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vectra polaris tm  (Akoya Biosciences)
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Akoya Biosciences vectra polaris tm
Vectra Polaris Tm, supplied by Akoya Biosciences, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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image lab tm software  (Bio-Rad)
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Bio-Rad image lab tm software
Tor1 activation in NKKY101 strain causes Hsp90 activation via CK2 kinase. A, CDR6/ROA1 deletion suppresses CK2 activity. CK2 activity was monitored in an in vitro assay using protein lysates from C. albicans WT and NKKY101 strains, using recombinant Sic1 as a substrate. The assay was performed in biological duplicates with technical replicates. Error bars, S.D.; *, p < 0.05 (Student's t test). B, the CDR6/ROA1 deletion causes Hog1 activation. NaCl was used as a positive control to detect the active phosphorylated form of Hog1. The phosphorylated Hog1 level is low in the WT and CDR6/ROA1 revertant NKKY102 strains under basal conditions and induced in the presence of NaCl. However, the phosphorylated Hog1 level is high in the CDR6/ROA1 null strain NKKY101 even in basal conditions. The addition of NaCl increased the phosphorylated Hog1 in the null strain. Bands were quantified using Bio-Rad <t>Image</t> <t>Lab</t> <t>software,</t> and the ratio of phosphorylated Hog1 to total Hog1 was plotted for WT, NKKY101, and NKKY102 strains for basal conditions (without NaCl induction). A similar trend of phosphorylated Hog1 was observed in biological triplicate experiments for basal conditions (Fig. S5). C, Hog1 activation in CDR6/ROA1 null strain NKKY101 is Tor1-dependent. Rapamycin was used as a Tor1 inhibitor. The phosphorylated Hog1 level decreased in CDR6/ROA1 null strain NKKY101 when treated with rapamycin (4 and 8 ng/ml) in comparison with untreated conditions. D, validation of microarray data of HSP70 expression by qRT-PCR in NKKY101 mutant compared with WT. Data (mean ± S.E. (error bars) of biological replicate with technical triplicates) were normalized to an internal ACT1 mRNA control and represent percentage relative expression in the mutant cultures compared with the wild-type cells. Statistical analysis was performed using Student's t test (**, p ≤ 0.01). E, model for Hsp90 activation. Deletion of CDR6/ROA1 activates the Tor1, which down-regulates the KNS1 transcript, resulting in decreased CK2 kinase activity. This decrease in CK2 kinase activity causes activation of Hsp90 and its client proteins.
Image Lab Tm Software, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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arraycam tm 400-s microarray imaging system  (Grace Bio-Labs)
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Grace Bio-Labs arraycam tm 400-s microarray imaging system
Tor1 activation in NKKY101 strain causes Hsp90 activation via CK2 kinase. A, CDR6/ROA1 deletion suppresses CK2 activity. CK2 activity was monitored in an in vitro assay using protein lysates from C. albicans WT and NKKY101 strains, using recombinant Sic1 as a substrate. The assay was performed in biological duplicates with technical replicates. Error bars, S.D.; *, p < 0.05 (Student's t test). B, the CDR6/ROA1 deletion causes Hog1 activation. NaCl was used as a positive control to detect the active phosphorylated form of Hog1. The phosphorylated Hog1 level is low in the WT and CDR6/ROA1 revertant NKKY102 strains under basal conditions and induced in the presence of NaCl. However, the phosphorylated Hog1 level is high in the CDR6/ROA1 null strain NKKY101 even in basal conditions. The addition of NaCl increased the phosphorylated Hog1 in the null strain. Bands were quantified using Bio-Rad <t>Image</t> <t>Lab</t> <t>software,</t> and the ratio of phosphorylated Hog1 to total Hog1 was plotted for WT, NKKY101, and NKKY102 strains for basal conditions (without NaCl induction). A similar trend of phosphorylated Hog1 was observed in biological triplicate experiments for basal conditions (Fig. S5). C, Hog1 activation in CDR6/ROA1 null strain NKKY101 is Tor1-dependent. Rapamycin was used as a Tor1 inhibitor. The phosphorylated Hog1 level decreased in CDR6/ROA1 null strain NKKY101 when treated with rapamycin (4 and 8 ng/ml) in comparison with untreated conditions. D, validation of microarray data of HSP70 expression by qRT-PCR in NKKY101 mutant compared with WT. Data (mean ± S.E. (error bars) of biological replicate with technical triplicates) were normalized to an internal ACT1 mRNA control and represent percentage relative expression in the mutant cultures compared with the wild-type cells. Statistical analysis was performed using Student's t test (**, p ≤ 0.01). E, model for Hsp90 activation. Deletion of CDR6/ROA1 activates the Tor1, which down-regulates the KNS1 transcript, resulting in decreased CK2 kinase activity. This decrease in CK2 kinase activity causes activation of Hsp90 and its client proteins.
Arraycam Tm 400 S Microarray Imaging System, supplied by Grace Bio-Labs, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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gene tac tm uc 4 microarray scanner  (Genomic Solutions Inc)
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Genomic Solutions Inc gene tac tm uc 4 microarray scanner
