and cell-cycle arrest and negatively regulates mTOR/MYC pathways in multiple myeloma cells. A, MM1.S and NCI-H929 cells were treated with ON123300 at three different concentrations (5 nmol/L, 10 nmol/L, and 50 nmol/L) for 24 hours, followed by analysis for apoptosis with Annexin V/PI double staining. ON123300 triggered a significant increase in both early (Annexin V+/PI−) and late (Annexin V+/PI−) apoptotic cell populations in both cell lines (mean ± SD; n = 3). B, MM1.S and NCI-H929 cells were treated with ON123300 (10 nmol/L and 50 nmol/L) for 24 hours, followed by analysis for cell proliferation by EdU incorporation assay with APC/PI double staining. Quantification of cell-incorporated (EdU) and total DNA content in control- and ON123300-treated cells showed a significant G 0 –G 1 cell-cycle arrest in treated cells. C, MM1.S and NCI-H929 cells were treated with ON123300 (50 nmol/L) for 4, 6, and 12 hours, followed by Western blot analysis. As seen, treatment with ON123300 increased the expression of AMPK and SIRT1, resulting in decreased acetylation of MYC and total MYC. Alternatively, ON123300 also inhibits Rb/mTOR pathway via reduction in phosphoRb and phosphoS6K in both cell lines.

Techniques Used: Double Staining, Western Blot, Expressing

ARK5 depletion inhibits multiple myeloma cell growth via Rb/mTOR/MYC pathways and induces apoptosis and cell-cycle arrest. A, ARK5 repression significantly attenuated phosphoS6K, phosphoRb, MYC, and acetyl MYC activities in multiple myeloma. Conversely, depletion of ARK5 increased AMPK and SIRT1. Western blot analysis showing the levels of ARK5, SIRT1, MYC, acetyl MYC, total S6K, Rb, phosphoS6K, and phosphoRb proteins after 24-hour transfection in MM1.S and NCI-H929 siRNA–transfected cells. There was no difference in total Rb and total S6K between the groups. B and C, MM1.S and NCI-H929 cells were subjected to SIRT1 depletion by siRNA and SIRT1 activation with SRT1720. Western blotting confirmed that depletion of SIRT1 increased the acetylation activities of MYC, whereas the activation with SRT1720 resulted in decreased acetylation of MYC in a dose- and time-dependent manner. D, transfection in MM1.S and NCI-H929 cells induced apoptosis in ARK5-depleted cells as compared with nontransfected cells after 24-hour transfection confirmed with Annexin V/PI double staining. E, transfection in MM1.S and NCI-H929 cells also induced cell-cycle arrest in ARK5-depleted cells confirmed by EdU cell proliferation assay. Forty percent of MM1.S cells transfected with scrambled control siRNA showed EdU incorporation. EdU incorporation in cells transfected with ARK5 siRNA was approximately half that of the negative control. In NCI-H929 cells, 50% of cells transfected with negative control siRNA showed EdU incorporation, and EdU incorporation in cells transfected with ARK5 siRNA was less than half that.
Figure Legend Snippet: ARK5 depletion inhibits multiple myeloma cell growth via Rb/mTOR/MYC pathways and induces apoptosis and cell-cycle arrest. A, ARK5 repression significantly attenuated phosphoS6K, phosphoRb, MYC, and acetyl MYC activities in multiple myeloma. Conversely, depletion of ARK5 increased AMPK and SIRT1. Western blot analysis showing the levels of ARK5, SIRT1, MYC, acetyl MYC, total S6K, Rb, phosphoS6K, and phosphoRb proteins after 24-hour transfection in MM1.S and NCI-H929 siRNA–transfected cells. There was no difference in total Rb and total S6K between the groups. B and C, MM1.S and NCI-H929 cells were subjected to SIRT1 depletion by siRNA and SIRT1 activation with SRT1720. Western blotting confirmed that depletion of SIRT1 increased the acetylation activities of MYC, whereas the activation with SRT1720 resulted in decreased acetylation of MYC in a dose- and time-dependent manner. D, transfection in MM1.S and NCI-H929 cells induced apoptosis in ARK5-depleted cells as compared with nontransfected cells after 24-hour transfection confirmed with Annexin V/PI double staining. E, transfection in MM1.S and NCI-H929 cells also induced cell-cycle arrest in ARK5-depleted cells confirmed by EdU cell proliferation assay. Forty percent of MM1.S cells transfected with scrambled control siRNA showed EdU incorporation. EdU incorporation in cells transfected with ARK5 siRNA was approximately half that of the negative control. In NCI-H929 cells, 50% of cells transfected with negative control siRNA showed EdU incorporation, and EdU incorporation in cells transfected with ARK5 siRNA was less than half that.

