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differentiation thp 1 cells  (ATCC)


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    ATCC differentiation thp 1 cells
    Differentiation Thp 1 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 20139 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/differentiation+thp+1+cells/THP-1/pm41708812-79-3-6
    Average 99 stars, based on 20139 article reviews
    differentiation thp 1 cells - by Bioz Stars, 2026-09
    99/100 stars

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    Related Articles

    Transfection:

    Article Title: Intratracheal administration of mitochondrial DNA directly provokes lung inflammation through the TLR9-p38 MAPK pathway.
    Article Snippet: An increasing number of studies have focused on the phenomenon that mitochondrial DNA (mtDNA) activates innate immunity responses.. However, the specific role of mtDNA in inflammatory lung disease remains elusive.. This study was designed to examine the proinflammatory effects of mtDNA in lungs and to investigate the putative mechanisms.

    Cell Culture:

    Article Title: Intratracheal administration of mitochondrial DNA directly provokes lung inflammation through the TLR9-p38 MAPK pathway.
    Article Snippet: An increasing number of studies have focused on the phenomenon that mitochondrial DNA (mtDNA) activates innate immunity responses.. However, the specific role of mtDNA in inflammatory lung disease remains elusive.. This study was designed to examine the proinflammatory effects of mtDNA in lungs and to investigate the putative mechanisms.

    Article Title: MOV10, a novel immunotherapy and prognostic biomarker, contributes to glioma development by regulating autophagy.
    Article Snippet: .. Macrophage generation and differentiation THP-1 cells (ATCC, catalog number: TIB-202) were cultured in RPMI-1640 medium (Gibco, 11875-093) containing 10% fetal bovine serum-FBS (Gibco, 10099-141) and 1% penicillin-streptomycin mixture (Gibco, 15140-122) and maintained at 37 °C in a 5% CO2 incubator. ..

    Article Title: Topotecan Alleviates Lipopolysaccharide-Mediated Acute Lung Injury Via the NF-κB Signaling Pathway.
    Article Snippet: Background: The topoisomerase 1 (Top1) inhibitor has been reported to inhibit inflammatory genes induced by virus and protect mice from sepsis.. Its role in acute lung injury (ALI) remains unknown.. This study aimed to explore the effects of topotecan (TPT), a Top 1 inhibitor, in lipopolysaccharide (LPS)-ALI.

    Article Title: Modifications in Gamma-aminobutyric Acid type A Receptor Subunit Gene Expression During Macrophage Differentiation and Propofol Administration in THP-1 Cells
    Article Snippet: Propofol was obtained from Wako Pure Chemical Industries (Osaka, Japan). .. Cell culture and differentiation THP-1 cells (ATCC; Manassas, VA, USA) resemble primary monocytes and macrophages in morphology and differentiation properties. ..



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    ( A-B ). Cell death <t>of</t> <t>THP-1</t> macrophages upon infection with S. flexneri 2457T ( A ), or electroporation with S. enterica serovar Minnesota LPS ( B ), measured by LDH release, as percentage of Triton X-100-induced cell lysis. N ≥ 4 biological replicates. ( C-D ). NLRP11 is required for the processing of CASP4 and gasdermin D (GSDMD) induced by S. flexneri infection ( C ), or S. enterica LPS electroporation ( D ). CASP4 is required for GSDMD processing induced by S. flexneri infection ( C ), or S. enterica LPS electroporation ( D ). Processing of CASP4 yields a p32 and/or p20 polypeptide, and processing of GSDMD yields a p30 polypeptide. Representative western blots. Molecular weight markers in kDa. DKO, NLRP11 −/− CASP4 −/− double knockout. Mean ± SEM. Two-way ANOVA with Tukey’s post hoc test *, P<0.05; **, P<0.01; ****, P<0.0001.
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    ( A-B ). Cell death <t>of</t> <t>THP-1</t> macrophages upon infection with S. flexneri 2457T ( A ), or electroporation with S. enterica serovar Minnesota LPS ( B ), measured by LDH release, as percentage of Triton X-100-induced cell lysis. N ≥ 4 biological replicates. ( C-D ). NLRP11 is required for the processing of CASP4 and gasdermin D (GSDMD) induced by S. flexneri infection ( C ), or S. enterica LPS electroporation ( D ). CASP4 is required for GSDMD processing induced by S. flexneri infection ( C ), or S. enterica LPS electroporation ( D ). Processing of CASP4 yields a p32 and/or p20 polypeptide, and processing of GSDMD yields a p30 polypeptide. Representative western blots. Molecular weight markers in kDa. DKO, NLRP11 −/− CASP4 −/− double knockout. Mean ± SEM. Two-way ANOVA with Tukey’s post hoc test *, P<0.05; **, P<0.01; ****, P<0.0001.
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    ( A-B ). Cell death of THP-1 macrophages upon infection with S. flexneri 2457T ( A ), or electroporation with S. enterica serovar Minnesota LPS ( B ), measured by LDH release, as percentage of Triton X-100-induced cell lysis. N ≥ 4 biological replicates. ( C-D ). NLRP11 is required for the processing of CASP4 and gasdermin D (GSDMD) induced by S. flexneri infection ( C ), or S. enterica LPS electroporation ( D ). CASP4 is required for GSDMD processing induced by S. flexneri infection ( C ), or S. enterica LPS electroporation ( D ). Processing of CASP4 yields a p32 and/or p20 polypeptide, and processing of GSDMD yields a p30 polypeptide. Representative western blots. Molecular weight markers in kDa. DKO, NLRP11 −/− CASP4 −/− double knockout. Mean ± SEM. Two-way ANOVA with Tukey’s post hoc test *, P<0.05; **, P<0.01; ****, P<0.0001.

    Journal: bioRxiv

    Article Title: NLRP11 promotes non-canonical inflammasome activation in human macrophages by enhancing caspase-4 recognition of cytosolic lipopolysaccharide

    doi: 10.64898/2026.02.02.703338

    Figure Lengend Snippet: ( A-B ). Cell death of THP-1 macrophages upon infection with S. flexneri 2457T ( A ), or electroporation with S. enterica serovar Minnesota LPS ( B ), measured by LDH release, as percentage of Triton X-100-induced cell lysis. N ≥ 4 biological replicates. ( C-D ). NLRP11 is required for the processing of CASP4 and gasdermin D (GSDMD) induced by S. flexneri infection ( C ), or S. enterica LPS electroporation ( D ). CASP4 is required for GSDMD processing induced by S. flexneri infection ( C ), or S. enterica LPS electroporation ( D ). Processing of CASP4 yields a p32 and/or p20 polypeptide, and processing of GSDMD yields a p30 polypeptide. Representative western blots. Molecular weight markers in kDa. DKO, NLRP11 −/− CASP4 −/− double knockout. Mean ± SEM. Two-way ANOVA with Tukey’s post hoc test *, P<0.05; **, P<0.01; ****, P<0.0001.

    Article Snippet: PMA-differentiated THP-1 cells were primed with 1 μg/mL E. coli O111:B4 LPS (InvivoGen, tlrl-eblps) for 2.5 h and treated with 10 μM nigericin (InvivoGen, tlrl-nig) for 15 min prior to the assay when indicated.

    Techniques: Infection, Electroporation, Lysis, Western Blot, Molecular Weight, Double Knockout

    ( A-B ). Cell death of THP-1 macrophages upon infection with S. flexneri ( A ) or electroporation with E. coli O111:B4 LPS ( B ) measured by LDH release, as percentage of Triton X-100-induced cell lysis. Complementation of indicated THP-1 knockouts by transduction with indicated NLRP11 or CASP4 constructs. N ≥ 4 biological replicates. ( C ) Identification of CASP4 residues D174, and K19 KVR53-55 QEK62-64 as required for efficient processing of CASP4 and GSDMD induced by LPS electroporation. Representative western blots. Molecular weight markers in kDa. Mean ± SEM. Two-way ANOVA with Tukey’s post hoc test. ns, not significant; *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001.

    Journal: bioRxiv

    Article Title: NLRP11 promotes non-canonical inflammasome activation in human macrophages by enhancing caspase-4 recognition of cytosolic lipopolysaccharide

    doi: 10.64898/2026.02.02.703338

    Figure Lengend Snippet: ( A-B ). Cell death of THP-1 macrophages upon infection with S. flexneri ( A ) or electroporation with E. coli O111:B4 LPS ( B ) measured by LDH release, as percentage of Triton X-100-induced cell lysis. Complementation of indicated THP-1 knockouts by transduction with indicated NLRP11 or CASP4 constructs. N ≥ 4 biological replicates. ( C ) Identification of CASP4 residues D174, and K19 KVR53-55 QEK62-64 as required for efficient processing of CASP4 and GSDMD induced by LPS electroporation. Representative western blots. Molecular weight markers in kDa. Mean ± SEM. Two-way ANOVA with Tukey’s post hoc test. ns, not significant; *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001.

    Article Snippet: PMA-differentiated THP-1 cells were primed with 1 μg/mL E. coli O111:B4 LPS (InvivoGen, tlrl-eblps) for 2.5 h and treated with 10 μM nigericin (InvivoGen, tlrl-nig) for 15 min prior to the assay when indicated.

    Techniques: Infection, Electroporation, Lysis, Transduction, Construct, Western Blot, Molecular Weight

    ( A-C ). LPS binding to anti-FLAG-coated plates pre-incubated with lysates of HEK293T cells expressing FLAG-NLRP11 and/or CASP4-FLAG. Addition of purified E. coli O111:B4 LPS ( A ), intact E. coli O126:H7 bacteria ( B ), or intact S. flexneri WT, Δ rfe , or Δ galU bacteria ( C ). Bound LPS was normalized to levels in the CASP4*-alone condition ( A ), CASP4* with E. coli O126:H7 ( B ), or CASP4* with WT S. flexneri ( C ). Panel C also shows the structure of LPS; vertical lines indicate the location of truncations in LPS produced by S. flexneri Δ rfe and S. flexneri Δ galU . ( D-E ) Increasing interaction between NLRP11 and CASP4 as a function of concentration of added HEK293T FLAG-NLRP11 lysate, without ( D ) or with ( E ) addition of LPS. FLAG-NLRP11 in transfected HEK293T cells bound to plates coated with purified WT CASP4 or indicated CASP4 derivatives at 10 μg/mL; detection of bound FLAG. N = 3 biological replicates. a.u., arbitrary units. ( F ) LPS binding to plates pre-incubated with lysates of HEK293T cells expressing FLAG-NLRP11 and indicated purified derivatives of CASP4*. ( G-H ) Levels of soluble cytosolic LPS (cLPS) not bound to macromolecular complexes. S. flexneri -infected THP-1 macrophages lysed with 0.02% digitonin. Shown is LPS within the separated and filtered cytosolic fractions. Quantified by LAL assay. CASP4*, catalytically inactive caspase. CASP4 K19E KVR QEK, LPS-binding defective caspase. CASP4 KVR, KVR53-55EEA. DKO, NLRP11 −/− CASP4 −/− double knockout. Mean ± SEM. Two-way ANOVA with Tukey’s post hoc test; ns, not significant; *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001.

    Journal: bioRxiv

    Article Title: NLRP11 promotes non-canonical inflammasome activation in human macrophages by enhancing caspase-4 recognition of cytosolic lipopolysaccharide

    doi: 10.64898/2026.02.02.703338

    Figure Lengend Snippet: ( A-C ). LPS binding to anti-FLAG-coated plates pre-incubated with lysates of HEK293T cells expressing FLAG-NLRP11 and/or CASP4-FLAG. Addition of purified E. coli O111:B4 LPS ( A ), intact E. coli O126:H7 bacteria ( B ), or intact S. flexneri WT, Δ rfe , or Δ galU bacteria ( C ). Bound LPS was normalized to levels in the CASP4*-alone condition ( A ), CASP4* with E. coli O126:H7 ( B ), or CASP4* with WT S. flexneri ( C ). Panel C also shows the structure of LPS; vertical lines indicate the location of truncations in LPS produced by S. flexneri Δ rfe and S. flexneri Δ galU . ( D-E ) Increasing interaction between NLRP11 and CASP4 as a function of concentration of added HEK293T FLAG-NLRP11 lysate, without ( D ) or with ( E ) addition of LPS. FLAG-NLRP11 in transfected HEK293T cells bound to plates coated with purified WT CASP4 or indicated CASP4 derivatives at 10 μg/mL; detection of bound FLAG. N = 3 biological replicates. a.u., arbitrary units. ( F ) LPS binding to plates pre-incubated with lysates of HEK293T cells expressing FLAG-NLRP11 and indicated purified derivatives of CASP4*. ( G-H ) Levels of soluble cytosolic LPS (cLPS) not bound to macromolecular complexes. S. flexneri -infected THP-1 macrophages lysed with 0.02% digitonin. Shown is LPS within the separated and filtered cytosolic fractions. Quantified by LAL assay. CASP4*, catalytically inactive caspase. CASP4 K19E KVR QEK, LPS-binding defective caspase. CASP4 KVR, KVR53-55EEA. DKO, NLRP11 −/− CASP4 −/− double knockout. Mean ± SEM. Two-way ANOVA with Tukey’s post hoc test; ns, not significant; *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001.

    Article Snippet: PMA-differentiated THP-1 cells were primed with 1 μg/mL E. coli O111:B4 LPS (InvivoGen, tlrl-eblps) for 2.5 h and treated with 10 μM nigericin (InvivoGen, tlrl-nig) for 15 min prior to the assay when indicated.

    Techniques: Binding Assay, Incubation, Expressing, Purification, Bacteria, Produced, Concentration Assay, Transfection, Infection, LAL Assay, Double Knockout