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    Santa Cruz Biotechnology anti hog1 antibody
    The cross-talk between thermal adaptation and cell wall stress resistance is not mediated via stress cross-protection. (A) Stress cross-protection in C. albicans wild-type cells (NGY152: Table 1 ) was not observed for cells pre-treated with a heat stress and then subjected to cell wall stress, but was observed for cells exposed to a secondary oxidative stress. The data represent cell survival after exposure to a 30°C–42°C heat shock followed by a subsequent cell wall (CFW, CR), osmotic (NaCl) or peroxide (H 2 O 2 ) stress (see Materials and Methods ) and the data are expressed relative to unstressed cells (dark bars). Control cells (grey bars), were not exposed to the prior 30°C–42°C heat shock. (B) The reciprocal assay was performed, whereby C. albicans wild type cells were exposed to a prior stress (cell wall: CFW, CR; osmotic: NaCl; peroxide: H 2 O 2 ) followed by a 30°C–42°C heat shock (dark bars). These data are expressed relative to unstressed cells. Control cells (grey bars) correspond to cells exposed only to the 30°C–42°C heat shock. (C) Wild type, <t>hog1</t> Δ (JC50) or cap1 Δ cells (JC128: Table 1 ) were pre-treated with a 30°C–42°C heat shock, followed by a H 2 O 2 stress (dark bars). Control cells (grey bars) were not exposed to the 30°C–42°C heat shock. The data represent the level of survival compared to unstressed cells. All data are the means from three independent assays: ** paired, two-tailed t-test, p
    Anti Hog1 Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti hog1 antibody/product/Santa Cruz Biotechnology
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti hog1 antibody - by Bioz Stars, 2021-09
    96/100 stars
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    93
    Santa Cruz Biotechnology hog1
    The <t>Hog1</t> signaling profile is insufficient to predict downstream output
    Hog1, 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/result/hog1/product/Santa Cruz Biotechnology
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    hog1 - by Bioz Stars, 2021-09
    93/100 stars
      Buy from Supplier

    Image Search Results


    The cross-talk between thermal adaptation and cell wall stress resistance is not mediated via stress cross-protection. (A) Stress cross-protection in C. albicans wild-type cells (NGY152: Table 1 ) was not observed for cells pre-treated with a heat stress and then subjected to cell wall stress, but was observed for cells exposed to a secondary oxidative stress. The data represent cell survival after exposure to a 30°C–42°C heat shock followed by a subsequent cell wall (CFW, CR), osmotic (NaCl) or peroxide (H 2 O 2 ) stress (see Materials and Methods ) and the data are expressed relative to unstressed cells (dark bars). Control cells (grey bars), were not exposed to the prior 30°C–42°C heat shock. (B) The reciprocal assay was performed, whereby C. albicans wild type cells were exposed to a prior stress (cell wall: CFW, CR; osmotic: NaCl; peroxide: H 2 O 2 ) followed by a 30°C–42°C heat shock (dark bars). These data are expressed relative to unstressed cells. Control cells (grey bars) correspond to cells exposed only to the 30°C–42°C heat shock. (C) Wild type, hog1 Δ (JC50) or cap1 Δ cells (JC128: Table 1 ) were pre-treated with a 30°C–42°C heat shock, followed by a H 2 O 2 stress (dark bars). Control cells (grey bars) were not exposed to the 30°C–42°C heat shock. The data represent the level of survival compared to unstressed cells. All data are the means from three independent assays: ** paired, two-tailed t-test, p

    Journal: PLoS Pathogens

    Article Title: Hsp90 Orchestrates Transcriptional Regulation by Hsf1 and Cell Wall Remodelling by MAPK Signalling during Thermal Adaptation in a Pathogenic Yeast

    doi: 10.1371/journal.ppat.1003069

    Figure Lengend Snippet: The cross-talk between thermal adaptation and cell wall stress resistance is not mediated via stress cross-protection. (A) Stress cross-protection in C. albicans wild-type cells (NGY152: Table 1 ) was not observed for cells pre-treated with a heat stress and then subjected to cell wall stress, but was observed for cells exposed to a secondary oxidative stress. The data represent cell survival after exposure to a 30°C–42°C heat shock followed by a subsequent cell wall (CFW, CR), osmotic (NaCl) or peroxide (H 2 O 2 ) stress (see Materials and Methods ) and the data are expressed relative to unstressed cells (dark bars). Control cells (grey bars), were not exposed to the prior 30°C–42°C heat shock. (B) The reciprocal assay was performed, whereby C. albicans wild type cells were exposed to a prior stress (cell wall: CFW, CR; osmotic: NaCl; peroxide: H 2 O 2 ) followed by a 30°C–42°C heat shock (dark bars). These data are expressed relative to unstressed cells. Control cells (grey bars) correspond to cells exposed only to the 30°C–42°C heat shock. (C) Wild type, hog1 Δ (JC50) or cap1 Δ cells (JC128: Table 1 ) were pre-treated with a 30°C–42°C heat shock, followed by a H 2 O 2 stress (dark bars). Control cells (grey bars) were not exposed to the 30°C–42°C heat shock. The data represent the level of survival compared to unstressed cells. All data are the means from three independent assays: ** paired, two-tailed t-test, p

