uk er mp20 ly 6c Search Results


93
Novus Biologicals ly6c
Monocyte‐derived TNF‐α acts on MYC + CD63 + EC through TNFR1. A) Spatial feature plots showing the cell types in EC7 expansion units for ST. B) CellPhoneDB analysis showing the cell–cell interactions for scRNA‐seq. C) Mas1 −/− mice were pre‐administrated with clodronate liposomes or control liposomes for 24 h before APAP challenge ( n = 4 per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. D) WT and Mas1 −/− mice were pre‐administrated with cenicriviroc for 2 h before APAP challenge ( n = 4 per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. E) CellPhoneDB analysis showing the major interaction pairs between <t>Ly6c</t> hi monocyte‐Mψ5 or Ly6c hi monocyte‐EC7 for scRNA‐seq. In F‐G, Mas1 −/− mice were pre‐administrated with cediranib or control for 2 h before APAP challenge ( n = 4 per group). F) Representative staining of H&E and mIHC are shown. Scale bar: 50 µm. G) Quantification of necrotic area for H&E as shown in F ( n = 4 mice per group; two‐sided Student's t‐test; p = 1.55 × 10 −4 ) and serum ALT ( n = 4 mice per group; two‐sided Student's t‐test; p = 2.64 × 10 −8 ). H) Multiplex fluorescence of CD31 + MYC + CD63 + LSECs and key glycolytic enzymes (PKM and PFKFB3). Scale bar: 100 µm. The mouse primary LSECs were treated with or without BMDM‐CM for 24 h. I) Quantification of CD31 + MYC + CD63 + PFKFB3 + PKM + LSECs for multiplex fluorescence as shown in H ( n = 4 samples per group; two‐sided Mann‐Whitney U test, p = 2.86 × 10 −2 ). J) Glycolytic rate assay showing glycolytic function of LSECs treated with or without BMDM‐CM for 24 h. ( n = 5 or 6 samples per group; two‐sided Student's t‐test, p = 7.50 × 10 −3 and 3.77 × 10 −3 from left to right). K) Multiplex fluorescence of CD31 + MYC + CD63 + LSECs and key glycolytic enzymes (PKM and PFKFB3). Scale bar: 100 µm. The mouse primary LSECs were treated with or without TNF‐α (20 ng ml −1 ) for 24 h. L) Quantification of CD31 + MYC + CD63 + PFKFB3 + PKM + LSECs for multiplex fluorescence as shown in K ( n = 4 samples per group; two‐sided Student's t‐test, p = 2.00 × 10 −2 ). M) Glycolytic rate assay showing glycolytic function of LSECs treated with or without TNF‐α (20 ng ml −1 ) for 24 h. ( n = 5 or 6 samples per group; two‐sided Student's t‐test, p = 8.00 × 10 −6 and 1.30 × 10 −5 from top to bottom). N) mIHC of CD31 + MYC + ECs, F4/80 + MMP12 + Mψ and CCR2 + monocytes are shown. Scale bar: 200 µm, 50 µm and 20 µm. Spatial localizations of CD31 + MYC + ECs, CCR2 + monocytes, and F4/80 + MMP12 + Mψ within injured region are shown. In all graphs data are presented as mean ± SD, * p < 0.05; ** p < 0.01; *** p < 0.001.
Ly6c, supplied by Novus Biologicals, 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/result/ly6c/product/Novus Biologicals
Average 93 stars, based on 1 article reviews
ly6c - by Bioz Stars, 2026-03
93/100 stars
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94
R&D Systems percpconjugated anti ly6c
Monocyte‐derived TNF‐α acts on MYC + CD63 + EC through TNFR1. A) Spatial feature plots showing the cell types in EC7 expansion units for ST. B) CellPhoneDB analysis showing the cell–cell interactions for scRNA‐seq. C) Mas1 −/− mice were pre‐administrated with clodronate liposomes or control liposomes for 24 h before APAP challenge ( n = 4 per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. D) WT and Mas1 −/− mice were pre‐administrated with cenicriviroc for 2 h before APAP challenge ( n = 4 per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. E) CellPhoneDB analysis showing the major interaction pairs between <t>Ly6c</t> hi monocyte‐Mψ5 or Ly6c hi monocyte‐EC7 for scRNA‐seq. In F‐G, Mas1 −/− mice were pre‐administrated with cediranib or control for 2 h before APAP challenge ( n = 4 per group). F) Representative staining of H&E and mIHC are shown. Scale bar: 50 µm. G) Quantification of necrotic area for H&E as shown in F ( n = 4 mice per group; two‐sided Student's t‐test; p = 1.55 × 10 −4 ) and serum ALT ( n = 4 mice per group; two‐sided Student's t‐test; p = 2.64 × 10 −8 ). H) Multiplex fluorescence of CD31 + MYC + CD63 + LSECs and key glycolytic enzymes (PKM and PFKFB3). Scale bar: 100 µm. The mouse primary LSECs were treated with or without BMDM‐CM for 24 h. I) Quantification of CD31 + MYC + CD63 + PFKFB3 + PKM + LSECs for multiplex fluorescence as shown in H ( n = 4 samples per group; two‐sided Mann‐Whitney U