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human monocytic aml cell line thp  (ATCC)


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    Structured Review

    ATCC human monocytic aml cell line thp
    FcγR-dependent and independent mechanisms of h128-3-induced LILRB4 internalization on monocytic AML. Depending on the monocytic <t>AML</t> <t>cell</t> surface levels of functional FcγRs, h128-3 binds and internalizes its LILRB4 target receptor on these malignant cells by three potential mechanisms: (1) on all monocytic AML cells, h128-3 crosslinking of LILRB4 receptors triggers clathrin-mediated endocytosis and lysosomal receptor degradation; (2) on FcγR high monocytic AML cells, high-affinity FcγRI scaffolds h128-3 to target LILRB4, leading to internalization and degradation; and (3) on FcγRI − FcγRIIA + monocytic AML cells, low-affinity FcγRIIA scaffolds h128-3 by avidity to target LILRB4, prompting its internalization and degradation.
    Human Monocytic Aml Cell Line Thp, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 20870 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human monocytic aml cell line thp/product/ATCC
    Average 99 stars, based on 20870 article reviews
    human monocytic aml cell line thp - by Bioz Stars, 2026-02
    99/100 stars

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    1) Product Images from "Fc gamma receptors promote antibody-induced LILRB4 internalization and immune regulation of monocytic AML"

    Article Title: Fc gamma receptors promote antibody-induced LILRB4 internalization and immune regulation of monocytic AML

    Journal: Antibody Therapeutics

    doi: 10.1093/abt/tbad025

    FcγR-dependent and independent mechanisms of h128-3-induced LILRB4 internalization on monocytic AML. Depending on the monocytic AML cell surface levels of functional FcγRs, h128-3 binds and internalizes its LILRB4 target receptor on these malignant cells by three potential mechanisms: (1) on all monocytic AML cells, h128-3 crosslinking of LILRB4 receptors triggers clathrin-mediated endocytosis and lysosomal receptor degradation; (2) on FcγR high monocytic AML cells, high-affinity FcγRI scaffolds h128-3 to target LILRB4, leading to internalization and degradation; and (3) on FcγRI − FcγRIIA + monocytic AML cells, low-affinity FcγRIIA scaffolds h128-3 by avidity to target LILRB4, prompting its internalization and degradation.
    Figure Legend Snippet: FcγR-dependent and independent mechanisms of h128-3-induced LILRB4 internalization on monocytic AML. Depending on the monocytic AML cell surface levels of functional FcγRs, h128-3 binds and internalizes its LILRB4 target receptor on these malignant cells by three potential mechanisms: (1) on all monocytic AML cells, h128-3 crosslinking of LILRB4 receptors triggers clathrin-mediated endocytosis and lysosomal receptor degradation; (2) on FcγR high monocytic AML cells, high-affinity FcγRI scaffolds h128-3 to target LILRB4, leading to internalization and degradation; and (3) on FcγRI − FcγRIIA + monocytic AML cells, low-affinity FcγRIIA scaffolds h128-3 by avidity to target LILRB4, prompting its internalization and degradation.

    Techniques Used: Functional Assay



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    ATCC human monocytic aml cell line thp
    FcγR-dependent and independent mechanisms of h128-3-induced LILRB4 internalization on monocytic AML. Depending on the monocytic <t>AML</t> <t>cell</t> surface levels of functional FcγRs, h128-3 binds and internalizes its LILRB4 target receptor on these malignant cells by three potential mechanisms: (1) on all monocytic AML cells, h128-3 crosslinking of LILRB4 receptors triggers clathrin-mediated endocytosis and lysosomal receptor degradation; (2) on FcγR high monocytic AML cells, high-affinity FcγRI scaffolds h128-3 to target LILRB4, leading to internalization and degradation; and (3) on FcγRI − FcγRIIA + monocytic AML cells, low-affinity FcγRIIA scaffolds h128-3 by avidity to target LILRB4, prompting its internalization and degradation.
    Human Monocytic Aml Cell Line Thp, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human monocytic aml cell line thp/product/ATCC
    Average 99 stars, based on 1 article reviews
    human monocytic aml cell line thp - by Bioz Stars, 2026-02
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    DSMZ human monocytic aml cell line mono mac
    FcγR-dependent and independent mechanisms of h128-3-induced LILRB4 internalization on monocytic AML. Depending on the monocytic <t>AML</t> <t>cell</t> surface levels of functional FcγRs, h128-3 binds and internalizes its LILRB4 target receptor on these malignant cells by three potential mechanisms: (1) on all monocytic AML cells, h128-3 crosslinking of LILRB4 receptors triggers clathrin-mediated endocytosis and lysosomal receptor degradation; (2) on FcγR high monocytic AML cells, high-affinity FcγRI scaffolds h128-3 to target LILRB4, leading to internalization and degradation; and (3) on FcγRI − FcγRIIA + monocytic AML cells, low-affinity FcγRIIA scaffolds h128-3 by avidity to target LILRB4, prompting its internalization and degradation.
    Human Monocytic Aml Cell Line Mono Mac, supplied by DSMZ, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human monocytic aml cell lines
    FcγR-dependent and independent mechanisms of h128-3-induced LILRB4 internalization on monocytic AML. Depending on the monocytic <t>AML</t> <t>cell</t> surface levels of functional FcγRs, h128-3 binds and internalizes its LILRB4 target receptor on these malignant cells by three potential mechanisms: (1) on all monocytic AML cells, h128-3 crosslinking of LILRB4 receptors triggers clathrin-mediated endocytosis and lysosomal receptor degradation; (2) on FcγR high monocytic AML cells, high-affinity FcγRI scaffolds h128-3 to target LILRB4, leading to internalization and degradation; and (3) on FcγRI − FcγRIIA + monocytic AML cells, low-affinity FcγRIIA scaffolds h128-3 by avidity to target LILRB4, prompting its internalization and degradation.
    Human Monocytic Aml Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human monocytic aml cell lines/product/ATCC
    Average 99 stars, based on 1 article reviews
    human monocytic aml cell lines - by Bioz Stars, 2026-02
    99/100 stars
      Buy from Supplier

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    ATCC human monocytic leukemia cell line
    Pro-inflammatory milieu induced by coculturing of <t>human</t> lung cancer A427 <t>cell</t> <t>line</t> and human <t>monocytic</t> AML-193 cell line. A427 cells were cultured along with AML-193 at ratios of 1:1, 1:10, 1:15, 1:25 and 1:50. The 1:15 ratio produced a high inflammatory response. When cultured alone, neither of the cell lines were able to produce an inflammatory response for (A) TNF-α and (B) IL-6. Data are represented as mean + standard deviation. of three independent experiments. *P<0.05, **P<0.01 vs. A427. TNF, tumor necrosis factor; IL, interleukin.
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    FcγR-dependent and independent mechanisms of h128-3-induced LILRB4 internalization on monocytic AML. Depending on the monocytic AML cell surface levels of functional FcγRs, h128-3 binds and internalizes its LILRB4 target receptor on these malignant cells by three potential mechanisms: (1) on all monocytic AML cells, h128-3 crosslinking of LILRB4 receptors triggers clathrin-mediated endocytosis and lysosomal receptor degradation; (2) on FcγR high monocytic AML cells, high-affinity FcγRI scaffolds h128-3 to target LILRB4, leading to internalization and degradation; and (3) on FcγRI − FcγRIIA + monocytic AML cells, low-affinity FcγRIIA scaffolds h128-3 by avidity to target LILRB4, prompting its internalization and degradation.

    Journal: Antibody Therapeutics

    Article Title: Fc gamma receptors promote antibody-induced LILRB4 internalization and immune regulation of monocytic AML

    doi: 10.1093/abt/tbad025

    Figure Lengend Snippet: FcγR-dependent and independent mechanisms of h128-3-induced LILRB4 internalization on monocytic AML. Depending on the monocytic AML cell surface levels of functional FcγRs, h128-3 binds and internalizes its LILRB4 target receptor on these malignant cells by three potential mechanisms: (1) on all monocytic AML cells, h128-3 crosslinking of LILRB4 receptors triggers clathrin-mediated endocytosis and lysosomal receptor degradation; (2) on FcγR high monocytic AML cells, high-affinity FcγRI scaffolds h128-3 to target LILRB4, leading to internalization and degradation; and (3) on FcγRI − FcγRIIA + monocytic AML cells, low-affinity FcγRIIA scaffolds h128-3 by avidity to target LILRB4, prompting its internalization and degradation.

    Article Snippet: Human monocytic AML cell line THP-1 was obtained from ATCC and maintained in a humidified atmosphere of 5% CO 2 at 37°C, in R10 [RPMI supplemented with 10% FBS (HyClone) and 100 U/ml penicillin and 100 μg/ml streptomycin (Life Technologies)].

    Techniques: Functional Assay

    FcγR-dependent and independent mechanisms of h128-3-induced LILRB4 internalization on monocytic AML. Depending on the monocytic AML cell surface levels of functional FcγRs, h128-3 binds and internalizes its LILRB4 target receptor on these malignant cells by three potential mechanisms: (1) on all monocytic AML cells, h128-3 crosslinking of LILRB4 receptors triggers clathrin-mediated endocytosis and lysosomal receptor degradation; (2) on FcγR high monocytic AML cells, high-affinity FcγRI scaffolds h128-3 to target LILRB4, leading to internalization and degradation; and (3) on FcγRI − FcγRIIA + monocytic AML cells, low-affinity FcγRIIA scaffolds h128-3 by avidity to target LILRB4, prompting its internalization and degradation.

    Journal: Antibody Therapeutics

    Article Title: Fc gamma receptors promote antibody-induced LILRB4 internalization and immune regulation of monocytic AML

    doi: 10.1093/abt/tbad025

    Figure Lengend Snippet: FcγR-dependent and independent mechanisms of h128-3-induced LILRB4 internalization on monocytic AML. Depending on the monocytic AML cell surface levels of functional FcγRs, h128-3 binds and internalizes its LILRB4 target receptor on these malignant cells by three potential mechanisms: (1) on all monocytic AML cells, h128-3 crosslinking of LILRB4 receptors triggers clathrin-mediated endocytosis and lysosomal receptor degradation; (2) on FcγR high monocytic AML cells, high-affinity FcγRI scaffolds h128-3 to target LILRB4, leading to internalization and degradation; and (3) on FcγRI − FcγRIIA + monocytic AML cells, low-affinity FcγRIIA scaffolds h128-3 by avidity to target LILRB4, prompting its internalization and degradation.

    Article Snippet: Human monocytic AML cell line Mono-mac-6 was obtained from DSMZ and maintained in a humidified atmosphere of 5% CO 2 at 37°C, in RPMI supplemented with 10% FBS (HyClone), 1 mM sodium pyruvate, non-essential amino acids (Thermo Fisher), 10 μg/ml human insulin (Sigma) and 100 U/ml penicillin and 100 μg/ml streptomycin (Life Technologies).

    Techniques: Functional Assay

    Pro-inflammatory milieu induced by coculturing of human lung cancer A427 cell line and human monocytic AML-193 cell line. A427 cells were cultured along with AML-193 at ratios of 1:1, 1:10, 1:15, 1:25 and 1:50. The 1:15 ratio produced a high inflammatory response. When cultured alone, neither of the cell lines were able to produce an inflammatory response for (A) TNF-α and (B) IL-6. Data are represented as mean + standard deviation. of three independent experiments. *P<0.05, **P<0.01 vs. A427. TNF, tumor necrosis factor; IL, interleukin.

    Journal: Experimental and Therapeutic Medicine

    Article Title: Biochanin A extirpates the epithelial-mesenchymal transition in a human lung cancer

    doi: 10.3892/etm.2018.5731

    Figure Lengend Snippet: Pro-inflammatory milieu induced by coculturing of human lung cancer A427 cell line and human monocytic AML-193 cell line. A427 cells were cultured along with AML-193 at ratios of 1:1, 1:10, 1:15, 1:25 and 1:50. The 1:15 ratio produced a high inflammatory response. When cultured alone, neither of the cell lines were able to produce an inflammatory response for (A) TNF-α and (B) IL-6. Data are represented as mean + standard deviation. of three independent experiments. *P<0.05, **P<0.01 vs. A427. TNF, tumor necrosis factor; IL, interleukin.

    Article Snippet: Human lung adenocarcinoma cell line (A427) and human monocytic leukemia cell line (AML-193) were obtained from American Type Culture Collection (Manassas, VA, USA).

    Techniques: Cell Culture, Produced, Standard Deviation