human hepatoma cells number hepg2-500 Search Results


hepg2 human hepatoma cells  (ATCC)
99
ATCC hepg2 human hepatoma cells
Hepg2 Human Hepatoma Cells, 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
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transit lt1  (Mirus Bio)
99
Mirus Bio transit lt1
Transit Lt1, supplied by Mirus Bio, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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transit lt1 - by Bioz Stars, 2026-03
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human hepatoma cells hepg2-500  (Cosmo Bio USA)
90
Cosmo Bio USA human hepatoma cells hepg2-500
Human Hepatoma Cells Hepg2 500, supplied by Cosmo Bio USA, 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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human hepatoma cells hepg2-500 - by Bioz Stars, 2026-03
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full-length recombinant human tfpi activity standard  (American Diagnostica)
90
American Diagnostica full-length recombinant human tfpi activity standard
Full Length Recombinant Human Tfpi Activity Standard, supplied by American Diagnostica, 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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antibodies against cyp1a1  (Santa Cruz Biotechnology)
94
Santa Cruz Biotechnology antibodies against cyp1a1
A) <t>HepG2</t> cells were treated with 10 µM visnagin, 10 µM khellin, and/or DMSO for 4 h, 8 h, 16 h, and 24 h. The results from PCR are shown as fold of DMSO-treated control cells. The data are mean from three independent experiments and were normalized to beta-actin transcription. * - value is significantly different from DMSO-treated cells ( p < 0.05). B) HepG2 cells were pre-treated with 20 µM MNF for 1 h and then exposed to 10 µM visnagin or 10 µM khellin for additional 16 h. The results from PCR are shown as fold of DMSO-treated control cells. The data are mean from three independent experiments and were normalized to beta-actin transcription. * - value is significantly different from DMSO-treated cells ( p < 0.05). # - value is significantly reduced in comparison to cells treated with VIS and KHEL, respectively; ( p < 0.05). C) HepG2 cells were treated with visnagin (VIS; 1 µM-20 µM), khellin (KHEL; 1 µM-20 µM), 1 µM 3MC, 5 nM TCDD, and/or vehicle (DMSO; 0.1% v/v) for 48 h. Thereafter, western blotting analyses for detection of <t>CYP1A1</t> and actin were performed as described in Materials and Methods section. The representative western blot analysis of two independent experiments (passages) is presented. D) HepG2 cells were treated with visnagin (VIS; 1 µM-20 µM), khellin (KHEL; 1 µM-20 µM), 1 µM 3MC, 5 nM TCDD, and/or vehicle (DMSO; 0.1% v/v) for either 16 h (upper panel) or 48 h (lower panel). EROD activity was determined as described in Materials and Method section. Analyses were performed in three independent experiments and are shown as fold induction over untreated cells. * - value is significantly different from DMSO-treated cells ( p < 0.05). E) HepG2 cells were treated with TCDD (5 nM) for 48 h. Thereafter, substrate mixture was supplemented with increasing doses of visnagin (VIS 1 nM -20 µM) or khellin (KHEL; 1 nM -20 µM) and EROD activity was determined as described in Materials and Methods section. Data are mean from three independent experiments and are expressed as percentage (%) of TCDD-mediated induction (i.e. induction by TCDD = 100%). * - value is significantly different from TCDD-treated cells ( p < 0.005).
Antibodies Against Cyp1a1, supplied by Santa Cruz Biotechnology, 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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antibodies against cyp1a1 - by Bioz Stars, 2026-03
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anti human tfpi antibody  (Danaher Inc)
86
Danaher Inc anti human tfpi antibody
A GO term enrichment analysis of differentially expressed genes in F4/80 + CD169 + Vcam-1 + macrophages between <t>TFPI</t> f/f and TFPI f/f;EpoR mice. B Heatmap of differential gene expression. C mRNA expression of ALAS2, ALAD, HMBS, UROS, UROD, CPOX, <t>and</t> <t>Fech</t> in F4/80 + CD169 + Vcam-1 + macrophages of TFPI f/f;EpoR mice ( n = 5). D mRNA expression of ALAS2, ALAD, HMBS, UROS, UROD, CPOX, and Fech in F4/80 + CD169 + Vcam-1 + macrophages of rTFPI-treated mice ( n = 5). E Fech mRNA expression in F4/80 + CD169 + Vcam-1 + macrophages and Ter119 + cells of TFPI f/f;EpoR mice ( n = 5). (F and G) Heme content in F4/80 + CD169 + Vcam-1 + macrophages F and Ter119 + cells G of TFPI f/f;EpoR mice ( n = 5). H Heme content in Ter119 + cells of TFPI f/f;EpoR ;CD169 DTR/+ mice after DT treatment ( n = 5). I Heme content in Ter119 + cells of TFPI f/f;EpoR mice after clodronate liposomes treatment ( n = 5). J p-GATA1 and GATA1 protein levels in F4/80 + CD169 + Vcam-1 + macrophages of TFPI f/f;EpoR mice ( n = 3). K GATA1 protein expression of F4/80 + CD169 + Vcam-1 + macrophages after GATA1 shRNA treatment ( n = 3). L Heme content in F4/80 + CD169 + Vcam-1 + macrophages of TFPI f/f mice after treated with rTFPI and GATA1 shRNA ( n = 5). Statistical analysis was performed using one-way ANOVA ( A , and C – L ). Data are shown as mean ± SEM and are representative of two ( E – I ) or three (C, D, and J-L) independent experiments. Source data are provided as a Source Data file.
Anti Human Tfpi Antibody, supplied by Danaher Inc, 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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rabbit anti glut1  (Proteintech)
96
Proteintech rabbit anti glut1
KEY RESOURCES TABLE
Rabbit Anti Glut1, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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monoclonal antibody directed against human tfpi  (American Diagnostica)
90
American Diagnostica monoclonal antibody directed against human tfpi
KEY RESOURCES TABLE
Monoclonal Antibody Directed Against Human Tfpi, supplied by American Diagnostica, 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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rabbit polyclonal anti-human tfpi  (Kaketsuken K k)
90
Kaketsuken K k rabbit polyclonal anti-human tfpi
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Rabbit Polyclonal Anti Human Tfpi, supplied by Kaketsuken K k, 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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hepg2 human hepatocellular liver carcinoma whole cell lysate  (OriGene)
N/A
HepG2 Human hepatocellular liver carcinoma Whole Cell Lysate
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rabbit anti human ct1  (RayBiotech)
N/A
Rabbit Anti Human CT1 Antibody
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A) HepG2 cells were treated with 10 µM visnagin, 10 µM khellin, and/or DMSO for 4 h, 8 h, 16 h, and 24 h. The results from PCR are shown as fold of DMSO-treated control cells. The data are mean from three independent experiments and were normalized to beta-actin transcription. * - value is significantly different from DMSO-treated cells ( p < 0.05). B) HepG2 cells were pre-treated with 20 µM MNF for 1 h and then exposed to 10 µM visnagin or 10 µM khellin for additional 16 h. The results from PCR are shown as fold of DMSO-treated control cells. The data are mean from three independent experiments and were normalized to beta-actin transcription. * - value is significantly different from DMSO-treated cells ( p < 0.05). # - value is significantly reduced in comparison to cells treated with VIS and KHEL, respectively; ( p < 0.05). C) HepG2 cells were treated with visnagin (VIS; 1 µM-20 µM), khellin (KHEL; 1 µM-20 µM), 1 µM 3MC, 5 nM TCDD, and/or vehicle (DMSO; 0.1% v/v) for 48 h. Thereafter, western blotting analyses for detection of CYP1A1 and actin were performed as described in Materials and Methods section. The representative western blot analysis of two independent experiments (passages) is presented. D) HepG2 cells were treated with visnagin (VIS; 1 µM-20 µM), khellin (KHEL; 1 µM-20 µM), 1 µM 3MC, 5 nM TCDD, and/or vehicle (DMSO; 0.1% v/v) for either 16 h (upper panel) or 48 h (lower panel). EROD activity was determined as described in Materials and Method section. Analyses were performed in three independent experiments and are shown as fold induction over untreated cells. * - value is significantly different from DMSO-treated cells ( p < 0.05). E) HepG2 cells were treated with TCDD (5 nM) for 48 h. Thereafter, substrate mixture was supplemented with increasing doses of visnagin (VIS 1 nM -20 µM) or khellin (KHEL; 1 nM -20 µM) and EROD activity was determined as described in Materials and Methods section. Data are mean from three independent experiments and are expressed as percentage (%) of TCDD-mediated induction (i.e. induction by TCDD = 100%). * - value is significantly different from TCDD-treated cells ( p < 0.005).

Journal: PLoS ONE

Article Title: Khellin and Visnagin Differentially Modulate AHR Signaling and Downstream CYP1A Activity in Human Liver Cells

doi: 10.1371/journal.pone.0074917

Figure Lengend Snippet: A) HepG2 cells were treated with 10 µM visnagin, 10 µM khellin, and/or DMSO for 4 h, 8 h, 16 h, and 24 h. The results from PCR are shown as fold of DMSO-treated control cells. The data are mean from three independent experiments and were normalized to beta-actin transcription. * - value is significantly different from DMSO-treated cells ( p < 0.05). B) HepG2 cells were pre-treated with 20 µM MNF for 1 h and then exposed to 10 µM visnagin or 10 µM khellin for additional 16 h. The results from PCR are shown as fold of DMSO-treated control cells. The data are mean from three independent experiments and were normalized to beta-actin transcription. * - value is significantly different from DMSO-treated cells ( p < 0.05). # - value is significantly reduced in comparison to cells treated with VIS and KHEL, respectively; ( p < 0.05). C) HepG2 cells were treated with visnagin (VIS; 1 µM-20 µM), khellin (KHEL; 1 µM-20 µM), 1 µM 3MC, 5 nM TCDD, and/or vehicle (DMSO; 0.1% v/v) for 48 h. Thereafter, western blotting analyses for detection of CYP1A1 and actin were performed as described in Materials and Methods section. The representative western blot analysis of two independent experiments (passages) is presented. D) HepG2 cells were treated with visnagin (VIS; 1 µM-20 µM), khellin (KHEL; 1 µM-20 µM), 1 µM 3MC, 5 nM TCDD, and/or vehicle (DMSO; 0.1% v/v) for either 16 h (upper panel) or 48 h (lower panel). EROD activity was determined as described in Materials and Method section. Analyses were performed in three independent experiments and are shown as fold induction over untreated cells. * - value is significantly different from DMSO-treated cells ( p < 0.05). E) HepG2 cells were treated with TCDD (5 nM) for 48 h. Thereafter, substrate mixture was supplemented with increasing doses of visnagin (VIS 1 nM -20 µM) or khellin (KHEL; 1 nM -20 µM) and EROD activity was determined as described in Materials and Methods section. Data are mean from three independent experiments and are expressed as percentage (%) of TCDD-mediated induction (i.e. induction by TCDD = 100%). * - value is significantly different from TCDD-treated cells ( p < 0.005).

Article Snippet: Blots were probed with primary antibodies against CYP1A1 (goat polyclonal, sc-9828, G-18, diluted 1:500 – for detection in human hepatocytes; rabbit polyclonal, sc-20772, H-70, diluted 1:500 – for detection in HepG2 cells), CYP1B1 (mouse monoclonal, sc-374228, G-4, 1:1000), actin (goat polyclonal; sc-1616, 1-19, diluted 1:2000), all purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA) or GAPDH (rabbit monoclonal, 2118, 14C10, diluted 1:1000) purchased from Cell Signaling Technology, overnight at 4°C.

Techniques: Control, Comparison, Western Blot, Activity Assay

Influence of visnagin and khellin treatment on CYP1A1 mRNA expression in human primary hepatocytes.

Journal: PLoS ONE

Article Title: Khellin and Visnagin Differentially Modulate AHR Signaling and Downstream CYP1A Activity in Human Liver Cells

doi: 10.1371/journal.pone.0074917

Figure Lengend Snippet: Influence of visnagin and khellin treatment on CYP1A1 mRNA expression in human primary hepatocytes.

Article Snippet: Blots were probed with primary antibodies against CYP1A1 (goat polyclonal, sc-9828, G-18, diluted 1:500 – for detection in human hepatocytes; rabbit polyclonal, sc-20772, H-70, diluted 1:500 – for detection in HepG2 cells), CYP1B1 (mouse monoclonal, sc-374228, G-4, 1:1000), actin (goat polyclonal; sc-1616, 1-19, diluted 1:2000), all purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA) or GAPDH (rabbit monoclonal, 2118, 14C10, diluted 1:1000) purchased from Cell Signaling Technology, overnight at 4°C.

Techniques: Expressing

A GO term enrichment analysis of differentially expressed genes in F4/80 + CD169 + Vcam-1 + macrophages between TFPI f/f and TFPI f/f;EpoR mice. B Heatmap of differential gene expression. C mRNA expression of ALAS2, ALAD, HMBS, UROS, UROD, CPOX, and Fech in F4/80 + CD169 + Vcam-1 + macrophages of TFPI f/f;EpoR mice ( n = 5). D mRNA expression of ALAS2, ALAD, HMBS, UROS, UROD, CPOX, and Fech in F4/80 + CD169 + Vcam-1 + macrophages of rTFPI-treated mice ( n = 5). E Fech mRNA expression in F4/80 + CD169 + Vcam-1 + macrophages and Ter119 + cells of TFPI f/f;EpoR mice ( n = 5). (F and G) Heme content in F4/80 + CD169 + Vcam-1 + macrophages F and Ter119 + cells G of TFPI f/f;EpoR mice ( n = 5). H Heme content in Ter119 + cells of TFPI f/f;EpoR ;CD169 DTR/+ mice after DT treatment ( n = 5). I Heme content in Ter119 + cells of TFPI f/f;EpoR mice after clodronate liposomes treatment ( n = 5). J p-GATA1 and GATA1 protein levels in F4/80 + CD169 + Vcam-1 + macrophages of TFPI f/f;EpoR mice ( n = 3). K GATA1 protein expression of F4/80 + CD169 + Vcam-1 + macrophages after GATA1 shRNA treatment ( n = 3). L Heme content in F4/80 + CD169 + Vcam-1 + macrophages of TFPI f/f mice after treated with rTFPI and GATA1 shRNA ( n = 5). Statistical analysis was performed using one-way ANOVA ( A , and C – L ). Data are shown as mean ± SEM and are representative of two ( E – I ) or three (C, D, and J-L) independent experiments. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: TFPI from erythroblasts drives heme production in central macrophages promoting erythropoiesis in polycythemia

doi: 10.1038/s41467-024-48328-8

Figure Lengend Snippet: A GO term enrichment analysis of differentially expressed genes in F4/80 + CD169 + Vcam-1 + macrophages between TFPI f/f and TFPI f/f;EpoR mice. B Heatmap of differential gene expression. C mRNA expression of ALAS2, ALAD, HMBS, UROS, UROD, CPOX, and Fech in F4/80 + CD169 + Vcam-1 + macrophages of TFPI f/f;EpoR mice ( n = 5). D mRNA expression of ALAS2, ALAD, HMBS, UROS, UROD, CPOX, and Fech in F4/80 + CD169 + Vcam-1 + macrophages of rTFPI-treated mice ( n = 5). E Fech mRNA expression in F4/80 + CD169 + Vcam-1 + macrophages and Ter119 + cells of TFPI f/f;EpoR mice ( n = 5). (F and G) Heme content in F4/80 + CD169 + Vcam-1 + macrophages F and Ter119 + cells G of TFPI f/f;EpoR mice ( n = 5). H Heme content in Ter119 + cells of TFPI f/f;EpoR ;CD169 DTR/+ mice after DT treatment ( n = 5). I Heme content in Ter119 + cells of TFPI f/f;EpoR mice after clodronate liposomes treatment ( n = 5). J p-GATA1 and GATA1 protein levels in F4/80 + CD169 + Vcam-1 + macrophages of TFPI f/f;EpoR mice ( n = 3). K GATA1 protein expression of F4/80 + CD169 + Vcam-1 + macrophages after GATA1 shRNA treatment ( n = 3). L Heme content in F4/80 + CD169 + Vcam-1 + macrophages of TFPI f/f mice after treated with rTFPI and GATA1 shRNA ( n = 5). Statistical analysis was performed using one-way ANOVA ( A , and C – L ). Data are shown as mean ± SEM and are representative of two ( E – I ) or three (C, D, and J-L) independent experiments. Source data are provided as a Source Data file.

Article Snippet: Anti-mouse TFPI antibody (1:500, ab180619, Abcam, Cambridge, UK), anti-human TFPI antibody (1:500, ab260042, Abcam) anti-mouse Fech antibody (1:1000, 14466-1-AP, Proteintech, Wuhan, China), anti-mouse Thbd antibody (1:1000, ab230010, Abcam), anti-human Thbd antibody (1:1000, ab109189, Abcam), anti-mouse GATA1 antibody (1:1000, sc-265, Santa Cruz Biotechnology, Santa Cruz, CA, USA), anti-mouse PC antibody (1:1000, ab313386, Abcam), anti-Flag antibody (1:1000, F3165, Sigma-Aldrich), anti-Myc antibody (1:1000, 2276, Cell Signaling Technology), anti-GST antibody (1:1000, 2622, Cell Signaling Technology), anti-p-GATA1 antibody (1:500, PA5-104243, Thermo Fisher Scientific, Waltham, MA, USA), anti-β-actin antibody (1:1000, sc-47778, Santa Cruz Biotechnology) and anti-GAPDH antibody (1:1000, sc-365062, Santa Cruz Biotechnology).

Techniques: Expressing, Liposomes, shRNA

A mRNA expression of TF in F4/80 + CD169 + Vcam-1 + macrophages of Jak2 V617F -mutated or hypoxia-exposed mice ( n = 5). B TF procoagulant activity and plasma TAT levels in mice after TF mAb treatment ( n = 5). C Heme content in F4/80 + CD169 + Vcam-1 + macrophages of TFPI f/f;EpoR mice after TF mAb treatment ( n = 5). D Fech mRNA expression in F4/80 + CD169 + Vcam-1 + macrophages of TFPI f/f;EpoR mice after TF mAb treatment ( n = 5). E PB Hb in TFPI f/f;EpoR mice after TF mAb treatment ( n = 5). F Co-IP analysis of the interaction between TFPI and Thbd in HEK293T cells ( n = 2). G Schematic illustration of Thbd and TFPI constructs. H Co-IP analysis of the interaction of TFPI with the different domains of Thbd in HEK293T cells ( n = 2). I Co-IP analysis of the interaction between TFPI and Thbd in F4/80 + CD169 + Vcam-1 + macrophages ( n = 2). J Pull down analysis of the interaction between the TFPI and Thbd ( n = 2). K Thbd protein expression in F4/80 + CD169 + Vcam-1 + macrophages after Thbd shRNA treatment ( n = 3). L Fech mRNA expression in F4/80 + CD169 + Vcam-1 + macrophages after Thbd shRNA and rTFPI treatment ( n = 5). M Fech mRNA expression in HEK293T cells after Thbd transfection and rTFPI treatment ( n = 5). Statistical analysis was performed using one-way ANOVA ( B – E and K – M ). Data are shown as mean ± SEM and are representative of two ( B – J ) or three ( A and K – M ) independent experiments. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: TFPI from erythroblasts drives heme production in central macrophages promoting erythropoiesis in polycythemia

doi: 10.1038/s41467-024-48328-8

Figure Lengend Snippet: A mRNA expression of TF in F4/80 + CD169 + Vcam-1 + macrophages of Jak2 V617F -mutated or hypoxia-exposed mice ( n = 5). B TF procoagulant activity and plasma TAT levels in mice after TF mAb treatment ( n = 5). C Heme content in F4/80 + CD169 + Vcam-1 + macrophages of TFPI f/f;EpoR mice after TF mAb treatment ( n = 5). D Fech mRNA expression in F4/80 + CD169 + Vcam-1 + macrophages of TFPI f/f;EpoR mice after TF mAb treatment ( n = 5). E PB Hb in TFPI f/f;EpoR mice after TF mAb treatment ( n = 5). F Co-IP analysis of the interaction between TFPI and Thbd in HEK293T cells ( n = 2). G Schematic illustration of Thbd and TFPI constructs. H Co-IP analysis of the interaction of TFPI with the different domains of Thbd in HEK293T cells ( n = 2). I Co-IP analysis of the interaction between TFPI and Thbd in F4/80 + CD169 + Vcam-1 + macrophages ( n = 2). J Pull down analysis of the interaction between the TFPI and Thbd ( n = 2). K Thbd protein expression in F4/80 + CD169 + Vcam-1 + macrophages after Thbd shRNA treatment ( n = 3). L Fech mRNA expression in F4/80 + CD169 + Vcam-1 + macrophages after Thbd shRNA and rTFPI treatment ( n = 5). M Fech mRNA expression in HEK293T cells after Thbd transfection and rTFPI treatment ( n = 5). Statistical analysis was performed using one-way ANOVA ( B – E and K – M ). Data are shown as mean ± SEM and are representative of two ( B – J ) or three ( A and K – M ) independent experiments. Source data are provided as a Source Data file.

Article Snippet: Anti-mouse TFPI antibody (1:500, ab180619, Abcam, Cambridge, UK), anti-human TFPI antibody (1:500, ab260042, Abcam) anti-mouse Fech antibody (1:1000, 14466-1-AP, Proteintech, Wuhan, China), anti-mouse Thbd antibody (1:1000, ab230010, Abcam), anti-human Thbd antibody (1:1000, ab109189, Abcam), anti-mouse GATA1 antibody (1:1000, sc-265, Santa Cruz Biotechnology, Santa Cruz, CA, USA), anti-mouse PC antibody (1:1000, ab313386, Abcam), anti-Flag antibody (1:1000, F3165, Sigma-Aldrich), anti-Myc antibody (1:1000, 2276, Cell Signaling Technology), anti-GST antibody (1:1000, 2622, Cell Signaling Technology), anti-p-GATA1 antibody (1:500, PA5-104243, Thermo Fisher Scientific, Waltham, MA, USA), anti-β-actin antibody (1:1000, sc-47778, Santa Cruz Biotechnology) and anti-GAPDH antibody (1:1000, sc-365062, Santa Cruz Biotechnology).

Techniques: Expressing, Activity Assay, Co-Immunoprecipitation Assay, Construct, shRNA, Transfection

A mRNA expression of aPC in F4/80 + CD169 + Vcam-1 + macrophages of Jak2 V617F -mutated and hypoxia-exposed mice ( n = 5). B aPC protein expression of F4/80 + CD169 + Vcam-1 + macrophages after intraosseous infusion of lentivirus-expressing aPC shRNA ( n = 3). C Frequency of RIII, RIV, and RV erythroblast populations in Thbd f/f;LysM mice after intraosseous infusion of lentivirus-expressing aPC shRNA ( n = 5). D KEGG analysis of downregulated genes in F4/80 + CD169 + Vcam-1 + macrophages in TFPI f/f;EpoR mice. E Heme content in F4/80 + CD169 + Vcam-1 + macrophages treated with rTFPI combined with JNK, FOXO, and ERK1/2 inhibitors ( n = 5). F Heme content in F4/80 + CD169 + Vcam-1 + macrophages after treated with rTFPI combined with ERK1/2 inhibitor and GATA1 shRNA ( n = 10). G Phosphorylation level of ERK1/2 protein in F4/80 + CD169 + Vcam-1 + macrophages after rTFPI treatment ( n = 3). H Phosphorylation level of GATA1 protein in F4/80 + CD169 + Vcam-1 + macrophages of Thbd f/f;LysM mice after rTFPI treatment ( n = 3). I Phosphorylation level of GATA1 protein in F4/80 + CD169 + Vcam-1 + macrophages treated with rTFPI and ERK1/2 inhibitor ( n = 3). J Phosphorylation level of GATA1 protein in F4/80 + CD169 + Vcam-1 + macrophages of Thbd f/f;LysM mice at different time points after rTFPI treatment ( n = 3). K ALAS2 and Fech mRNA expression in F4/80 + CD169 + Vcam-1 + macrophages of Thbd f/f;LysM mice after rTFPI treatment ( n = 5). L ALAS2 and Fech mRNA expression in F4/80 + CD169 + Vcam-1 + macrophages after treated with rTFPI and ERK1/2 inhibitor ( n = 5). M ALAS2 and Fech mRNA expression in F4/80 + CD169 + Vcam-1 + macrophages after treated with rTFPI and GATA1 shRNA ( n = 5). Statistical analysis was performed using one-way ANOVA ( B , C , E , F , and K – M ). Data are shown as mean ± SEM and are representative of two ( C , E , and F ) or three ( A , B , and G – M ) independent experiments. N The signaling pathway of TFPI/Thbd mediated heme synthesis in F4/80 + CD169 + Vcam-1 + macrophages. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: TFPI from erythroblasts drives heme production in central macrophages promoting erythropoiesis in polycythemia

doi: 10.1038/s41467-024-48328-8

Figure Lengend Snippet: A mRNA expression of aPC in F4/80 + CD169 + Vcam-1 + macrophages of Jak2 V617F -mutated and hypoxia-exposed mice ( n = 5). B aPC protein expression of F4/80 + CD169 + Vcam-1 + macrophages after intraosseous infusion of lentivirus-expressing aPC shRNA ( n = 3). C Frequency of RIII, RIV, and RV erythroblast populations in Thbd f/f;LysM mice after intraosseous infusion of lentivirus-expressing aPC shRNA ( n = 5). D KEGG analysis of downregulated genes in F4/80 + CD169 + Vcam-1 + macrophages in TFPI f/f;EpoR mice. E Heme content in F4/80 + CD169 + Vcam-1 + macrophages treated with rTFPI combined with JNK, FOXO, and ERK1/2 inhibitors ( n = 5). F Heme content in F4/80 + CD169 + Vcam-1 + macrophages after treated with rTFPI combined with ERK1/2 inhibitor and GATA1 shRNA ( n = 10). G Phosphorylation level of ERK1/2 protein in F4/80 + CD169 + Vcam-1 + macrophages after rTFPI treatment ( n = 3). H Phosphorylation level of GATA1 protein in F4/80 + CD169 + Vcam-1 + macrophages of Thbd f/f;LysM mice after rTFPI treatment ( n = 3). I Phosphorylation level of GATA1 protein in F4/80 + CD169 + Vcam-1 + macrophages treated with rTFPI and ERK1/2 inhibitor ( n = 3). J Phosphorylation level of GATA1 protein in F4/80 + CD169 + Vcam-1 + macrophages of Thbd f/f;LysM mice at different time points after rTFPI treatment ( n = 3). K ALAS2 and Fech mRNA expression in F4/80 + CD169 + Vcam-1 + macrophages of Thbd f/f;LysM mice after rTFPI treatment ( n = 5). L ALAS2 and Fech mRNA expression in F4/80 + CD169 + Vcam-1 + macrophages after treated with rTFPI and ERK1/2 inhibitor ( n = 5). M ALAS2 and Fech mRNA expression in F4/80 + CD169 + Vcam-1 + macrophages after treated with rTFPI and GATA1 shRNA ( n = 5). Statistical analysis was performed using one-way ANOVA ( B , C , E , F , and K – M ). Data are shown as mean ± SEM and are representative of two ( C , E , and F ) or three ( A , B , and G – M ) independent experiments. N The signaling pathway of TFPI/Thbd mediated heme synthesis in F4/80 + CD169 + Vcam-1 + macrophages. Source data are provided as a Source Data file.

Article Snippet: Anti-mouse TFPI antibody (1:500, ab180619, Abcam, Cambridge, UK), anti-human TFPI antibody (1:500, ab260042, Abcam) anti-mouse Fech antibody (1:1000, 14466-1-AP, Proteintech, Wuhan, China), anti-mouse Thbd antibody (1:1000, ab230010, Abcam), anti-human Thbd antibody (1:1000, ab109189, Abcam), anti-mouse GATA1 antibody (1:1000, sc-265, Santa Cruz Biotechnology, Santa Cruz, CA, USA), anti-mouse PC antibody (1:1000, ab313386, Abcam), anti-Flag antibody (1:1000, F3165, Sigma-Aldrich), anti-Myc antibody (1:1000, 2276, Cell Signaling Technology), anti-GST antibody (1:1000, 2622, Cell Signaling Technology), anti-p-GATA1 antibody (1:500, PA5-104243, Thermo Fisher Scientific, Waltham, MA, USA), anti-β-actin antibody (1:1000, sc-47778, Santa Cruz Biotechnology) and anti-GAPDH antibody (1:1000, sc-365062, Santa Cruz Biotechnology).

Techniques: Expressing, shRNA

A Protocol used for human EBI formation. B TFPI expression in erythroblasts (EB) and macrophages (Ma) ( n = 3). C Thbd expression in erythroblasts and macrophages. Null means no expression ( n = 3). D hemoglobin and heme content in erythroblasts, heme content and Fech mRNA expression in macrophages of EBIs formed by macrophages and erythroblasts treated with TFPI shRNA ( n = 5). E hemoglobin and heme content in erythroblasts, heme content and Fech mRNA expression in macrophages of EBIs formed by macrophages and erythroblasts treated with TFPI shRNA and rTFPI ( n = 5). Statistical analysis was performed using one-way ANOVA ( B – E ). Data are shown as mean ± SEM and are representative of two (D and E) or three (B and C) independent experiments. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: TFPI from erythroblasts drives heme production in central macrophages promoting erythropoiesis in polycythemia

doi: 10.1038/s41467-024-48328-8

Figure Lengend Snippet: A Protocol used for human EBI formation. B TFPI expression in erythroblasts (EB) and macrophages (Ma) ( n = 3). C Thbd expression in erythroblasts and macrophages. Null means no expression ( n = 3). D hemoglobin and heme content in erythroblasts, heme content and Fech mRNA expression in macrophages of EBIs formed by macrophages and erythroblasts treated with TFPI shRNA ( n = 5). E hemoglobin and heme content in erythroblasts, heme content and Fech mRNA expression in macrophages of EBIs formed by macrophages and erythroblasts treated with TFPI shRNA and rTFPI ( n = 5). Statistical analysis was performed using one-way ANOVA ( B – E ). Data are shown as mean ± SEM and are representative of two (D and E) or three (B and C) independent experiments. Source data are provided as a Source Data file.

Article Snippet: Anti-mouse TFPI antibody (1:500, ab180619, Abcam, Cambridge, UK), anti-human TFPI antibody (1:500, ab260042, Abcam) anti-mouse Fech antibody (1:1000, 14466-1-AP, Proteintech, Wuhan, China), anti-mouse Thbd antibody (1:1000, ab230010, Abcam), anti-human Thbd antibody (1:1000, ab109189, Abcam), anti-mouse GATA1 antibody (1:1000, sc-265, Santa Cruz Biotechnology, Santa Cruz, CA, USA), anti-mouse PC antibody (1:1000, ab313386, Abcam), anti-Flag antibody (1:1000, F3165, Sigma-Aldrich), anti-Myc antibody (1:1000, 2276, Cell Signaling Technology), anti-GST antibody (1:1000, 2622, Cell Signaling Technology), anti-p-GATA1 antibody (1:500, PA5-104243, Thermo Fisher Scientific, Waltham, MA, USA), anti-β-actin antibody (1:1000, sc-47778, Santa Cruz Biotechnology) and anti-GAPDH antibody (1:1000, sc-365062, Santa Cruz Biotechnology).

Techniques: Expressing, shRNA

KEY RESOURCES TABLE

Journal: Cell reports

Article Title: Single-cell transcriptomics of human-skin-equivalent organoids

doi: 10.1016/j.celrep.2023.112511

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: The following antibodies were used: chicken anti-KRT14 (1:500; BioLegend; SIG-3476), rabbit anti-KI67 (1:500; Abcam; ab15580), rabbit anti-COL17A1 (1:100; One World Labs; ap9099c), rabbit anti-KRT19 (1:250; Cell signaling; 13092), mouse anti-KRT15 (1:500; Santa Cruz; sc-47697), rabbit anti-VIM (1:500; Cell Signaling; D21H3), mouse anti-PSCA (1:500; Santa Cruz; sc-80654), mouse anti-FLG (1:500; Santa Cruz; sc-66192), mouse anti-DSG1 (1:500; Santa Cruz; sc-137164), mouse anti-SLUG (1:500; Santa Cruz; sc-166476), rabbit anti-KRT16 (1:500; Invitrogen; PA5–99172), rabbit anti-cCASP3 (1:500; Cell Signaling; 9579T), rabbit anti-KRT4 (1:500; Fisher Scientific; 16572–1-AP), rabbit anti-GLUT1 (1:500; Proteintech; 218291AP), rabbit anti-HIF1a (1:500; Proteintech; 501733175), and rabbit anti-LOR (1:500; Abcam; ab85679).

Techniques: Recombinant, Multiplex Assay, Software