Techniques Used: Western Blot, Transfection, Activation Assay, Double Staining, Proliferation Assay, Negative Control

ON123300 overcomes bone marrow stromal protection. A, ON123300 overcomes the cytoprotective effects of the multiple myeloma–host bone marrow microenvironment as observed in MM1.S and NCI-H929 cells. MM1.S cells were cultured alone or with BMSCs for 48 hours in the presence or absence of ON123300 (50 nmol/L) and confirmed with Annexin V/PI double staining. As shown, there was significant inhibition of BMSC-induced proliferation of multiple myeloma cells in response to ON123300 treatment. B, MM1.S and NCI-H929 cells were treated with proteasome inhibitor bortezomib at different concentrations (1–6 nmol/L) in the presence or absence of BMSCs for 48 hours and then analyzed for cytotoxicity by CellTiter-Blue assay. As shown, there was no significant inhibition of BMSC-induced proliferation of multiple myeloma cells in response to bortezomib treatment.
Figure Legend Snippet: ON123300 overcomes bone marrow stromal protection. A, ON123300 overcomes the cytoprotective effects of the multiple myeloma–host bone marrow microenvironment as observed in MM1.S and NCI-H929 cells. MM1.S cells were cultured alone or with BMSCs for 48 hours in the presence or absence of ON123300 (50 nmol/L) and confirmed with Annexin V/PI double staining. As shown, there was significant inhibition of BMSC-induced proliferation of multiple myeloma cells in response to ON123300 treatment. B, MM1.S and NCI-H929 cells were treated with proteasome inhibitor bortezomib at different concentrations (1–6 nmol/L) in the presence or absence of BMSCs for 48 hours and then analyzed for cytotoxicity by CellTiter-Blue assay. As shown, there was no significant inhibition of BMSC-induced proliferation of multiple myeloma cells in response to bortezomib treatment.

Techniques Used: Cell Culture, Double Staining, Inhibition, CtB Assay

Anti–multiple myeloma activity of ON123300, a multitargeted kinase inhibitor. A, structure of ON123300-8-Cyclopentyl-2-[4-(4-methylpiperazin-1-yl)-phenylamino]-7-oxo-7,8-dihydro-pyrido[2,3-d]pyrimidine-6-carbonitrile. B, ARK5 protein expression was confirmed by Western blot in multiple myeloma (MM) cell lines and primary cells. ARK5 level was significantly higher in the cell lines MM1.S, NCI-H929, JJN3, EJM, and in primary samples with 1q21 deletion and cMAF translocation. The numerical values indicate densitometric analysis of band intensity using ImageJ. C, ON123300 decreased cell viability by approximately 30% to 70% (IC 50 , 50–200 nmol/L) in 8/8 multiple myeloma cell lines examined. On the basis of IC 50 of 50 nmol/L, we could separate the cell lines into two groups: four cell lines (MM.1R, KMS11, RPMI-8226, and ARP1) had IC 50 of 50–150 nmol/L, and four cell lines (MM1.S, EJM, JJN3, and NCI-H929) were very sensitive (IC 50
Figure Legend Snippet: Anti–multiple myeloma activity of ON123300, a multitargeted kinase inhibitor. A, structure of ON123300-8-Cyclopentyl-2-[4-(4-methylpiperazin-1-yl)-phenylamino]-7-oxo-7,8-dihydro-pyrido[2,3-d]pyrimidine-6-carbonitrile. B, ARK5 protein expression was confirmed by Western blot in multiple myeloma (MM) cell lines and primary cells. ARK5 level was significantly higher in the cell lines MM1.S, NCI-H929, JJN3, EJM, and in primary samples with 1q21 deletion and cMAF translocation. The numerical values indicate densitometric analysis of band intensity using ImageJ. C, ON123300 decreased cell viability by approximately 30% to 70% (IC 50 , 50–200 nmol/L) in 8/8 multiple myeloma cell lines examined. On the basis of IC 50 of 50 nmol/L, we could separate the cell lines into two groups: four cell lines (MM.1R, KMS11, RPMI-8226, and ARP1) had IC 50 of 50–150 nmol/L, and four cell lines (MM1.S, EJM, JJN3, and NCI-H929) were very sensitive (IC 50

