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ml anti nrcam antibody  (Proteintech)


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    Proteintech ml anti nrcam antibody
    Identification of ASM-dependent host co-receptors for S. aureus by an APEX2-based proximity labeling screen. (A) Decorated bacteria are still internalized by host cells in an ASM-dependent manner. HuLEC was treated with amitriptyline, ionomycin, and β-toxin and then infected with APEX2-decorated S. aureus JE2. Invasion efficiency was determined by lysostaphin protection assay and colony-forming units (CFU) recovery assays. Numbers of bacteria internalized by treated cells were normalized to untreated controls (set to 100%, dotted line). (B–D) Establishment of the ASM and Ca 2+ -dependent host-pathogen interactome. HuLEC was pretreated with either amitriptyline, the bacterial SMase β-toxin, and ionomycin or left untreated. Cells were infected with APEX2-decorated S. aureus , and interaction partners were determined by proximity labeling. (B) Abundance of individual proteins was compared to untreated controls, and median log2 fold changes were determined ( n = 3). (C) Proteins with a median log2 fold change ≤−1 were selected as candidate targets for each condition. (D) A list of candidate receptors that were downregulated in at least six of nine replicates (regardless of the treatment) were considered as “consistently reduced.” (E and F) Blockade of <t>NRCAM</t> and MFI2 with antibodies reduces the invasion efficiency of S. aureus . HuLEC was pretreated with antibodies targeting NRCAM (E) or melanotransferrin (MFI2), NT5E/CD73 (F), or the respective solvent control. Then, cells were infected with S. aureus for 10 min, and invasion efficiency was determined by a lysostaphin protection assay and CFU counting ( n ≥ 4). (G) S. aureus invasion is reduced in a PTK7 knockout (K.O.) cell line. The invasion efficiency of S. aureus JE2 after 10 min or 30 min was determined in a HeLa cell line lacking PTK7 and was compared to WT cells ( n = 7). (H) S. aureus invasion is reduced in CD109 and MET K.O. cell lines. The invasion efficiency of S. aureus JE2 after 10 min was determined in a HeLa cell line lacking CD109 ( n = 9), and MET ( n = 5) and compared to WT cells. Statistics: unpaired Student‘s t -test (E and G) or one sample t -test (F and H). * P ≤ 0.05, ** P ≤ 0.01, *** P < 0.001, and **** P < 0.0001.
    Ml Anti Nrcam Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ml+anti+nrcam+antibody/pmc12077161-17-1-5?v=Proteintech
    Average 93 stars, based on 5 article reviews
    ml anti nrcam antibody - by Bioz Stars, 2026-07
    93/100 stars

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    1) Product Images from "Identification of the Staphylococcus aureus endothelial cell surface interactome by proximity labeling"

    Article Title: Identification of the Staphylococcus aureus endothelial cell surface interactome by proximity labeling

    Journal: mBio

    doi: 10.1128/mbio.03654-24

    Identification of ASM-dependent host co-receptors for S. aureus by an APEX2-based proximity labeling screen. (A) Decorated bacteria are still internalized by host cells in an ASM-dependent manner. HuLEC was treated with amitriptyline, ionomycin, and β-toxin and then infected with APEX2-decorated S. aureus JE2. Invasion efficiency was determined by lysostaphin protection assay and colony-forming units (CFU) recovery assays. Numbers of bacteria internalized by treated cells were normalized to untreated controls (set to 100%, dotted line). (B–D) Establishment of the ASM and Ca 2+ -dependent host-pathogen interactome. HuLEC was pretreated with either amitriptyline, the bacterial SMase β-toxin, and ionomycin or left untreated. Cells were infected with APEX2-decorated S. aureus , and interaction partners were determined by proximity labeling. (B) Abundance of individual proteins was compared to untreated controls, and median log2 fold changes were determined ( n = 3). (C) Proteins with a median log2 fold change ≤−1 were selected as candidate targets for each condition. (D) A list of candidate receptors that were downregulated in at least six of nine replicates (regardless of the treatment) were considered as “consistently reduced.” (E and F) Blockade of NRCAM and MFI2 with antibodies reduces the invasion efficiency of S. aureus . HuLEC was pretreated with antibodies targeting NRCAM (E) or melanotransferrin (MFI2), NT5E/CD73 (F), or the respective solvent control. Then, cells were infected with S. aureus for 10 min, and invasion efficiency was determined by a lysostaphin protection assay and CFU counting ( n ≥ 4). (G) S. aureus invasion is reduced in a PTK7 knockout (K.O.) cell line. The invasion efficiency of S. aureus JE2 after 10 min or 30 min was determined in a HeLa cell line lacking PTK7 and was compared to WT cells ( n = 7). (H) S. aureus invasion is reduced in CD109 and MET K.O. cell lines. The invasion efficiency of S. aureus JE2 after 10 min was determined in a HeLa cell line lacking CD109 ( n = 9), and MET ( n = 5) and compared to WT cells. Statistics: unpaired Student‘s t -test (E and G) or one sample t -test (F and H). * P ≤ 0.05, ** P ≤ 0.01, *** P < 0.001, and **** P < 0.0001.
    Figure Legend Snippet: Identification of ASM-dependent host co-receptors for S. aureus by an APEX2-based proximity labeling screen. (A) Decorated bacteria are still internalized by host cells in an ASM-dependent manner. HuLEC was treated with amitriptyline, ionomycin, and β-toxin and then infected with APEX2-decorated S. aureus JE2. Invasion efficiency was determined by lysostaphin protection assay and colony-forming units (CFU) recovery assays. Numbers of bacteria internalized by treated cells were normalized to untreated controls (set to 100%, dotted line). (B–D) Establishment of the ASM and Ca 2+ -dependent host-pathogen interactome. HuLEC was pretreated with either amitriptyline, the bacterial SMase β-toxin, and ionomycin or left untreated. Cells were infected with APEX2-decorated S. aureus , and interaction partners were determined by proximity labeling. (B) Abundance of individual proteins was compared to untreated controls, and median log2 fold changes were determined ( n = 3). (C) Proteins with a median log2 fold change ≤−1 were selected as candidate targets for each condition. (D) A list of candidate receptors that were downregulated in at least six of nine replicates (regardless of the treatment) were considered as “consistently reduced.” (E and F) Blockade of NRCAM and MFI2 with antibodies reduces the invasion efficiency of S. aureus . HuLEC was pretreated with antibodies targeting NRCAM (E) or melanotransferrin (MFI2), NT5E/CD73 (F), or the respective solvent control. Then, cells were infected with S. aureus for 10 min, and invasion efficiency was determined by a lysostaphin protection assay and CFU counting ( n ≥ 4). (G) S. aureus invasion is reduced in a PTK7 knockout (K.O.) cell line. The invasion efficiency of S. aureus JE2 after 10 min or 30 min was determined in a HeLa cell line lacking PTK7 and was compared to WT cells ( n = 7). (H) S. aureus invasion is reduced in CD109 and MET K.O. cell lines. The invasion efficiency of S. aureus JE2 after 10 min was determined in a HeLa cell line lacking CD109 ( n = 9), and MET ( n = 5) and compared to WT cells. Statistics: unpaired Student‘s t -test (E and G) or one sample t -test (F and H). * P ≤ 0.05, ** P ≤ 0.01, *** P < 0.001, and **** P < 0.0001.

    Techniques Used: Labeling, Bacteria, Infection, Solvent, Control, Knock-Out



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    ml anti nrcam antibody  (Proteintech)
    93
    Proteintech ml anti nrcam antibody
    Identification of ASM-dependent host co-receptors for S. aureus by an APEX2-based proximity labeling screen. (A) Decorated bacteria are still internalized by host cells in an ASM-dependent manner. HuLEC was treated with amitriptyline, ionomycin, and β-toxin and then infected with APEX2-decorated S. aureus JE2. Invasion efficiency was determined by lysostaphin protection assay and colony-forming units (CFU) recovery assays. Numbers of bacteria internalized by treated cells were normalized to untreated controls (set to 100%, dotted line). (B–D) Establishment of the ASM and Ca 2+ -dependent host-pathogen interactome. HuLEC was pretreated with either amitriptyline, the bacterial SMase β-toxin, and ionomycin or left untreated. Cells were infected with APEX2-decorated S. aureus , and interaction partners were determined by proximity labeling. (B) Abundance of individual proteins was compared to untreated controls, and median log2 fold changes were determined ( n = 3). (C) Proteins with a median log2 fold change ≤−1 were selected as candidate targets for each condition. (D) A list of candidate receptors that were downregulated in at least six of nine replicates (regardless of the treatment) were considered as “consistently reduced.” (E and F) Blockade of <t>NRCAM</t> and MFI2 with antibodies reduces the invasion efficiency of S. aureus . HuLEC was pretreated with antibodies targeting NRCAM (E) or melanotransferrin (MFI2), NT5E/CD73 (F), or the respective solvent control. Then, cells were infected with S. aureus for 10 min, and invasion efficiency was determined by a lysostaphin protection assay and CFU counting ( n ≥ 4). (G) S. aureus invasion is reduced in a PTK7 knockout (K.O.) cell line. The invasion efficiency of S. aureus JE2 after 10 min or 30 min was determined in a HeLa cell line lacking PTK7 and was compared to WT cells ( n = 7). (H) S. aureus invasion is reduced in CD109 and MET K.O. cell lines. The invasion efficiency of S. aureus JE2 after 10 min was determined in a HeLa cell line lacking CD109 ( n = 9), and MET ( n = 5) and compared to WT cells. Statistics: unpaired Student‘s t -test (E and G) or one sample t -test (F and H). * P ≤ 0.05, ** P ≤ 0.01, *** P < 0.001, and **** P < 0.0001.
    Ml Anti Nrcam Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ml+anti+nrcam+antibody/pmc12077161-17-1-5?v=Proteintech
    Average 93 stars, based on 1 article reviews
    ml anti nrcam antibody - by Bioz Stars, 2026-07
    93/100 stars
    		  Buy from Supplier

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    Identification of ASM-dependent host co-receptors for S. aureus by an APEX2-based proximity labeling screen. (A) Decorated bacteria are still internalized by host cells in an ASM-dependent manner. HuLEC was treated with amitriptyline, ionomycin, and β-toxin and then infected with APEX2-decorated S. aureus JE2. Invasion efficiency was determined by lysostaphin protection assay and colony-forming units (CFU) recovery assays. Numbers of bacteria internalized by treated cells were normalized to untreated controls (set to 100%, dotted line). (B–D) Establishment of the ASM and Ca 2+ -dependent host-pathogen interactome. HuLEC was pretreated with either amitriptyline, the bacterial SMase β-toxin, and ionomycin or left untreated. Cells were infected with APEX2-decorated S. aureus , and interaction partners were determined by proximity labeling. (B) Abundance of individual proteins was compared to untreated controls, and median log2 fold changes were determined ( n = 3). (C) Proteins with a median log2 fold change ≤−1 were selected as candidate targets for each condition. (D) A list of candidate receptors that were downregulated in at least six of nine replicates (regardless of the treatment) were considered as “consistently reduced.” (E and F) Blockade of NRCAM and MFI2 with antibodies reduces the invasion efficiency of S. aureus . HuLEC was pretreated with antibodies targeting NRCAM (E) or melanotransferrin (MFI2), NT5E/CD73 (F), or the respective solvent control. Then, cells were infected with S. aureus for 10 min, and invasion efficiency was determined by a lysostaphin protection assay and CFU counting ( n ≥ 4). (G) S. aureus invasion is reduced in a PTK7 knockout (K.O.) cell line. The invasion efficiency of S. aureus JE2 after 10 min or 30 min was determined in a HeLa cell line lacking PTK7 and was compared to WT cells ( n = 7). (H) S. aureus invasion is reduced in CD109 and MET K.O. cell lines. The invasion efficiency of S. aureus JE2 after 10 min was determined in a HeLa cell line lacking CD109 ( n = 9), and MET ( n = 5) and compared to WT cells. Statistics: unpaired Student‘s t -test (E and G) or one sample t -test (F and H). * P ≤ 0.05, ** P ≤ 0.01, *** P < 0.001, and **** P < 0.0001.

    Journal: mBio

    Article Title: Identification of the Staphylococcus aureus endothelial cell surface interactome by proximity labeling

    doi: 10.1128/mbio.03654-24

    Figure Lengend Snippet: Identification of ASM-dependent host co-receptors for S. aureus by an APEX2-based proximity labeling screen. (A) Decorated bacteria are still internalized by host cells in an ASM-dependent manner. HuLEC was treated with amitriptyline, ionomycin, and β-toxin and then infected with APEX2-decorated S. aureus JE2. Invasion efficiency was determined by lysostaphin protection assay and colony-forming units (CFU) recovery assays. Numbers of bacteria internalized by treated cells were normalized to untreated controls (set to 100%, dotted line). (B–D) Establishment of the ASM and Ca 2+ -dependent host-pathogen interactome. HuLEC was pretreated with either amitriptyline, the bacterial SMase β-toxin, and ionomycin or left untreated. Cells were infected with APEX2-decorated S. aureus , and interaction partners were determined by proximity labeling. (B) Abundance of individual proteins was compared to untreated controls, and median log2 fold changes were determined ( n = 3). (C) Proteins with a median log2 fold change ≤−1 were selected as candidate targets for each condition. (D) A list of candidate receptors that were downregulated in at least six of nine replicates (regardless of the treatment) were considered as “consistently reduced.” (E and F) Blockade of NRCAM and MFI2 with antibodies reduces the invasion efficiency of S. aureus . HuLEC was pretreated with antibodies targeting NRCAM (E) or melanotransferrin (MFI2), NT5E/CD73 (F), or the respective solvent control. Then, cells were infected with S. aureus for 10 min, and invasion efficiency was determined by a lysostaphin protection assay and CFU counting ( n ≥ 4). (G) S. aureus invasion is reduced in a PTK7 knockout (K.O.) cell line. The invasion efficiency of S. aureus JE2 after 10 min or 30 min was determined in a HeLa cell line lacking PTK7 and was compared to WT cells ( n = 7). (H) S. aureus invasion is reduced in CD109 and MET K.O. cell lines. The invasion efficiency of S. aureus JE2 after 10 min was determined in a HeLa cell line lacking CD109 ( n = 9), and MET ( n = 5) and compared to WT cells. Statistics: unpaired Student‘s t -test (E and G) or one sample t -test (F and H). * P ≤ 0.05, ** P ≤ 0.01, *** P < 0.001, and **** P < 0.0001.

    Article Snippet: 30 ng/mL anti-NRCAM antibody , Proteintech/21608–1-AP , 75 min , Removed prior to infection.

    Techniques: Labeling, Bacteria, Infection, Solvent, Control, Knock-Out