    Article Snippet: To detect total Hog1 an anti-Hog1 antibody (Santa Cruz Biotechnology, y-215) was diluted 1∶1000 in PBS-T+5% milk.

    Techniques: Two Tailed Test

    Hsp90 coordinates the activities of multiple signalling pathways that contribute to thermotolerance in C. albicans - a model. Hsf1 activation is required for thermotolerance [42] . Hog1, Mkc1 and Cek1 signalling are also required for thermotolerance ( Figure 3 ), but these MAP kinases are not essential for Hsf1 phosphorylation ( Figure 4 ). Instead, these pathways promote thermotolerance in part via cell wall remodelling [81] , [90] . Hsp90 coordinates much of this activity. Hsf1 ( Figures 1 and 2 ), Hog1, Mkc1 and Cek1 ( Figure 10 ) are all Hsp90 client proteins [62] , [86] . Changes in ambient temperature affect interactions between Hsp90 and Hsf1 ( Figure 2 ), and probably affect Hsp90 interactions with Hog1, Mkc1 and Cek1 [49] thereby modulating the activities of these signalling pathways and their inputs to thermal adaptation. Increases in ambient temperature activate Hsf1, thereby inducing the expression of protein chaperones (HSPs) including Hsp90, which promotes thermal adaptation in the shorter term. Hsp90 then down-regulates Hsf1 and modulates Mkc1, Hog1 and Cek1 signalling, which in the longer term influences cell wall architecture ( Figure 11 ), leading to the thermotolerance of C. albicans .

    Journal: PLoS Pathogens

    Article Title: Hsp90 Orchestrates Transcriptional Regulation by Hsf1 and Cell Wall Remodelling by MAPK Signalling during Thermal Adaptation in a Pathogenic Yeast

    doi: 10.1371/journal.ppat.1003069

    Figure Lengend Snippet: Hsp90 coordinates the activities of multiple signalling pathways that contribute to thermotolerance in C. albicans - a model. Hsf1 activation is required for thermotolerance [42] . Hog1, Mkc1 and Cek1 signalling are also required for thermotolerance ( Figure 3 ), but these MAP kinases are not essential for Hsf1 phosphorylation ( Figure 4 ). Instead, these pathways promote thermotolerance in part via cell wall remodelling [81] , [90] . Hsp90 coordinates much of this activity. Hsf1 ( Figures 1 and 2 ), Hog1, Mkc1 and Cek1 ( Figure 10 ) are all Hsp90 client proteins [62] , [86] . Changes in ambient temperature affect interactions between Hsp90 and Hsf1 ( Figure 2 ), and probably affect Hsp90 interactions with Hog1, Mkc1 and Cek1 [49] thereby modulating the activities of these signalling pathways and their inputs to thermal adaptation. Increases in ambient temperature activate Hsf1, thereby inducing the expression of protein chaperones (HSPs) including Hsp90, which promotes thermal adaptation in the shorter term. Hsp90 then down-regulates Hsf1 and modulates Mkc1, Hog1 and Cek1 signalling, which in the longer term influences cell wall architecture ( Figure 11 ), leading to the thermotolerance of C. albicans .

    Article Snippet: To detect total Hog1 an anti-Hog1 antibody (Santa Cruz Biotechnology, y-215) was diluted 1∶1000 in PBS-T+5% milk.

    Techniques: Activation Assay, Activity Assay, Expressing

    Hsp90 depletion affects MAP kinase signalling in the presence and absence of stress. C. albicans wild-type and tetO-HSP90 cells (SN95 and CaLC1411: Table 1 ) were treated with 0 or 20 µg/ml doxycycline for seven hours. Mkc1, Cek1 and Hog1 phosphorylation levels were then assayed by western analysis in unstressed cells or cells treated as follows: (A) 30 minute 30°C–42°C heat shock; (B) 30 minutes with 100 µg/ml Calcofluor White (CFW); (C) 10 minutes with 5 mM H 2 O 2 ; or (D) 12 minutes with 1 M NaCl. Total Mkc1 levels were assayed using Mkc1-6xHis-FLAG tagged cells in SN95 (CaLC681) and tetO-HSP90 (caLC648) cells ( Table 1 ). Hsp90 levels and total kinase levels for Hog1 were also examined by western blotting relative to the internal Act1 loading control.