Techniques Used: Activity Assay, Expressing, Western Blot, Translocation Assay

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Enzyme-linked Immunospot:

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Article Snippet: .. Cell Culture The OCI-Ly1 cells were cultured in medium containing 90% Iscove medium (Cellgro, Manassas, VA), 10% fetal bovine serum (Gemini, Irvine, CA), and 1% penicillin/streptomycin (Invitrogen, Carlsbad, CA). ..

Article Title: Similar degrees of obesity induced by diet or aging cause strikingly different immunologic and metabolic outcomes. Similar degrees of obesity induced by diet or aging cause strikingly different immunologic and metabolic outcomes
Article Snippet: .. Tissue and plasma measurements The isolated immune cells from liver and SVC from AT were cultured for 18 h in complete DMEM medium (Cellgro, Manassas, VA). .. The harvested media was analyzed for various cytokines (TNF‐α, INF‐γ, IL‐6, MCP‐1, IL‐4, IL‐13, IL‐10) using Luminex (Invitrogen).

Article Title: Dual Targeting of CDK4 and ARK5 Using a Novel Kinase Inhibitor ON123300 Exerts Potent Anticancer Activity against Multiple Myeloma
Article Snippet: .. Multiple myeloma cell lines MM.1R, KMS11, ARP1, RPMI-8226, MM1.S, EJM, JJN3, and NCI-H929 were cultured in RPMI1640 medium (CellGro) supplemented with 10% FBS (Gemini Bio Products), N-2-hydroxyethylpiperazine-N′-2-ethanesulfonic acid, 100 U/mL penicillin G, and 100 μg/mL streptomycin (CellGro). ..

Article Title: Converting cell lines representing hematological malignancies from glucocorticoid-resistant to glucocorticoid-sensitive: signaling pathway interactions
Article Snippet: Paragraph title: 2.2. Cell culture and drug treatments ... RPMI 8226, IM-9, Ramos and Molt 4 cells were grown in RPMI 1640 (Cellgro Media Tech, Herndon, VA) at pH 7.4 supplemented with 10% fetal bovine serum (FBS, Atlanta Biologicals, Norcross, GA).

Article Title: Attenuation of dengue virus infection by adeno-associated virus-mediated siRNA delivery
Article Snippet: .. After 2 h at 37°C/5%CO2 the nonadherent cells were removed and the adherent cells were cultured with fresh DMEM supplemented with 10% FBS (Cellgro), 200 ng/ml IL-4 (BD-Pharmingen) and 50 ng/ml GM-CSF (BD-Pharmingen) for 7 days prior to infection with DEN. .. Blocking dengue virus infection in vitro 1 × 105 Vero cells or DCs were seeded into six-well tissue culture plates and infected with different numbers of recombinant AAV carrying the DEN-siRNA silencing cassette.

Expressing:

Article Title: Inhibition of HIV-1 endocytosis allows lipid mixing at the plasma membrane, but not complete fusion
Article Snippet: Cells and Reagents HeLa-derived indicator TZM-bl cells expressing CD4, CXCR4 and CCR5 (donated by Drs. J.C. Kappes and X. Wu [ ]), human T4-lymphoblastoid CEMss cells (donated by Dr. P. Nara [ ]), CEM-NKR-CCR5-Luc cells (donated by Drs. J. Moore and C. Spenlehauer [ ]), PM-1 cells (donated by Drs. P. Lusso and R. Gallo [ ]) and human astroglioma U87-MG-derived U87.CD4.CCR5 cells (donated by Dr. H. Deng and Dr. D.R. .. U87.CD4.CCR5 were maintained in DMEM supplemented with 15% FBS, 100U penicillin-streptomycin, 0.5 mg/ml G418 sulfate (Cellgro), and 1 μg/ml puromycin (Sigma, St. Louis, MO).

Gradient Centrifugation:

Article Title: Inhibition of HIV-1 endocytosis allows lipid mixing at the plasma membrane, but not complete fusion
Article Snippet: U87.CD4.CCR5 were maintained in DMEM supplemented with 15% FBS, 100U penicillin-streptomycin, 0.5 mg/ml G418 sulfate (Cellgro), and 1 μg/ml puromycin (Sigma, St. Louis, MO). .. Primary peripheral blood mononuclear cells (PBMCs) were purified from the peripheral blood of healthy donor (approval from Emory IRB000045690 "Phlebotomy of Healthy Adults for Research in Infectious Diseases and Immunology") by Ficoll-Paque Plus (GE Healthcare, Piscataway, NJ) density gradient centrifugation.

Modification:

Article Title: Inhibition of HIV-1 endocytosis allows lipid mixing at the plasma membrane, but not complete fusion
Article Snippet: TZM-bl were grown in Dulbecco's Modified Eagle Medium (DMEM, Cellgro, Manassas, VA), whereas CEMss, CEM-NKR-CCR5-Luc, Jurkat, and PM-1 cells were grown in RPMI-1640 (Cellgro) supplemented with 10% Fetal Bovine Serum (FBS, HyClone Laboratories, Logan, UT) and 100 U penicillin-streptomycin (Gemini Bio-Products, West Sacramento, CA). .. U87.CD4.CCR5 were maintained in DMEM supplemented with 15% FBS, 100U penicillin-streptomycin, 0.5 mg/ml G418 sulfate (Cellgro), and 1 μg/ml puromycin (Sigma, St. Louis, MO).

Article Title: Converting cell lines representing hematological malignancies from glucocorticoid-resistant to glucocorticoid-sensitive: signaling pathway interactions
Article Snippet: RPMI 8226, IM-9, Ramos and Molt 4 cells were grown in RPMI 1640 (Cellgro Media Tech, Herndon, VA) at pH 7.4 supplemented with 10% fetal bovine serum (FBS, Atlanta Biologicals, Norcross, GA). .. OPM-I cells were cultured in RPMI 1640 at pH 7.4 supplemented with 10% defined FBS (HyClone, Logan, UT); HL-60, K-562 and Mo cells were grown in Iscove’s modification of DMEM (Cellgro Media Tech, Herndon, VA) at pH 7.4, supplemented with 10% FBS (Atlanta Biologicals).

Centrifugation:

Article Title: KSHV confers a survival advantage to endothelial cells
Article Snippet: A KSHV-negative lymphoma cell line, BJAB, and the body-cavity-based lymphoma cell line BCBL-1 were grown in RPMI media (Cellgro) with 10% FBS. .. The conditional media from BJAB and BCBL-1 cells was harvested by centrifugation at 3500 rpm for 10 min. Growth factor-reduced Matrigel (BD Biosciences) was added to the wells of a pre-chilled 24-well plate (0.25ml per well).

Article Title: Attenuation of dengue virus infection by adeno-associated virus-mediated siRNA delivery
Article Snippet: Buffy coats were diluted with one volume of DMEM (Cellgro) and PBMCs were isolated by density-gradient centrifugation using Histopaque-1077 (SIGMA) according to the instructions. .. After 2 h at 37°C/5%CO2 the nonadherent cells were removed and the adherent cells were cultured with fresh DMEM supplemented with 10% FBS (Cellgro), 200 ng/ml IL-4 (BD-Pharmingen) and 50 ng/ml GM-CSF (BD-Pharmingen) for 7 days prior to infection with DEN.

Recombinant:

Article Title: Immunity to Human Immunodeficiency Virus (HIV) in Children with Chronic HIV Infection Receiving Highly Active Antiretroviral Therapy
Article Snippet: Frozen cells were thawed and resuspended at 107 cells/ml in ELISPOT assay medium (RPMI 1640, 10% human serum, 10 mM HEPES [Cellgro], 2 mM l -glutamine, 100 U of penicillin-streptomycin/ml). .. This mixture was then added to 96 microtiter wells precoated with anti-human recombinant IFN-γ monoclonal antibody (Endogen).

other:

Article Title: COT/MAP3K8 drives resistance to RAF inhibition through MAP kinase pathway reactivation
Article Snippet: M307 was grown in RPMI (Cellgro), 10% FBS and 1% penicillin/streptomycin supplemented with 1 mM sodium pyruvate.

Derivative Assay:

Article Title: EFFICACY OF PANOBINOSTAT AND MARIZOMIB IN ACUTE MYELOID LEUKEMIA AND BORTEZOMIB-RESISTANT MODELS
Article Snippet: The human leukemia AML3 (human AML FAB-M4) and ML-1 (derived from an M5 AML relapse in a patient initially diagnosed with T-cell ALL) cell lines were purchased from ATCC (Manassas, VA). .. RPMI-8226 MM parental cells and bortezomib-resistant RPMI-8226vr10 cells were maintained in RPMI media with 2 mM L-glutamine containing 10% FBS, 100 IU/mL penicillin, and 100 μg/mL streptomycin (Cellgro, Mediatech, Herndon, VA).

Luminex:

Article Title: Similar degrees of obesity induced by diet or aging cause strikingly different immunologic and metabolic outcomes. Similar degrees of obesity induced by diet or aging cause strikingly different immunologic and metabolic outcomes
Article Snippet: Tissue and plasma measurements The isolated immune cells from liver and SVC from AT were cultured for 18 h in complete DMEM medium (Cellgro, Manassas, VA). .. Tissue and plasma measurements The isolated immune cells from liver and SVC from AT were cultured for 18 h in complete DMEM medium (Cellgro, Manassas, VA).

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    Cellgro elispot assay medium
    HIV- and CMV-specific CMI in HIV- infected children on HAART. Data represent results of assays performed with PBMC from 12 HIV-seropositive pediatric patients, 9 of whom were also CMV seropositive. Results for each patient contributed 2 to 6 data points. Dotted lines indicate thresholds for positive results. Solid lines indicate medians. (A) HIV LPA responses were significantly lower than those for CMV with respect to proportion of positive results ( P = 0.02) and amplitude of response ( P = 0.006). (B) The difference in the proportions of positive <t>ELISPOT</t> assay results for HIV and CMV did not reach statistical significance ( P = 0.06), but the magnitude of the response was significantly lower for HIV than for CMV ( P = 0.007).(C) ICCK responses were similar for HIV- and CMV-seropositive patients with respect to proportion of positive results ( P = 0.16) and magnitude of the response ( P = 0.3).
    Elispot Assay Medium, supplied by Cellgro, used in various techniques. Bioz Stars score: 84/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    HIV- and CMV-specific CMI in HIV- infected children on HAART. Data represent results of assays performed with PBMC from 12 HIV-seropositive pediatric patients, 9 of whom were also CMV seropositive. Results for each patient contributed 2 to 6 data points. Dotted lines indicate thresholds for positive results. Solid lines indicate medians. (A) HIV LPA responses were significantly lower than those for CMV with respect to proportion of positive results ( P = 0.02) and amplitude of response ( P = 0.006). (B) The difference in the proportions of positive <t>ELISPOT</t> assay results for HIV and CMV did not reach statistical significance ( P = 0.06), but the magnitude of the response was significantly lower for HIV than for CMV ( P = 0.007).(C) ICCK responses were similar for HIV- and CMV-seropositive patients with respect to proportion of positive results ( P = 0.16) and magnitude of the response ( P = 0.3).
    Hepes Buffered Phenol Red Free Rpmi 1640, supplied by Cellgro, used in various techniques. Bioz Stars score: 84/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    HIV- and CMV-specific CMI in HIV- infected children on HAART. Data represent results of assays performed with PBMC from 12 HIV-seropositive pediatric patients, 9 of whom were also CMV seropositive. Results for each patient contributed 2 to 6 data points. Dotted lines indicate thresholds for positive results. Solid lines indicate medians. (A) HIV LPA responses were significantly lower than those for CMV with respect to proportion of positive results ( P = 0.02) and amplitude of response ( P = 0.006). (B) The difference in the proportions of positive <t>ELISPOT</t> assay results for HIV and CMV did not reach statistical significance ( P = 0.06), but the magnitude of the response was significantly lower for HIV than for CMV ( P = 0.007).(C) ICCK responses were similar for HIV- and CMV-seropositive patients with respect to proportion of positive results ( P = 0.16) and magnitude of the response ( P = 0.3).
    Free Hepes Buffered Hanks, supplied by Cellgro, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cellgro hepes
    HIV- and CMV-specific CMI in HIV- infected children on HAART. Data represent results of assays performed with PBMC from 12 HIV-seropositive pediatric patients, 9 of whom were also CMV seropositive. Results for each patient contributed 2 to 6 data points. Dotted lines indicate thresholds for positive results. Solid lines indicate medians. (A) HIV LPA responses were significantly lower than those for CMV with respect to proportion of positive results ( P = 0.02) and amplitude of response ( P = 0.006). (B) The difference in the proportions of positive <t>ELISPOT</t> assay results for HIV and CMV did not reach statistical significance ( P = 0.06), but the magnitude of the response was significantly lower for HIV than for CMV ( P = 0.007).(C) ICCK responses were similar for HIV- and CMV-seropositive patients with respect to proportion of positive results ( P = 0.16) and magnitude of the response ( P = 0.3).
    Hepes, supplied by Cellgro, used in various techniques. Bioz Stars score: 97/100, based on 17 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    HIV- and CMV-specific CMI in HIV- infected children on HAART. Data represent results of assays performed with PBMC from 12 HIV-seropositive pediatric patients, 9 of whom were also CMV seropositive. Results for each patient contributed 2 to 6 data points. Dotted lines indicate thresholds for positive results. Solid lines indicate medians. (A) HIV LPA responses were significantly lower than those for CMV with respect to proportion of positive results ( P = 0.02) and amplitude of response ( P = 0.006). (B) The difference in the proportions of positive ELISPOT assay results for HIV and CMV did not reach statistical significance ( P = 0.06), but the magnitude of the response was significantly lower for HIV than for CMV ( P = 0.007).(C) ICCK responses were similar for HIV- and CMV-seropositive patients with respect to proportion of positive results ( P = 0.16) and magnitude of the response ( P = 0.3).

    Journal: Clinical and Diagnostic Laboratory Immunology

    Article Title: Immunity to Human Immunodeficiency Virus (HIV) in Children with Chronic HIV Infection Receiving Highly Active Antiretroviral Therapy

    doi: 10.1128/CDLI.10.5.821-825.2003

    Figure Lengend Snippet: HIV- and CMV-specific CMI in HIV- infected children on HAART. Data represent results of assays performed with PBMC from 12 HIV-seropositive pediatric patients, 9 of whom were also CMV seropositive. Results for each patient contributed 2 to 6 data points. Dotted lines indicate thresholds for positive results. Solid lines indicate medians. (A) HIV LPA responses were significantly lower than those for CMV with respect to proportion of positive results ( P = 0.02) and amplitude of response ( P = 0.006). (B) The difference in the proportions of positive ELISPOT assay results for HIV and CMV did not reach statistical significance ( P = 0.06), but the magnitude of the response was significantly lower for HIV than for CMV ( P = 0.007).(C) ICCK responses were similar for HIV- and CMV-seropositive patients with respect to proportion of positive results ( P = 0.16) and magnitude of the response ( P = 0.3).

    Article Snippet: Frozen cells were thawed and resuspended at 107 cells/ml in ELISPOT assay medium (RPMI 1640, 10% human serum, 10 mM HEPES [Cellgro], 2 mM l -glutamine, 100 U of penicillin-streptomycin/ml).

    Techniques: Infection, Enzyme-linked Immunospot