test, p = 2.86 × 10 −2 ). J) Glycolytic rate assay showing glycolytic function of LSECs treated with or without BMDM‐CM for 24 h. ( n = 5 or 6 samples per group; two‐sided Student's t‐test, p = 7.50 × 10 −3 and 3.77 × 10 −3 from left to right). K) Multiplex fluorescence of CD31 + MYC + CD63 + LSECs and key glycolytic enzymes (PKM and PFKFB3). Scale bar: 100 µm. The mouse primary LSECs were treated with or without TNF‐α (20 ng ml −1 ) for 24 h. L) Quantification of CD31 + MYC + CD63 + PFKFB3 + PKM + LSECs for multiplex fluorescence as shown in K ( n = 4 samples per group; two‐sided Student's t‐test, p = 2.00 × 10 −2 ). M) Glycolytic rate assay showing glycolytic function of LSECs treated with or without TNF‐α (20 ng ml −1 ) for 24 h. ( n = 5 or 6 samples per group; two‐sided Student's t‐test, p = 8.00 × 10 −6 and 1.30 × 10 −5 from top to bottom). N) mIHC of CD31 + MYC + ECs, F4/80 + MMP12 + Mψ and CCR2 + monocytes are shown. Scale bar: 200 µm, 50 µm and 20 µm. Spatial localizations of CD31 + MYC + ECs, CCR2 + monocytes, and F4/80 + MMP12 + Mψ within injured region are shown. In all graphs data are presented as mean ± SD, * p < 0.05; ** p < 0.01; *** p < 0.001.
Percpconjugated Anti Ly6c, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/percpconjugated anti ly6c/product/R&D Systems
Average 94 stars, based on 1 article reviews
percpconjugated anti ly6c - by Bioz Stars, 2026-03
94/100 stars
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93
Novus Biologicals ly6c pe cy5 5
Monocyte‐derived TNF‐α acts on MYC + CD63 + EC through TNFR1. A) Spatial feature plots showing the cell types in EC7 expansion units for ST. B) CellPhoneDB analysis showing the cell–cell interactions for scRNA‐seq. C) Mas1 −/− mice were pre‐administrated with clodronate liposomes or control liposomes for 24 h before APAP challenge ( n = 4 per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. D) WT and Mas1 −/− mice were pre‐administrated with cenicriviroc for 2 h before APAP challenge ( n = 4 per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. E) CellPhoneDB analysis showing the major interaction pairs between <t>Ly6c</t> hi monocyte‐Mψ5 or Ly6c hi monocyte‐EC7 for scRNA‐seq. In F‐G, Mas1 −/− mice were pre‐administrated with cediranib or control for 2 h before APAP challenge ( n = 4 per group). F) Representative staining of H&E and mIHC are shown. Scale bar: 50 µm. G) Quantification of necrotic area for H&E as shown in F ( n = 4 mice per group; two‐sided Student's t‐test; p = 1.55 × 10 −4 ) and serum ALT ( n = 4 mice per group; two‐sided Student's t‐test; p = 2.64 × 10 −8 ). H) Multiplex fluorescence of CD31 + MYC + CD63 + LSECs and key glycolytic enzymes (PKM and PFKFB3). Scale bar: 100 µm. The mouse primary LSECs were treated with or without BMDM‐CM for 24 h. I) Quantification of CD31 + MYC + CD63 + PFKFB3 + PKM + LSECs for multiplex fluorescence as shown in H ( n = 4 samples per group; two‐sided Mann‐Whitney U test, p = 2.86 × 10 −2 ). J) Glycolytic rate assay showing glycolytic function of LSECs treated with or without BMDM‐CM for 24 h. ( n = 5 or 6 samples per group; two‐sided Student's t‐test, p = 7.50 × 10 −3 and 3.77 × 10 −3 from left to right). K) Multiplex fluorescence of CD31 + MYC + CD63 + LSECs and key glycolytic enzymes (PKM and PFKFB3). Scale bar: 100 µm. The mouse primary LSECs were treated with or without TNF‐α (20 ng ml −1 ) for 24 h. L) Quantification of CD31 + MYC + CD63 + PFKFB3 + PKM + LSECs for multiplex fluorescence as shown in K ( n = 4 samples per group; two‐sided Student's t‐test, p = 2.00 × 10 −2 ). M) Glycolytic rate assay showing glycolytic function of LSECs treated with or without TNF‐α (20 ng ml −1 ) for 24 h. ( n = 5 or 6 samples per group; two‐sided Student's t‐test, p = 8.00 × 10 −6 and 1.30 × 10 −5 from top to bottom). N) mIHC of CD31 + MYC + ECs, F4/80 + MMP12 + Mψ and CCR2 + monocytes are shown. Scale bar: 200 µm, 50 µm and 20 µm. Spatial localizations of CD31 + MYC + ECs, CCR2 + monocytes, and F4/80 + MMP12 + Mψ within injured region are shown. In all graphs data are presented as mean ± SD, * p < 0.05; ** p < 0.01; *** p < 0.001.
Ly6c Pe Cy5 5, supplied by Novus Biologicals, 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/result/ly6c pe cy5 5/product/Novus Biologicals
Average 93 stars, based on 1 article reviews
ly6c pe cy5 5 - by Bioz Stars, 2026-03
93/100 stars
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Image Search Results


Monocyte‐derived TNF‐α acts on MYC + CD63 + EC through TNFR1. A) Spatial feature plots showing the cell types in EC7 expansion units for ST. B) CellPhoneDB analysis showing the cell–cell interactions for scRNA‐seq. C) Mas1 −/− mice were pre‐administrated with clodronate liposomes or control liposomes for 24 h before APAP challenge ( n = 4 per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. D) WT and Mas1 −/− mice were pre‐administrated with cenicriviroc for 2 h before APAP challenge ( n = 4 per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. E) CellPhoneDB analysis showing the major interaction pairs between Ly6c hi monocyte‐Mψ5 or Ly6c hi monocyte‐EC7 for scRNA‐seq. In F‐G, Mas1 −/− mice were pre‐administrated with cediranib or control for 2 h before APAP challenge ( n = 4 per group). F) Representative staining of H&E and mIHC are shown. Scale bar: 50 µm. G) Quantification of necrotic area for H&E as shown in F ( n = 4 mice per group; two‐sided Student's t‐test; p = 1.55 × 10 −4 ) and serum ALT ( n = 4 mice per group; two‐sided Student's t‐test; p = 2.64 × 10 −8 ). H) Multiplex fluorescence of CD31 + MYC + CD63 + LSECs and key glycolytic enzymes (PKM and PFKFB3). Scale bar: 100 µm. The mouse primary LSECs were treated with or without BMDM‐CM for 24 h. I) Quantification of CD31 + MYC + CD63 + PFKFB3 + PKM + LSECs for multiplex fluorescence as shown in H ( n = 4 samples per group; two‐sided Mann‐Whitney U test, p = 2.86 × 10 −2 ). J) Glycolytic rate assay showing glycolytic function of LSECs treated with or without BMDM‐CM for 24 h. ( n = 5 or 6 samples per group; two‐sided Student's t‐test, p = 7.50 × 10 −3 and 3.77 × 10 −3 from left to right). K) Multiplex fluorescence of CD31 + MYC + CD63 + LSECs and key glycolytic enzymes (PKM and PFKFB3). Scale bar: 100 µm. The mouse primary LSECs were treated with or without TNF‐α (20 ng ml −1 ) for 24 h. L) Quantification of CD31 + MYC + CD63 + PFKFB3 + PKM + LSECs for multiplex fluorescence as shown in K ( n = 4 samples per group; two‐sided Student's t‐test, p = 2.00 × 10 −2 ). M) Glycolytic rate assay showing glycolytic function of LSECs treated with or without TNF‐α (20 ng ml −1 ) for 24 h. ( n = 5 or 6 samples per group; two‐sided Student's t‐test, p = 8.00 × 10 −6 and 1.30 × 10 −5 from top to bottom). N) mIHC of CD31 + MYC + ECs, F4/80 + MMP12 + Mψ and CCR2 + monocytes are shown. Scale bar: 200 µm, 50 µm and 20 µm. Spatial localizations of CD31 + MYC + ECs, CCR2 + monocytes, and F4/80 + MMP12 + Mψ within injured region are shown. In all graphs data are presented as mean ± SD, * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Advanced Science

Article Title: Myeloid‐Mas Signaling Modulates Pathogenic Crosstalk among MYC + CD63 + Endothelial Cells, MMP12 + Macrophages, and Monocytes in Acetaminophen‐Induced Liver Injury

doi: 10.1002/advs.202306066

Figure Lengend Snippet: Monocyte‐derived TNF‐α acts on MYC + CD63 + EC through TNFR1. A) Spatial feature plots showing the cell types in EC7 expansion units for ST. B) CellPhoneDB analysis showing the cell–cell interactions for scRNA‐seq. C) Mas1 −/− mice were pre‐administrated with clodronate liposomes or control liposomes for 24 h before APAP challenge ( n = 4 per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. D) WT and Mas1 −/− mice were pre‐administrated with cenicriviroc for 2 h before APAP challenge ( n = 4 per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. E) CellPhoneDB analysis showing the major interaction pairs between Ly6c hi monocyte‐Mψ5 or Ly6c hi monocyte‐EC7 for scRNA‐seq. In F‐G, Mas1 −/− mice were pre‐administrated with cediranib or control for 2 h before APAP challenge ( n = 4 per group). F) Representative staining of H&E and mIHC are shown. Scale bar: 50 µm. G) Quantification of necrotic area for H&E as shown in F ( n = 4 mice per group; two‐sided Student's t‐test; p = 1.55 × 10 −4 ) and serum ALT ( n = 4 mice per group; two‐sided Student's t‐test; p = 2.64 × 10 −8 ). H) Multiplex fluorescence of CD31 + MYC + CD63 + LSECs and key glycolytic enzymes (PKM and PFKFB3). Scale bar: 100 µm. The mouse primary LSECs were treated with or without BMDM‐CM for 24 h. I) Quantification of CD31 + MYC + CD63 + PFKFB3 + PKM + LSECs for multiplex fluorescence as shown in H ( n = 4 samples per group; two‐sided Mann‐Whitney U test, p = 2.86 × 10 −2 ). J) Glycolytic rate assay showing glycolytic function of LSECs treated with or without BMDM‐CM for 24 h. ( n = 5 or 6 samples per group; two‐sided Student's t‐test, p = 7.50 × 10 −3 and 3.77 × 10 −3 from left to right). K) Multiplex fluorescence of CD31 + MYC + CD63 + LSECs and key glycolytic enzymes (PKM and PFKFB3). Scale bar: 100 µm. The mouse primary LSECs were treated with or without TNF‐α (20 ng ml −1 ) for 24 h. L) Quantification of CD31 + MYC + CD63 + PFKFB3 + PKM + LSECs for multiplex fluorescence as shown in K ( n = 4 samples per group; two‐sided Student's t‐test, p = 2.00 × 10 −2 ). M) Glycolytic rate assay showing glycolytic function of LSECs treated with or without TNF‐α (20 ng ml −1 ) for 24 h. ( n = 5 or 6 samples per group; two‐sided Student's t‐test, p = 8.00 × 10 −6 and 1.30 × 10 −5 from top to bottom). N) mIHC of CD31 + MYC + ECs, F4/80 + MMP12 + Mψ and CCR2 + monocytes are shown. Scale bar: 200 µm, 50 µm and 20 µm. Spatial localizations of CD31 + MYC + ECs, CCR2 + monocytes, and F4/80 + MMP12 + Mψ within injured region are shown. In all graphs data are presented as mean ± SD, * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: For the experimental preparations in Figure , Figure and (Supporting Information), CD31 (5 µg, 102416, Biolegend), Ly6C (10 µg, NB100‐65413AF594, Novus), CD63 (4 µg, 143920, Biolegend) and PBS (60 µL) were injected into mice through the tail vein.

Techniques: Derivative Assay, Liposomes, Control, Staining, Multiplex Assay, Fluorescence, MANN-WHITNEY

Myeloid Mas modulates AILI through the highly pro‐inflammatory and glycolytic microenvironment. A) Mas1 f/f , LysM cre Mas1 f/f , Alb cre Mas1 f/f , Cdh5 cre Mas1 f/f , Lrat cre Mas1 f/f and Cd4 cre Mas1 f/f mice were administrated with APAP for 24 h ( n = 6 mice per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. B) mIHC of CD31 + MYC + ECs, F4/80 + MMP12 + Mψ, and CCR2 + monocytes are shown. Scale bar: 50 µm and 20 µm. C) The UMAP plot showing the subpopulation of Mψ. D) mIHC of CD31 + MYC + ECs, F4/80 + MMP12 + Mψ, and key glycolytic enzymes (PKM and PFKFB3). Scale bar: 20 µm. E) LysM cre Mas1 f/f mice were pre‐administrated with or without 3PO before APAP challenge ( n = 4 per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. F) Quantification of necrotic area for H&E as shown in E ( n = 4 mice per group; two‐sided Student's t‐test, p = 9.53 × 10 −7 ), serum ALT ( n = 4 mice per group; two‐sided Student's t‐test, p = 3.77 × 10 −7 ) and quantification of CD31 + MYC + ECs for mIHC as shown in E ( n = 4 mice per group; two‐sided Student's t‐test, p = 2.70 × 10 −5 ). G) Timelapse data of neutrophils (Ly6G) and monocytes (Ly6C) in the vessels (WGA) of living mouse livers were captured by DAOSLIMIT. Representative intravital images and the temporal traces of their number are shown. LysM cre Mas1 f/f mice were pre‐administrated with or without 3PO before APAP challenge. Scale bar: 50 µm. In all graphs, data are presented as mean ± SD, *** p < 0.001.

Journal: Advanced Science

Article Title: Myeloid‐Mas Signaling Modulates Pathogenic Crosstalk among MYC + CD63 + Endothelial Cells, MMP12 + Macrophages, and Monocytes in Acetaminophen‐Induced Liver Injury

doi: 10.1002/advs.202306066

Figure Lengend Snippet: Myeloid Mas modulates AILI through the highly pro‐inflammatory and glycolytic microenvironment. A) Mas1 f/f , LysM cre Mas1 f/f , Alb cre Mas1 f/f , Cdh5 cre Mas1 f/f , Lrat cre Mas1 f/f and Cd4 cre Mas1 f/f mice were administrated with APAP for 24 h ( n = 6 mice per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. B) mIHC of CD31 + MYC + ECs, F4/80 + MMP12 + Mψ, and CCR2 + monocytes are shown. Scale bar: 50 µm and 20 µm. C) The UMAP plot showing the subpopulation of Mψ. D) mIHC of CD31 + MYC + ECs, F4/80 + MMP12 + Mψ, and key glycolytic enzymes (PKM and PFKFB3). Scale bar: 20 µm. E) LysM cre Mas1 f/f mice were pre‐administrated with or without 3PO before APAP challenge ( n = 4 per group). Representative stainings of H&E and mIHC are shown. Scale bar: 50 µm. F) Quantification of necrotic area for H&E as shown in E ( n = 4 mice per group; two‐sided Student's t‐test, p = 9.53 × 10 −7 ), serum ALT ( n = 4 mice per group; two‐sided Student's t‐test, p = 3.77 × 10 −7 ) and quantification of CD31 + MYC + ECs for mIHC as shown in E ( n = 4 mice per group; two‐sided Student's t‐test, p = 2.70 × 10 −5 ). G) Timelapse data of neutrophils (Ly6G) and monocytes (Ly6C) in the vessels (WGA) of living mouse livers were captured by DAOSLIMIT. Representative intravital images and the temporal traces of their number are shown. LysM cre Mas1 f/f mice were pre‐administrated with or without 3PO before APAP challenge. Scale bar: 50 µm. In all graphs, data are presented as mean ± SD, *** p < 0.001.

Article Snippet: For the experimental preparations in Figure , Figure and (Supporting Information), CD31 (5 µg, 102416, Biolegend), Ly6C (10 µg, NB100‐65413AF594, Novus), CD63 (4 µg, 143920, Biolegend) and PBS (60 µL) were injected into mice through the tail vein.

Techniques: