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  • 98
    ATCC human non neoplastic astrocytic cell line sv40 fhas
    Human Non Neoplastic Astrocytic Cell Line Sv40 Fhas, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human non neoplastic astrocytic cell line sv40 fhas/product/ATCC
    Average 98 stars, based on 1 article reviews
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    human non neoplastic astrocytic cell line sv40 fhas - by Bioz Stars, 2020-12
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    94
    Thermo Fisher alexafluor 647 hydroxylamine fha
    Alexafluor 647 Hydroxylamine Fha, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    List Biological Laboratories native fha
    Silver-stained SDS-PAGE gel (A) and Western immunoblots (B) of the <t>S1S3FHA</t> fusion protein isolated from S. gordonii #8. In panel B, the protein was detected with a rabbit polyclonal anti-PT antibody (lane 1), an anti-S1 monoclonal antibody (lane 2), and an <t>anti-FHA</t> monoclonal antibody (lane 3).
    Native Fha, supplied by List Biological Laboratories, used in various techniques. Bioz Stars score: 85/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    89
    Glaxo Smith fha
    A test with anti-human IgG label demonstrated no unspecific binding to PT test line in ( a ) only <t>anti-FHA</t> (12, 13) and ( b ) both anti-FHA and <t>anti-PRN</t> (18, 19) IgG positive serum samples.
    Fha, supplied by Glaxo Smith, used in various techniques. Bioz Stars score: 89/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    89
    Novartis fha
    A test with anti-human IgG label demonstrated no unspecific binding to PT test line in ( a ) only <t>anti-FHA</t> (12, 13) and ( b ) both anti-FHA and <t>anti-PRN</t> (18, 19) IgG positive serum samples.
    Fha, supplied by Novartis, used in various techniques. Bioz Stars score: 89/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    fha  (Sanofi)
    93
    Sanofi fha
    A test with anti-human IgG label demonstrated no unspecific binding to PT test line in ( a ) only <t>anti-FHA</t> (12, 13) and ( b ) both anti-FHA and <t>anti-PRN</t> (18, 19) IgG positive serum samples.
    Fha, supplied by Sanofi, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Becton Dickinson fha
    A test with anti-human IgG label demonstrated no unspecific binding to PT test line in ( a ) only <t>anti-FHA</t> (12, 13) and ( b ) both anti-FHA and <t>anti-PRN</t> (18, 19) IgG positive serum samples.
    Fha, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 91/100, based on 29 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    89
    Cell Signaling Technology Inc fha
    A test with anti-human IgG label demonstrated no unspecific binding to PT test line in ( a ) only <t>anti-FHA</t> (12, 13) and ( b ) both anti-FHA and <t>anti-PRN</t> (18, 19) IgG positive serum samples.
    Fha, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 89/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Enzo Biochem fha
    A test with anti-human IgG label demonstrated no unspecific binding to PT test line in ( a ) only <t>anti-FHA</t> (12, 13) and ( b ) both anti-FHA and <t>anti-PRN</t> (18, 19) IgG positive serum samples.
    Fha, supplied by Enzo Biochem, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    89
    List Biological Laboratories fha
    A test with anti-human IgG label demonstrated no unspecific binding to PT test line in ( a ) only <t>anti-FHA</t> (12, 13) and ( b ) both anti-FHA and <t>anti-PRN</t> (18, 19) IgG positive serum samples.
    Fha, supplied by List Biological Laboratories, used in various techniques. Bioz Stars score: 89/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    fha  (Provivi)
    90
    Provivi fha
    A test with anti-human IgG label demonstrated no unspecific binding to PT test line in ( a ) only <t>anti-FHA</t> (12, 13) and ( b ) both anti-FHA and <t>anti-PRN</t> (18, 19) IgG positive serum samples.
    Fha, supplied by Provivi, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Addgene inc atg12
    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the <t>ATG12–ATG5</t> conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.
    Atg12, supplied by Addgene inc, used in various techniques. Bioz Stars score: 92/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Thermo Fisher chk2 fha domain phospho peptide binding assay streptavidin beads
    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the <t>ATG12–ATG5</t> conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.
    Chk2 Fha Domain Phospho Peptide Binding Assay Streptavidin Beads, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 92/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Millipore bordetella pertussis fha
    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the <t>ATG12–ATG5</t> conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.
    Bordetella Pertussis Fha, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    BioNet Asia fha bionet asia
    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the <t>ATG12–ATG5</t> conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.
    Fha Bionet Asia, supplied by BioNet Asia, 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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    85
    Glaxo Smith fha antigens
    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the <t>ATG12–ATG5</t> conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.
    Fha Antigens, supplied by Glaxo Smith, used in various techniques. Bioz Stars score: 85/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Novartis fha antigens
    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the <t>ATG12–ATG5</t> conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.
    Fha Antigens, supplied by Novartis, used in various techniques. Bioz Stars score: 85/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Illumina Inc fha deficient
    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the <t>ATG12–ATG5</t> conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.
    Fha Deficient, supplied by Illumina Inc, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Omron fha estate lugbe
    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the <t>ATG12–ATG5</t> conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.
    Fha Estate Lugbe, supplied by Omron, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    BEI Resources fha nr 31065
    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the <t>ATG12–ATG5</t> conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.
    Fha Nr 31065, supplied by BEI Resources, 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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    92
    Illumina Inc fha producing isolates
    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the <t>ATG12–ATG5</t> conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.
    Fha Producing Isolates, supplied by Illumina Inc, used in various techniques. Bioz Stars score: 92/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/fha producing isolates/product/Illumina Inc
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    92
    Glaxo Smith fha protein
    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the <t>ATG12–ATG5</t> conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.
    Fha Protein, supplied by Glaxo Smith, used in various techniques. Bioz Stars score: 92/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    fha  (Aventis)
    89
    Aventis fha
    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the <t>ATG12–ATG5</t> conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.
    Fha, supplied by Aventis, used in various techniques. Bioz Stars score: 89/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/fha/product/Aventis
    Average 89 stars, based on 10 article reviews
    Price from $9.99 to $1999.99
    fha - by Bioz Stars, 2020-12
    89/100 stars
      Buy from Supplier

    89
    Connaught Labs fha
    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the <t>ATG12–ATG5</t> conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.
    Fha, supplied by Connaught Labs, used in various techniques. Bioz Stars score: 89/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/fha/product/Connaught Labs
    Average 89 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    fha - by Bioz Stars, 2020-12
    89/100 stars
      Buy from Supplier

    Image Search Results


    Silver-stained SDS-PAGE gel (A) and Western immunoblots (B) of the S1S3FHA fusion protein isolated from S. gordonii #8. In panel B, the protein was detected with a rabbit polyclonal anti-PT antibody (lane 1), an anti-S1 monoclonal antibody (lane 2), and an anti-FHA monoclonal antibody (lane 3).

    Journal: Applied and Environmental Microbiology

    Article Title: Purification and Immunogenicity of a Recombinant Bordetella pertussis S1S3FHA Fusion Protein Expressed by Streptococcus gordonii

    doi: 10.1128/AEM.68.9.4253-4258.2002

    Figure Lengend Snippet: Silver-stained SDS-PAGE gel (A) and Western immunoblots (B) of the S1S3FHA fusion protein isolated from S. gordonii #8. In panel B, the protein was detected with a rabbit polyclonal anti-PT antibody (lane 1), an anti-S1 monoclonal antibody (lane 2), and an anti-FHA monoclonal antibody (lane 3).

    Article Snippet: The much lower titer against the native FHA than against rFHAI for anti-S1S3FHA sera may be explained by the many hidden epitopes in the native FHA.

    Techniques: Staining, SDS Page, Western Blot, Isolation

    A test with anti-human IgG label demonstrated no unspecific binding to PT test line in ( a ) only anti-FHA (12, 13) and ( b ) both anti-FHA and anti-PRN (18, 19) IgG positive serum samples.

    Journal: Diagnostics

    Article Title: Multiplex Point-of-Care Tests for the Determination of Antibodies after Acellular Pertussis Vaccination

    doi: 10.3390/diagnostics10040187

    Figure Lengend Snippet: A test with anti-human IgG label demonstrated no unspecific binding to PT test line in ( a ) only anti-FHA (12, 13) and ( b ) both anti-FHA and anti-PRN (18, 19) IgG positive serum samples.

    Article Snippet: Lateral flow test strips and multiplex assay: The preparation of the strips and the test procedure was performed following a similar method to Salminen et al. [ ] with the following modifications: The captured reagents on the test strips were purified PRN, PT and FHA—kindly provided by GlaxoSmithKline (Belgium), and rabbit anti-goat IgG antibody on the control line ( ).

    Techniques: Binding Assay

    The multiplex readouts from lateral flow test strips were measured as average time-resolved fluorescence signal by line scanning the nitrocellulose membrane starting from the control line (4 mm), followed by FHA (12 mm), PT (19 mm) and PRN (27 mm) test lines. Different combinations of anti-PRN, -PT and -FHA-specific IgG antibodies were tested: ( a ) All positive (samples 4, 5, 6, 7), ( b ) only PRN IgG positive (8, 9), ( c ) only PT positive (10, 11), ( d ) only FHA positive (12, 13), ( e ) both PRN and PT positive (14, 15), ( f ) both PT and FHA positive (16, 17), ( g ) both PRN and FHA positive, (18, 19), and ( h ) all negative samples (1, 2, 3). Please refer to Table 1 for antibody concentrations.

    Journal: Diagnostics

    Article Title: Multiplex Point-of-Care Tests for the Determination of Antibodies after Acellular Pertussis Vaccination

    doi: 10.3390/diagnostics10040187

    Figure Lengend Snippet: The multiplex readouts from lateral flow test strips were measured as average time-resolved fluorescence signal by line scanning the nitrocellulose membrane starting from the control line (4 mm), followed by FHA (12 mm), PT (19 mm) and PRN (27 mm) test lines. Different combinations of anti-PRN, -PT and -FHA-specific IgG antibodies were tested: ( a ) All positive (samples 4, 5, 6, 7), ( b ) only PRN IgG positive (8, 9), ( c ) only PT positive (10, 11), ( d ) only FHA positive (12, 13), ( e ) both PRN and PT positive (14, 15), ( f ) both PT and FHA positive (16, 17), ( g ) both PRN and FHA positive, (18, 19), and ( h ) all negative samples (1, 2, 3). Please refer to Table 1 for antibody concentrations.

    Article Snippet: Lateral flow test strips and multiplex assay: The preparation of the strips and the test procedure was performed following a similar method to Salminen et al. [ ] with the following modifications: The captured reagents on the test strips were purified PRN, PT and FHA—kindly provided by GlaxoSmithKline (Belgium), and rabbit anti-goat IgG antibody on the control line ( ).

    Techniques: Multiplex Assay, Fluorescence

    Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the ATG12–ATG5 conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.

    Journal: Autophagy

    Article Title: Crosstalk between lysine methylation and phosphorylation of ATG16L1 dictates the apoptosis of hypoxia/reoxygenation-induced cardiomyocytes

    doi: 10.1080/15548627.2017.1389357

    Figure Lengend Snippet: Crosstalk between methylation at K151 and phosphorylation at S139 of ATG16L1. ( A and B ) Immunoprecipitation was performed using anti-ATG16L1 antibody with extracts from untreated or H/R-treated NRVC cells transfected with a plasmid encoding WT SETD7, or sh Setd7 , or sh Kdm1a , WT ATG16L1, or ATG16L1 K151R expression vectors. Western blot analysis was performed with anti-ATG16L1-K151 or anti-phospho-Ser/Thr antibodies. ( C ) ATG16L1 protein was mixed with SETD7 with or without 1 μM cold SAM and then the mixture was subjected to in vitro phosphorylation with CSNK2 and γ 32 P-ATP. ( D ) ATG16L1 protein was preincubated with CSNK2 with or without 0.5 mM cold ATP and then the mixture was subjected to in vitro methylation reactions with SETD7 and H 3 -SAM. ( E ) Working model: (i) H/R decreases SETD7 expression and lysine methylation of ATG16L1, while it increases the KDM1A level and CSNK2 activity in cardiomyocytes; (ii) SETD7 methylates ATG16L1 at K151 in vivo and in vitro , whereas pre-phosphorylated ATG16L1 at S139 by CSNK2 blocks ATG16L1 methylation; and ATG16L1 methyl mark at K151 is removed by KDM1A; (iii) this methylation at K151 impairs the binding of ATG16L1 to the ATG12–ATG5 conjugate, leading to inhibition of autophagy and increased apoptosis in H/R-treated cardiomyocytes.

    Article Snippet: Other plasmids used were as follows: ATG5 (Addgene, 22948; deposited by Noboru Mizushima), FLAG-ATG16L1 constructs (Addgene, 24302; deposited by Noboru Mizushima), and ATG12 (Addgene, 27049; deposited by Jayanta Debnath).

    Techniques: Methylation, Immunoprecipitation, Transfection, Plasmid Preparation, Expressing, Western Blot, In Vitro, Activity Assay, In Vivo, Binding Assay, Inhibition

    Methylation of ATG16L1 at K151 selectively decreased its interaction with the ATG12–ATG5 conjugate. ( A ) H9c2 cells were transfected with plasmids containing empty vector, HA-SETD7 WT , or its inactive mutant HA-SETD7 H297A , and then exposed to H/R. Immunoprecipitation assay indicated that SETD7-dependent methylation of ATG16L1-V5 purified from H9c2 cells inhibited its binding to the ATG12–ATG5 conjugate. ( B ) In vitro binding assay showed that upon SETD7-mediated methylation, ATG16L1 purified from E. coli presented reduced binding, which was reversed by demethylation following (R)-RFI-2 treatment. Protein input and H 3 uptake into ATG16L1 are also shown. ( C ) Indicated E. coli -generated ATG16L1 and GST-ATG12–ATG5 fusion protein were used to perform the affinity isolation assay. Compared to untreated wild-type ATG16L1, SETD7 methylation or untreated ATG16L1 K151Q and K151R mutant showed opposite ATG12–ATG5 conjugate binding. Immunoblotting was carried out using the indicated antibodies. ( D ) NRVCs were or were not subjected to H/R treatment. Endogenous interaction between ATG16L1 and SETD7 or KDM1A was analyzed using co-immunoprecipitation with anti-ATG16L1. Immunoblotting was carried out using the indicated antibodies.

    Journal: Autophagy

    Article Title: Crosstalk between lysine methylation and phosphorylation of ATG16L1 dictates the apoptosis of hypoxia/reoxygenation-induced cardiomyocytes

    doi: 10.1080/15548627.2017.1389357

    Figure Lengend Snippet: Methylation of ATG16L1 at K151 selectively decreased its interaction with the ATG12–ATG5 conjugate. ( A ) H9c2 cells were transfected with plasmids containing empty vector, HA-SETD7 WT , or its inactive mutant HA-SETD7 H297A , and then exposed to H/R. Immunoprecipitation assay indicated that SETD7-dependent methylation of ATG16L1-V5 purified from H9c2 cells inhibited its binding to the ATG12–ATG5 conjugate. ( B ) In vitro binding assay showed that upon SETD7-mediated methylation, ATG16L1 purified from E. coli presented reduced binding, which was reversed by demethylation following (R)-RFI-2 treatment. Protein input and H 3 uptake into ATG16L1 are also shown. ( C ) Indicated E. coli -generated ATG16L1 and GST-ATG12–ATG5 fusion protein were used to perform the affinity isolation assay. Compared to untreated wild-type ATG16L1, SETD7 methylation or untreated ATG16L1 K151Q and K151R mutant showed opposite ATG12–ATG5 conjugate binding. Immunoblotting was carried out using the indicated antibodies. ( D ) NRVCs were or were not subjected to H/R treatment. Endogenous interaction between ATG16L1 and SETD7 or KDM1A was analyzed using co-immunoprecipitation with anti-ATG16L1. Immunoblotting was carried out using the indicated antibodies.

    Article Snippet: Other plasmids used were as follows: ATG5 (Addgene, 22948; deposited by Noboru Mizushima), FLAG-ATG16L1 constructs (Addgene, 24302; deposited by Noboru Mizushima), and ATG12 (Addgene, 27049; deposited by Jayanta Debnath).

    Techniques: Methylation, Transfection, Plasmid Preparation, Mutagenesis, Immunoprecipitation, Purification, Binding Assay, In Vitro, Generated, Isolation