    Journal: PLoS Pathogens

    Article Title: Hsp90 Orchestrates Transcriptional Regulation by Hsf1 and Cell Wall Remodelling by MAPK Signalling during Thermal Adaptation in a Pathogenic Yeast

    doi: 10.1371/journal.ppat.1003069

    Figure Lengend Snippet: Hsp90 depletion affects MAP kinase signalling in the presence and absence of stress. C. albicans wild-type and tetO-HSP90 cells (SN95 and CaLC1411: Table 1 ) were treated with 0 or 20 µg/ml doxycycline for seven hours. Mkc1, Cek1 and Hog1 phosphorylation levels were then assayed by western analysis in unstressed cells or cells treated as follows: (A) 30 minute 30°C–42°C heat shock; (B) 30 minutes with 100 µg/ml Calcofluor White (CFW); (C) 10 minutes with 5 mM H 2 O 2 ; or (D) 12 minutes with 1 M NaCl. Total Mkc1 levels were assayed using Mkc1-6xHis-FLAG tagged cells in SN95 (CaLC681) and tetO-HSP90 (caLC648) cells ( Table 1 ). Hsp90 levels and total kinase levels for Hog1 were also examined by western blotting relative to the internal Act1 loading control.

    Article Snippet: To detect total Hog1 an anti-Hog1 antibody (Santa Cruz Biotechnology, y-215) was diluted 1∶1000 in PBS-T+5% milk.

    Techniques: Western Blot

    Cross-talk between MAP kinase pathways during heat shock. Differential MAP kinase activation in response to a 30°C–42°C heat shock in MAP kinase mutants. (A) Activation of Hog1, Mkc1 and Cek1 was determined in an mkc1 Δ mutant relative to the internal Act1 control. (B) Activation of Hog1, Mkc1 and Cek1 was assayed in a cek1 Δ mutant relative to the internal Act1 control. (C) Activation of Hog1, Mkc1 and Cek1 was determined in a hog1 Δ mutant relative to the internal Act1 control.

    Journal: PLoS Pathogens

    Article Title: Hsp90 Orchestrates Transcriptional Regulation by Hsf1 and Cell Wall Remodelling by MAPK Signalling during Thermal Adaptation in a Pathogenic Yeast

    doi: 10.1371/journal.ppat.1003069

    Figure Lengend Snippet: Cross-talk between MAP kinase pathways during heat shock. Differential MAP kinase activation in response to a 30°C–42°C heat shock in MAP kinase mutants. (A) Activation of Hog1, Mkc1 and Cek1 was determined in an mkc1 Δ mutant relative to the internal Act1 control. (B) Activation of Hog1, Mkc1 and Cek1 was assayed in a cek1 Δ mutant relative to the internal Act1 control. (C) Activation of Hog1, Mkc1 and Cek1 was determined in a hog1 Δ mutant relative to the internal Act1 control.

    Article Snippet: To detect total Hog1 an anti-Hog1 antibody (Santa Cruz Biotechnology, y-215) was diluted 1∶1000 in PBS-T+5% milk.

    Techniques: Activation Assay, Mutagenesis

    Differential activation profiles of MAP kinases in response to heat shock. (A) Phosphorylation of C. albicans Mkc1, Cek1 and Hog1 during a 30°C–42°C heat shock revealed by western analysis using phospho-specific antibodies. Total kinase levels were monitored using antibodies against total Hog1, FLAG-tagged Mkc1 and TAP-tagged Cek1. Actin served as an internal loading control. (B) Expression of target genes for Mkc1 ( PGA13 ), Cek1 ( PMT4 ) and Hog1 ( RHR2 ) during a 30°C–42°C heat shock, as determined by qRT-PCR of the corresponding transcripts relative to the internal ACT1 mRNA control.