Tor1 activation in NKKY101 strain causes Hsp90 activation via CK2 kinase. A, CDR6/ROA1 deletion suppresses CK2 activity. CK2 activity was monitored in an in vitro assay using protein lysates from C. albicans WT and NKKY101 strains, using recombinant Sic1 as a substrate. The assay was performed in biological duplicates with technical replicates. Error bars, S.D.; *, p < 0.05 (Student's t test). B, the CDR6/ROA1 deletion causes Hog1 activation. NaCl was used as a positive control to detect the active phosphorylated form of Hog1. The phosphorylated Hog1 level is low in the WT and CDR6/ROA1 revertant NKKY102 strains under basal conditions and induced in the presence of NaCl. However, the phosphorylated Hog1 level is high in the CDR6/ROA1 null strain NKKY101 even in basal conditions. The addition of NaCl increased the phosphorylated Hog1 in the null strain. Bands were quantified using Bio-Rad <t>Image</t> <t>Lab</t> <t>software,</t> and the ratio of phosphorylated Hog1 to total Hog1 was plotted for WT, NKKY101, and NKKY102 strains for basal conditions (without NaCl induction). A similar trend of phosphorylated Hog1 was observed in biological triplicate experiments for basal conditions (Fig. S5). C, Hog1 activation in CDR6/ROA1 null strain NKKY101 is Tor1-dependent. Rapamycin was used as a Tor1 inhibitor. The phosphorylated Hog1 level decreased in CDR6/ROA1 null strain NKKY101 when treated with rapamycin (4 and 8 ng/ml) in comparison with untreated conditions. D, validation of microarray data of HSP70 expression by qRT-PCR in NKKY101 mutant compared with WT. Data (mean ± S.E. (error bars) of biological replicate with technical triplicates) were normalized to an internal ACT1 mRNA control and represent percentage relative expression in the mutant cultures compared with the wild-type cells. Statistical analysis was performed using Student's t test (**, p ≤ 0.01). E, model for Hsp90 activation. Deletion of CDR6/ROA1 activates the Tor1, which down-regulates the KNS1 transcript, resulting in decreased CK2 kinase activity. This decrease in CK2 kinase activity causes activation of Hsp90 and its client proteins.
Gene Tac Tm Uc 4 Microarray Scanner, supplied by Genomic Solutions Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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tm microarray imager software  (CustomArray Inc)
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CustomArray Inc tm microarray imager software
Tor1 activation in NKKY101 strain causes Hsp90 activation via CK2 kinase. A, CDR6/ROA1 deletion suppresses CK2 activity. CK2 activity was monitored in an in vitro assay using protein lysates from C. albicans WT and NKKY101 strains, using recombinant Sic1 as a substrate. The assay was performed in biological duplicates with technical replicates. Error bars, S.D.; *, p < 0.05 (Student's t test). B, the CDR6/ROA1 deletion causes Hog1 activation. NaCl was used as a positive control to detect the active phosphorylated form of Hog1. The phosphorylated Hog1 level is low in the WT and CDR6/ROA1 revertant NKKY102 strains under basal conditions and induced in the presence of NaCl. However, the phosphorylated Hog1 level is high in the CDR6/ROA1 null strain NKKY101 even in basal conditions. The addition of NaCl increased the phosphorylated Hog1 in the null strain. Bands were quantified using Bio-Rad <t>Image</t> <t>Lab</t> <t>software,</t> and the ratio of phosphorylated Hog1 to total Hog1 was plotted for WT, NKKY101, and NKKY102 strains for basal conditions (without NaCl induction). A similar trend of phosphorylated Hog1 was observed in biological triplicate experiments for basal conditions (Fig. S5). C, Hog1 activation in CDR6/ROA1 null strain NKKY101 is Tor1-dependent. Rapamycin was used as a Tor1 inhibitor. The phosphorylated Hog1 level decreased in CDR6/ROA1 null strain NKKY101 when treated with rapamycin (4 and 8 ng/ml) in comparison with untreated conditions. D, validation of microarray data of HSP70 expression by qRT-PCR in NKKY101 mutant compared with WT. Data (mean ± S.E. (error bars) of biological replicate with technical triplicates) were normalized to an internal ACT1 mRNA control and represent percentage relative expression in the mutant cultures compared with the wild-type cells. Statistical analysis was performed using Student's t test (**, p ≤ 0.01). E, model for Hsp90 activation. Deletion of CDR6/ROA1 activates the Tor1, which down-regulates the KNS1 transcript, resulting in decreased CK2 kinase activity. This decrease in CK2 kinase activity causes activation of Hsp90 and its client proteins.
Tm Microarray Imager Software, supplied by CustomArray Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Tor1 activation in NKKY101 strain causes Hsp90 activation via CK2 kinase. A, CDR6/ROA1 deletion suppresses CK2 activity. CK2 activity was monitored in an in vitro assay using protein lysates from C. albicans WT and NKKY101 strains, using recombinant Sic1 as a substrate. The assay was performed in biological duplicates with technical replicates. Error bars, S.D.; *, p < 0.05 (Student's t test). B, the CDR6/ROA1 deletion causes Hog1 activation. NaCl was used as a positive control to detect the active phosphorylated form of Hog1. The phosphorylated Hog1 level is low in the WT and CDR6/ROA1 revertant NKKY102 strains under basal conditions and induced in the presence of NaCl. However, the phosphorylated Hog1 level is high in the CDR6/ROA1 null strain NKKY101 even in basal conditions. The addition of NaCl increased the phosphorylated Hog1 in the null strain. Bands were quantified using Bio-Rad Image Lab software, and the ratio of phosphorylated Hog1 to total Hog1 was plotted for WT, NKKY101, and NKKY102 strains for basal conditions (without NaCl induction). A similar trend of phosphorylated Hog1 was observed in biological triplicate experiments for basal conditions (Fig. S5). C, Hog1 activation in CDR6/ROA1 null strain NKKY101 is Tor1-dependent. Rapamycin was used as a Tor1 inhibitor. The phosphorylated Hog1 level decreased in CDR6/ROA1 null strain NKKY101 when treated with rapamycin (4 and 8 ng/ml) in comparison with untreated conditions. D, validation of microarray data of HSP70 expression by qRT-PCR in NKKY101 mutant compared with WT. Data (mean ± S.E. (error bars) of biological replicate with technical triplicates) were normalized to an internal ACT1 mRNA control and represent percentage relative expression in the mutant cultures compared with the wild-type cells. Statistical analysis was performed using Student's t test (**, p ≤ 0.01). E, model for Hsp90 activation. Deletion of CDR6/ROA1 activates the Tor1, which down-regulates the KNS1 transcript, resulting in decreased CK2 kinase activity. This decrease in CK2 kinase activity causes activation of Hsp90 and its client proteins.

Journal: The Journal of Biological Chemistry

Article Title: Azole resistance in a Candida albicans mutant lacking the ABC transporter CDR6/ROA1 depends on TOR signaling

doi: 10.1074/jbc.M117.807032

Figure Lengend Snippet: Tor1 activation in NKKY101 strain causes Hsp90 activation via CK2 kinase. A, CDR6/ROA1 deletion suppresses CK2 activity. CK2 activity was monitored in an in vitro assay using protein lysates from C. albicans WT and NKKY101 strains, using recombinant Sic1 as a substrate. The assay was performed in biological duplicates with technical replicates. Error bars, S.D.; *, p < 0.05 (Student's t test). B, the CDR6/ROA1 deletion causes Hog1 activation. NaCl was used as a positive control to detect the active phosphorylated form of Hog1. The phosphorylated Hog1 level is low in the WT and CDR6/ROA1 revertant NKKY102 strains under basal conditions and induced in the presence of NaCl. However, the phosphorylated Hog1 level is high in the CDR6/ROA1 null strain NKKY101 even in basal conditions. The addition of NaCl increased the phosphorylated Hog1 in the null strain. Bands were quantified using Bio-Rad Image Lab software, and the ratio of phosphorylated Hog1 to total Hog1 was plotted for WT, NKKY101, and NKKY102 strains for basal conditions (without NaCl induction). A similar trend of phosphorylated Hog1 was observed in biological triplicate experiments for basal conditions (Fig. S5). C, Hog1 activation in CDR6/ROA1 null strain NKKY101 is Tor1-dependent. Rapamycin was used as a Tor1 inhibitor. The phosphorylated Hog1 level decreased in CDR6/ROA1 null strain NKKY101 when treated with rapamycin (4 and 8 ng/ml) in comparison with untreated conditions. D, validation of microarray data of HSP70 expression by qRT-PCR in NKKY101 mutant compared with WT. Data (mean ± S.E. (error bars) of biological replicate with technical triplicates) were normalized to an internal ACT1 mRNA control and represent percentage relative expression in the mutant cultures compared with the wild-type cells. Statistical analysis was performed using Student's t test (**, p ≤ 0.01). E, model for Hsp90 activation. Deletion of CDR6/ROA1 activates the Tor1, which down-regulates the KNS1 transcript, resulting in decreased CK2 kinase activity. This decrease in CK2 kinase activity causes activation of Hsp90 and its client proteins.

Article Snippet: Band intensities were quantified through Image Lab TM software (Bio-Rad), and Hog1 was used as a loading control.

Techniques: Activation Assay, Activity Assay, In Vitro, Recombinant, Positive Control, Software, Comparison, Biomarker Discovery, Microarray, Expressing, Quantitative RT-PCR, Mutagenesis, Control