    Journal: PLoS Pathogens

    Article Title: Hsp90 Orchestrates Transcriptional Regulation by Hsf1 and Cell Wall Remodelling by MAPK Signalling during Thermal Adaptation in a Pathogenic Yeast

    doi: 10.1371/journal.ppat.1003069

    Figure Lengend Snippet: Differential activation profiles of MAP kinases in response to heat shock. (A) Phosphorylation of C. albicans Mkc1, Cek1 and Hog1 during a 30°C–42°C heat shock revealed by western analysis using phospho-specific antibodies. Total kinase levels were monitored using antibodies against total Hog1, FLAG-tagged Mkc1 and TAP-tagged Cek1. Actin served as an internal loading control. (B) Expression of target genes for Mkc1 ( PGA13 ), Cek1 ( PMT4 ) and Hog1 ( RHR2 ) during a 30°C–42°C heat shock, as determined by qRT-PCR of the corresponding transcripts relative to the internal ACT1 mRNA control.

    Article Snippet: To detect total Hog1 an anti-Hog1 antibody (Santa Cruz Biotechnology, y-215) was diluted 1∶1000 in PBS-T+5% milk.

    Techniques: Activation Assay, Western Blot, Expressing, Quantitative RT-PCR

    Impact of MAP kinase cross-talk upon stress resistance during thermal adaptation. Cek1 signalling is required for the Calcofluor White resistance of hog1 cells at high temperatures. MIC assays were performed in YPD medium supplemented with different concentrations of NaCl, Calcofluor White or Congo Red. Plates were incubated statically at 25°C, 30°C, 37°C and 42°C for 48 hours. For each strain, optical densities were averaged for duplicate measurements and growth is quantitatively displayed with colour as indicated with the colour bar. Data are representative of three biological replicates. WT, wild type (NGY152: Table 1 ).

    Journal: PLoS Pathogens

    Article Title: Hsp90 Orchestrates Transcriptional Regulation by Hsf1 and Cell Wall Remodelling by MAPK Signalling during Thermal Adaptation in a Pathogenic Yeast

    doi: 10.1371/journal.ppat.1003069

    Figure Lengend Snippet: Impact of MAP kinase cross-talk upon stress resistance during thermal adaptation. Cek1 signalling is required for the Calcofluor White resistance of hog1 cells at high temperatures. MIC assays were performed in YPD medium supplemented with different concentrations of NaCl, Calcofluor White or Congo Red. Plates were incubated statically at 25°C, 30°C, 37°C and 42°C for 48 hours. For each strain, optical densities were averaged for duplicate measurements and growth is quantitatively displayed with colour as indicated with the colour bar. Data are representative of three biological replicates. WT, wild type (NGY152: Table 1 ).

    Article Snippet: To detect total Hog1 an anti-Hog1 antibody (Santa Cruz Biotechnology, y-215) was diluted 1∶1000 in PBS-T+5% milk.

    Techniques: Incubation

    The Hog1 signaling profile is insufficient to predict downstream output

    Journal: Science signaling

    Article Title: MAPK feedback encodes a switch and timer for tunable stress adaptation in yeast

    doi: 10.1126/scisignal.2005774

    Figure Lengend Snippet: The Hog1 signaling profile is insufficient to predict downstream output

    Article Snippet: The equation for the time-dependent behavior of nuclear Hog1 is given by d [ Hog 1 ∗ ] n d t = k n ⋅ [ Hog 1 ( t ) ∗ ] c − k c ⋅ [ Hog 1 ( t ) ∗ ] n (4) The equation that models time-dependent behavior of the species X is d [ X ∗ ] d t = k 8 ⋅ [ Hog 1 ( t ) ∗ ] n ⋅ ( [ X Total ] − [ X ( t ) ∗ ] ) K m 8 + ( [ X Total ] − [ X ( t ) ∗ ] ) − k 9 ⋅ [ X ( t ) ∗ ] K m 9 + [ X ( t ) ∗ ] (5) where the first term models Hog1-dependent X activation, and the second term models X deactivation.

    Techniques:

    The Hog1 signaling profile is a linear transducer that converts dose to duration

    Journal: Science signaling

    Article Title: MAPK feedback encodes a switch and timer for tunable stress adaptation in yeast

    doi: 10.1126/scisignal.2005774

    Figure Lengend Snippet: The Hog1 signaling profile is a linear transducer that converts dose to duration

    Article Snippet: The equation for the time-dependent behavior of nuclear Hog1 is given by d [ Hog 1 ∗ ] n d t = k n ⋅ [ Hog 1 ( t ) ∗ ] c − k c ⋅ [ Hog 1 ( t ) ∗ ] n (4) The equation that models time-dependent behavior of the species X is d [ X ∗ ] d t = k 8 ⋅ [ Hog 1 ( t ) ∗ ] n ⋅ ( [ X Total ] − [ X ( t ) ∗ ] ) K m 8 + ( [ X Total ] − [ X ( t ) ∗ ] ) − k 9 ⋅ [ X ( t ) ∗ ] K m 9 + [ X ( t ) ∗ ] (5) where the first term models Hog1-dependent X activation, and the second term models X deactivation.

    Techniques:

    Modeling positive and negative feedback by Hog1

    Journal: Science signaling

    Article Title: MAPK feedback encodes a switch and timer for tunable stress adaptation in yeast

    doi: 10.1126/scisignal.2005774

    Figure Lengend Snippet: Modeling positive and negative feedback by Hog1

    Article Snippet: The equation for the time-dependent behavior of nuclear Hog1 is given by d [ Hog 1 ∗ ] n d t = k n ⋅ [ Hog 1 ( t ) ∗ ] c − k c ⋅ [ Hog 1 ( t ) ∗ ] n (4) The equation that models time-dependent behavior of the species X is d [ X ∗ ] d t = k 8 ⋅ [ Hog 1 ( t ) ∗ ] n ⋅ ( [ X Total ] − [ X ( t ) ∗ ] ) K m 8 + ( [ X Total ] − [ X ( t ) ∗ ] ) − k 9 ⋅ [ X ( t ) ∗ ] K m 9 + [ X ( t ) ∗ ] (5) where the first term models Hog1-dependent X activation, and the second term models X deactivation.

    Techniques:

    Hog1 encodes dose-to-duration signaling through graded phosphorylation

    Journal: Science signaling

    Article Title: MAPK feedback encodes a switch and timer for tunable stress adaptation in yeast

    doi: 10.1126/scisignal.2005774

    Figure Lengend Snippet: Hog1 encodes dose-to-duration signaling through graded phosphorylation

    Article Snippet: The equation for the time-dependent behavior of nuclear Hog1 is given by d [ Hog 1 ∗ ] n d t = k n ⋅ [ Hog 1 ( t ) ∗ ] c − k c ⋅ [ Hog 1 ( t ) ∗ ] n (4) The equation that models time-dependent behavior of the species X is d [ X ∗ ] d t = k 8 ⋅ [ Hog 1 ( t ) ∗ ] n ⋅ ( [ X Total ] − [ X ( t ) ∗ ] ) K m 8 + ( [ X Total ] − [ X ( t ) ∗ ] ) − k 9 ⋅ [ X ( t ) ∗ ] K m 9 + [ X ( t ) ∗ ] (5) where the first term models Hog1-dependent X activation, and the second term models X deactivation.

    Techniques:

    Hog1 executes a tiered adaptive protein induction program over time

    Journal: Science signaling

    Article Title: MAPK feedback encodes a switch and timer for tunable stress adaptation in yeast

    doi: 10.1126/scisignal.2005774

    Figure Lengend Snippet: Hog1 executes a tiered adaptive protein induction program over time

    Article Snippet: The equation for the time-dependent behavior of nuclear Hog1 is given by d [ Hog 1 ∗ ] n d t = k n ⋅ [ Hog 1 ( t ) ∗ ] c − k c ⋅ [ Hog 1 ( t ) ∗ ] n (4) The equation that models time-dependent behavior of the species X is d [ X ∗ ] d t = k 8 ⋅ [ Hog 1 ( t ) ∗ ] n ⋅ ( [ X Total ] − [ X ( t ) ∗ ] ) K m 8 + ( [ X Total ] − [ X ( t ) ∗ ] ) − k 9 ⋅ [ X ( t ) ∗ ] K m 9 + [ X ( t ) ∗ ] (5) where the first term models Hog1-dependent X activation, and the second term models X deactivation.

    Techniques:

    The Hog1 signaling profile can be reengineered through component gene deletions

    Journal: Science signaling

    Article Title: MAPK feedback encodes a switch and timer for tunable stress adaptation in yeast

    doi: 10.1126/scisignal.2005774

    Figure Lengend Snippet: The Hog1 signaling profile can be reengineered through component gene deletions

    Article Snippet: The equation for the time-dependent behavior of nuclear Hog1 is given by d [ Hog 1 ∗ ] n d t = k n ⋅ [ Hog 1 ( t ) ∗ ] c − k c ⋅ [ Hog 1 ( t ) ∗ ] n (4) The equation that models time-dependent behavior of the species X is d [ X ∗ ] d t = k 8 ⋅ [ Hog 1 ( t ) ∗ ] n ⋅ ( [ X Total ] − [ X ( t ) ∗ ] ) K m 8 + ( [ X Total ] − [ X ( t ) ∗ ] ) − k 9 ⋅ [ X ( t ) ∗ ] K m 9 + [ X ( t ) ∗ ] (5) where the first term models Hog1-dependent X activation, and the second term models X deactivation.

    Techniques: