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Novus Biologicals kshv k8
Kshv K8, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 91/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/kshv+k8/pm41931390-243-28-30?v=Novus+Biologicals
Average 91 stars, based on 4 article reviews

kshv k8 - by Bioz Stars, 2026-07

91/100 stars

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KSHV lytic program targets KDM5A/B for proteasome degradation. (A) TREx.BCBL-1.RTA cells were treated with doxycycline (Dox, 1 µg/mL) for 2 days, followed by protein immunoblotting to quantify KDM5A/B proteins and KSHV lytic K8.1 protein. (B) KDM5A/B mRNA level in cell samples (A) was measured by RT-qPCR. (C) BJAB cells were treated similarly as (A) and analyzed by protein immunoblotting to quantify KDM5A/B proteins. (D) KDM5A/B mRNA level in cell samples (C) was measured by RT-qPCR. (E) TIME cells were spinoculated with KSHV BAC16 viruses. At 2 days post of infection (dpi), cells were collected and analyzed by protein immunoblotting to quantify KDM5A/B proteins and KSHV lytic K8.1 protein. (F) KDM5A/B mRNA level in cell samples (E) was measured by RT-qPCR. (G) TREx.BCBL-1.RTA cells were treated with Dox in the absence or presence of MG132 (1 µM) for 2 days, followed by protein immunoblotting to quantify KDM5A/B proteins and KSHV lytic K8.1 protein. (H, I) TREx.BCBL-1.RTA cells were treated with Dox in the absence or presence of MG132 (1 µM) for 2 days, followed by protein immunoprecipitation (IP) of KDM5A (H) or KDM5B (I) using their specific antibodies, followed by protein immunoblotting to quantify K48 or K63-linked polyubiquitination of KDM5A/B. Results were calculated from three independent experiments and presented as Mean ± SD (ns: not significant, * P < 0.05, ** P < 0.01, **** P < 0.0001; unpaired, two-tailed Student’s t -test).

Journal: bioRxiv

Article Title: Inhibition of KDM5A/B promotes antitumor innate immune responses in HHV-8/KSHV-positive B-cell lymphomas

doi: 10.64898/2026.01.28.702275

Figure Lengend Snippet: KSHV lytic program targets KDM5A/B for proteasome degradation. (A) TREx.BCBL-1.RTA cells were treated with doxycycline (Dox, 1 µg/mL) for 2 days, followed by protein immunoblotting to quantify KDM5A/B proteins and KSHV lytic K8.1 protein. (B) KDM5A/B mRNA level in cell samples (A) was measured by RT-qPCR. (C) BJAB cells were treated similarly as (A) and analyzed by protein immunoblotting to quantify KDM5A/B proteins. (D) KDM5A/B mRNA level in cell samples (C) was measured by RT-qPCR. (E) TIME cells were spinoculated with KSHV BAC16 viruses. At 2 days post of infection (dpi), cells were collected and analyzed by protein immunoblotting to quantify KDM5A/B proteins and KSHV lytic K8.1 protein. (F) KDM5A/B mRNA level in cell samples (E) was measured by RT-qPCR. (G) TREx.BCBL-1.RTA cells were treated with Dox in the absence or presence of MG132 (1 µM) for 2 days, followed by protein immunoblotting to quantify KDM5A/B proteins and KSHV lytic K8.1 protein. (H, I) TREx.BCBL-1.RTA cells were treated with Dox in the absence or presence of MG132 (1 µM) for 2 days, followed by protein immunoprecipitation (IP) of KDM5A (H) or KDM5B (I) using their specific antibodies, followed by protein immunoblotting to quantify K48 or K63-linked polyubiquitination of KDM5A/B. Results were calculated from three independent experiments and presented as Mean ± SD (ns: not significant, * P < 0.05, ** P < 0.01, **** P < 0.0001; unpaired, two-tailed Student’s t -test).

Article Snippet: The following antibodies were used in this study: anti-KDM5A (Active Motif, Cat# 91211); anti-KDM5B (Bethyl Laboratories, Cat# A301-813A); ant-KDM5C (Bethyl Laboratories, Cat# A301-034A); anti-KSHV K8.1 (Santa Cruz Biotechnology, Cat# sc-65446); anti-EBV EBNA1 (Santa Cruz Biotechnology, Cat# sc-81581); anti-GAPDH (Santa Cruz Biotechnology, Cat# sc-47724); normal rat IgG (Santa Cruz Biotechnology, Cat# sc-2026); anti-KSHV LANA (Advanced Biotechnologies, Cat# 13-210-100); anti-FLAG M2 (Sigma-Aldrich, Cat# F1804); anti-CD3-FITC (Miltenyi Biotec, Cat# 130-113-690); anti-CD19-PE (Santa Cruz Biotechnology, Cat# 130-113-731); anti-CD20 (BioLegend, Cat# 382802); anti-mouse HRP-linked (Cell Signaling Technology, Cat#7076S) and anti-rabbit HRP-linked (Santa Cruz Biotechnology, Cat# 7074S) antibodies; isotype control IgG including rabbit IgG (Santa Cruz Biotechnology, Cat# 3900S), mouse IgG 1 (Santa Cruz Biotechnology, Cat# 5415S), mouse IgG 2a (Santa Cruz Biotechnology, Cat# 61656S) and mouse IgG 2b (Santa Cruz Biotechnology, Cat# 53484S).

Techniques: Western Blot, Quantitative RT-PCR, Infection, Immunoprecipitation, Two Tailed Test

KDM5A/B suppress KSHV lytic reactivation from latency. (A, B) TREx.BCBL-1.RTA cells were transiently transfected with siRNAs targeting KDM5A (A) or KDM5B (B) through electroporation. At 3 days post of transfection, cells were collected and analyzed by RT-qPCR to quantify KDM5A/B knockdown. (C, D) TREx.BCBL-1.RTA cells with depletion of KDM5A (C) or KDM5B (D) were treated with Dox for 2 days, followed by RT-qPCR to quantify KSHV lytic genes K8 and K8.1. (E, F) KDM5A/B and KSHV K8.1 proteins in cell samples (C, D) with Dox treatment were measured by protein immunoblotting. (G, H) iSLK.BAC16 cells were transiently transfected with siRNAs targeting KDM5A (G) or KDM5B (H) for 3 days, followed by Dox treatment for 2 days. KDM5A/B knockdown were measured by RT-qPCR. (I, J) iSLK.BAC16 cells with depletion of KDM5A (I) or KDM5B (J) as well as Dox treatment was analyzed by RT-qPCR to quantify KSHV lytic genes K8 and K8.1. (K, L) KDM5A/B and KSHV K8.1 proteins in cell samples in cell samples (I, J) were measured by protein immunoblotting. (M, N) iSLK.r219 cells were transiently transfected with siRNAs targeting KDM5A (M) or KDM5B (N) for 3 days, followed by Dox treatment for 2 days. KDM5A/B knockdown were measured by RT-qPCR. KSHV lytic reactivation was visualized by fluorescence microscopy (RFP vs GFP signal). Results were calculated from three independent experiments and presented as Mean ± SD (*** P < 0.001, **** P < 0.0001; unpaired, two-tailed Student’s t -test for A; one-way ANOVA for I, J, two-way ANOVA for B, C, E, F, G).

Journal: bioRxiv

Article Title: Inhibition of KDM5A/B promotes antitumor innate immune responses in HHV-8/KSHV-positive B-cell lymphomas

doi: 10.64898/2026.01.28.702275

Figure Lengend Snippet: KDM5A/B suppress KSHV lytic reactivation from latency. (A, B) TREx.BCBL-1.RTA cells were transiently transfected with siRNAs targeting KDM5A (A) or KDM5B (B) through electroporation. At 3 days post of transfection, cells were collected and analyzed by RT-qPCR to quantify KDM5A/B knockdown. (C, D) TREx.BCBL-1.RTA cells with depletion of KDM5A (C) or KDM5B (D) were treated with Dox for 2 days, followed by RT-qPCR to quantify KSHV lytic genes K8 and K8.1. (E, F) KDM5A/B and KSHV K8.1 proteins in cell samples (C, D) with Dox treatment were measured by protein immunoblotting. (G, H) iSLK.BAC16 cells were transiently transfected with siRNAs targeting KDM5A (G) or KDM5B (H) for 3 days, followed by Dox treatment for 2 days. KDM5A/B knockdown were measured by RT-qPCR. (I, J) iSLK.BAC16 cells with depletion of KDM5A (I) or KDM5B (J) as well as Dox treatment was analyzed by RT-qPCR to quantify KSHV lytic genes K8 and K8.1. (K, L) KDM5A/B and KSHV K8.1 proteins in cell samples in cell samples (I, J) were measured by protein immunoblotting. (M, N) iSLK.r219 cells were transiently transfected with siRNAs targeting KDM5A (M) or KDM5B (N) for 3 days, followed by Dox treatment for 2 days. KDM5A/B knockdown were measured by RT-qPCR. KSHV lytic reactivation was visualized by fluorescence microscopy (RFP vs GFP signal). Results were calculated from three independent experiments and presented as Mean ± SD (*** P < 0.001, **** P < 0.0001; unpaired, two-tailed Student’s t -test for A; one-way ANOVA for I, J, two-way ANOVA for B, C, E, F, G).

Techniques: Transfection, Electroporation, Quantitative RT-PCR, Knockdown, Western Blot, Fluorescence, Microscopy, Two Tailed Test

KDM5 inhibition induces KSHV lytic reactivation from latency. (A) TREx.BCBL-1.RTA cells treated with JQKD82 (48 h) was analyzed by the ATP luminescent assay to measure drug’s cytotoxicity. (B) TREx.BCBL-1.RTA cells were treated with JQKD82 for 48 h and then Dox for another 48 h. Cells were collected for protein immunoblotting of KSHV lytic K8.1 protein. (C) mRNA level of KSHV lytic viral genes (ORF50/RTA, K8, K8.1) in cell samples (B) was measured by RT-qPCR. (D, E) BCBL-1 (D) or BC-3 cells (E) were treated with JQKD82 for 96 h and analyzed by RT-qPCR to quantify KSHV lytic genes K8 and K8.1. (F) iSLK.BAC16 cells were treated with JQKD82 for 48 h and then Dox for another 48 h. Cells were collected for protein immunoblotting to quantify KSHV K8.1 protein. (G) iSLK.BAC16 cells treated with JQKD82 in the absence or presence of Dox were collected and analyzed by RT-qPCR to quantify KSHV lytic genes K8 and K8.1. Results were calculated from three independent experiments and presented as Mean ± SD (** P < 0.01, *** P < 0.001, **** P < 0.0001; unpaired, two-tailed Student’s t -test for D, E; two-way ANOVA for C, G).

Journal: bioRxiv

Article Title: Inhibition of KDM5A/B promotes antitumor innate immune responses in HHV-8/KSHV-positive B-cell lymphomas

doi: 10.64898/2026.01.28.702275

Figure Lengend Snippet: KDM5 inhibition induces KSHV lytic reactivation from latency. (A) TREx.BCBL-1.RTA cells treated with JQKD82 (48 h) was analyzed by the ATP luminescent assay to measure drug’s cytotoxicity. (B) TREx.BCBL-1.RTA cells were treated with JQKD82 for 48 h and then Dox for another 48 h. Cells were collected for protein immunoblotting of KSHV lytic K8.1 protein. (C) mRNA level of KSHV lytic viral genes (ORF50/RTA, K8, K8.1) in cell samples (B) was measured by RT-qPCR. (D, E) BCBL-1 (D) or BC-3 cells (E) were treated with JQKD82 for 96 h and analyzed by RT-qPCR to quantify KSHV lytic genes K8 and K8.1. (F) iSLK.BAC16 cells were treated with JQKD82 for 48 h and then Dox for another 48 h. Cells were collected for protein immunoblotting to quantify KSHV K8.1 protein. (G) iSLK.BAC16 cells treated with JQKD82 in the absence or presence of Dox were collected and analyzed by RT-qPCR to quantify KSHV lytic genes K8 and K8.1. Results were calculated from three independent experiments and presented as Mean ± SD (** P < 0.01, *** P < 0.001, **** P < 0.0001; unpaired, two-tailed Student’s t -test for D, E; two-way ANOVA for C, G).

Techniques: Inhibition, Luminescence Assay, Western Blot, Quantitative RT-PCR, Two Tailed Test

( A ) Senescence was induced in primary human endothelial cells (HUVECs) by repeated subculture over 35 passages or treatment with doxorubicin. In doxycycline-inducible immortalized human endothelial cells (HuARLT cells), senescence was induced by culturing without doxycycline. SA-β-gal staining was used for validation of senescence through microscopy or flow cytometry. p, cell culture passages. dc, doxycycline. KSHV infectivity was measured by GFP expression in cells infected with recombinant KSHV BAC16. ( B ) Analysis of KSHV-infected cells in nonsenescent and senescent human endothelial cells by flow cytometry at 24 hpi. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. *** P < 0.001, unpaired 2-tailed Student’s t test. ( C ) Quantification of the KSHV genome in KSHV-infected nonsenescent and senescent human endothelial cells by quantitative PCR at 24 hpi. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. ** P < 0.01, *** P < 0.001, unpaired 2-tailed Student’s t test. ( D ) Assessment of the relative expression of KSHV ORF71 mRNA in KSHV-infected nonsenescent and senescent human endothelial cells using quantitative reverse transcription PCR at 24 hpi. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. ** P < 0.01, unpaired 2-tailed Student’s t test.

Journal: The Journal of Clinical Investigation

Article Title: Senescence of endothelial cells increases susceptibility to Kaposi’s sarcoma–associated herpesvirus infection via CD109-mediated viral entry

doi: 10.1172/JCI183561

Figure Lengend Snippet: ( A ) Senescence was induced in primary human endothelial cells (HUVECs) by repeated subculture over 35 passages or treatment with doxorubicin. In doxycycline-inducible immortalized human endothelial cells (HuARLT cells), senescence was induced by culturing without doxycycline. SA-β-gal staining was used for validation of senescence through microscopy or flow cytometry. p, cell culture passages. dc, doxycycline. KSHV infectivity was measured by GFP expression in cells infected with recombinant KSHV BAC16. ( B ) Analysis of KSHV-infected cells in nonsenescent and senescent human endothelial cells by flow cytometry at 24 hpi. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. *** P < 0.001, unpaired 2-tailed Student’s t test. ( C ) Quantification of the KSHV genome in KSHV-infected nonsenescent and senescent human endothelial cells by quantitative PCR at 24 hpi. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. ** P < 0.01, *** P < 0.001, unpaired 2-tailed Student’s t test. ( D ) Assessment of the relative expression of KSHV ORF71 mRNA in KSHV-infected nonsenescent and senescent human endothelial cells using quantitative reverse transcription PCR at 24 hpi. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. ** P < 0.01, unpaired 2-tailed Student’s t test.

Article Snippet: Mouse anti-KSHV K8.1 antibody (1:100 dilution; SC-65446; 4A4; Santa Cruz Biotechnology), rabbit anti-caveolin-1 (1:100 dilution; A1555; Abclonal), rabbit anti-CD109 (1:100 dilution; 486955; E8L2W; Cell Signaling Technology), rat anti-LANA (1:100 dilution; Ab4103; LN53; Abcam), and mouse anti-KSHV ORF 65 (1:100 dilution) ( ) were used as primary antibodies.

Techniques: Staining, Biomarker Discovery, Microscopy, Flow Cytometry, Cell Culture, Infection, Expressing, Recombinant, Real-time Polymerase Chain Reaction, Reverse Transcription

( A ) Immunofluorescence assay of the entry of KSHV into nonsenescent and senescent cells. KSHV was visualized at 4 hpi using KSHV ORF65 antibody. Phalloidin (F-actin) and DAPI were used to visualize the shapes of the cells and nuclei, respectively. Scale bars: 50 μm. ( B ) Analysis of the number of internalized KSHV particles per cell in the images in A and . Data are representative of 10 independent experiments. Data are shown as mean ± SD. n = 10. *** P < 0.001 using unpaired 2-tailed Student’s t test. ( C ) Quantification of the internalized KSHV genome in the KSHV-infected nonsenescent and senescent human endothelial cells by quantitative PCR. Genomic DNA was extracted from KSHV-infected cells at 4 hpi. The KSHV genome was quantified in the extracted DNA by quantitative PCR using primers for KSHV ORF26. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. ** P < 0.01; *** P < 0.001, unpaired 2-tailed Student’s t test.

Journal: The Journal of Clinical Investigation

Article Title: Senescence of endothelial cells increases susceptibility to Kaposi’s sarcoma–associated herpesvirus infection via CD109-mediated viral entry

doi: 10.1172/JCI183561

Figure Lengend Snippet: ( A ) Immunofluorescence assay of the entry of KSHV into nonsenescent and senescent cells. KSHV was visualized at 4 hpi using KSHV ORF65 antibody. Phalloidin (F-actin) and DAPI were used to visualize the shapes of the cells and nuclei, respectively. Scale bars: 50 μm. ( B ) Analysis of the number of internalized KSHV particles per cell in the images in A and . Data are representative of 10 independent experiments. Data are shown as mean ± SD. n = 10. *** P < 0.001 using unpaired 2-tailed Student’s t test. ( C ) Quantification of the internalized KSHV genome in the KSHV-infected nonsenescent and senescent human endothelial cells by quantitative PCR. Genomic DNA was extracted from KSHV-infected cells at 4 hpi. The KSHV genome was quantified in the extracted DNA by quantitative PCR using primers for KSHV ORF26. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. ** P < 0.01; *** P < 0.001, unpaired 2-tailed Student’s t test.

Techniques: Immunofluorescence, Infection, Real-time Polymerase Chain Reaction

( A ) Confocal microscopy images of KSHV binding to the cell surface. After infection, cells were immediately fixed and stained without permeabilization. Scale bars: 10 μm. ( B ) Analysis of the number of KSHV particles binding to the cell surface per cell in the images in A and . Data are representative of 10 independent experiments. Data are shown as mean ± SD. n = 10. *** P < 0.001, unpaired 2-tailed Student’s t test. ( C ) Quantification of the cell-surface–bound KSHV genome in KSHV-infected cells by quantitative PCR. After 1 hour of KSHV infection, the cells were immediately scraped and genomic DNA was extracted. The KSHV genome was quantified in the extracted DNA by quantitative PCR using primers for KSHV ORF26. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. ** P < 0.01; *** P < 0.001, unpaired 2-tailed Student’s t test.

Journal: The Journal of Clinical Investigation

Article Title: Senescence of endothelial cells increases susceptibility to Kaposi’s sarcoma–associated herpesvirus infection via CD109-mediated viral entry

doi: 10.1172/JCI183561

Figure Lengend Snippet: ( A ) Confocal microscopy images of KSHV binding to the cell surface. After infection, cells were immediately fixed and stained without permeabilization. Scale bars: 10 μm. ( B ) Analysis of the number of KSHV particles binding to the cell surface per cell in the images in A and . Data are representative of 10 independent experiments. Data are shown as mean ± SD. n = 10. *** P < 0.001, unpaired 2-tailed Student’s t test. ( C ) Quantification of the cell-surface–bound KSHV genome in KSHV-infected cells by quantitative PCR. After 1 hour of KSHV infection, the cells were immediately scraped and genomic DNA was extracted. The KSHV genome was quantified in the extracted DNA by quantitative PCR using primers for KSHV ORF26. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. ** P < 0.01; *** P < 0.001, unpaired 2-tailed Student’s t test.

Techniques: Confocal Microscopy, Binding Assay, Infection, Staining, Real-time Polymerase Chain Reaction

( A ) Heatmap of the differential expression of proteins from nonsenescent (+dc, culture with doxycycline) and senescent (–dc, culture without doxycycline) HuARLT cells with KSHV (K) or without KSHV (M). The cell lysate and cell pellet from each conditioned cell were analyzed by LC-MS/MS. ( B ) Western blot analysis of the selected candidate proteins. Cav-1, caveolin-1; ITG, integrin; dc, doxycycline. GAPDH was used as a housekeeping protein for normalization. ( C ) Flow cytometric analysis of candidate proteins in nonsenescent (+dc HuARLT and –dox HUVEC) and senescent (–dc HuARLT and +dox HUVEC) cells. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. * P < 0.05; ** P < 0.01; *** P < 0.001, unpaired 2-tailed Student’s t test.

Journal: The Journal of Clinical Investigation

Article Title: Senescence of endothelial cells increases susceptibility to Kaposi’s sarcoma–associated herpesvirus infection via CD109-mediated viral entry

doi: 10.1172/JCI183561

Figure Lengend Snippet: ( A ) Heatmap of the differential expression of proteins from nonsenescent (+dc, culture with doxycycline) and senescent (–dc, culture without doxycycline) HuARLT cells with KSHV (K) or without KSHV (M). The cell lysate and cell pellet from each conditioned cell were analyzed by LC-MS/MS. ( B ) Western blot analysis of the selected candidate proteins. Cav-1, caveolin-1; ITG, integrin; dc, doxycycline. GAPDH was used as a housekeeping protein for normalization. ( C ) Flow cytometric analysis of candidate proteins in nonsenescent (+dc HuARLT and –dox HUVEC) and senescent (–dc HuARLT and +dox HUVEC) cells. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. * P < 0.05; ** P < 0.01; *** P < 0.001, unpaired 2-tailed Student’s t test.

Techniques: Quantitative Proteomics, Liquid Chromatography with Mass Spectroscopy, Western Blot

Journal: The Journal of Clinical Investigation

Article Title: Senescence of endothelial cells increases susceptibility to Kaposi’s sarcoma–associated herpesvirus infection via CD109-mediated viral entry

doi: 10.1172/JCI183561

Figure Lengend Snippet: LC-MS/MS expression of KSHV receptor candidate in control and senescent HuARLT cells

Techniques: Expressing, Control

An equivalent quantity of KSHV was used to infect the same number of WT and KO HuARLT cells, with or without induction of senescence. KSHV was prepared as GFP infectious units of 1 to infect approximately 90% of nonsenescent WT cells, followed by the infection of a 2-fold serially diluted virus into each group of conditioned cells. KSHV infectivity was measured using GFP expression. ( A and B ) Fluorescence microscopic visualization of KSHV-infected cells for each KO clone in nonsenescent (+dc, A ) and senescent (–dc, B ) HuARLT cells. CAV1 , caveolin-1; ITGA2 , integrin-α 2 . Scale bar: 100 μm. ( C and D ) Flow cytometric analysis of KSHV-infected cells for each KO clone in nonsenescent (+dc, C ) and senescent (–dc, D ) HuARLT cells. At the indicated GFP infectious units (GIU), the percentage of KSHV-infected cells was compared among each group. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. *** P < 0.001, Dunnett’s test for multiple comparisons.

Journal: The Journal of Clinical Investigation

Article Title: Senescence of endothelial cells increases susceptibility to Kaposi’s sarcoma–associated herpesvirus infection via CD109-mediated viral entry

doi: 10.1172/JCI183561

Figure Lengend Snippet: An equivalent quantity of KSHV was used to infect the same number of WT and KO HuARLT cells, with or without induction of senescence. KSHV was prepared as GFP infectious units of 1 to infect approximately 90% of nonsenescent WT cells, followed by the infection of a 2-fold serially diluted virus into each group of conditioned cells. KSHV infectivity was measured using GFP expression. ( A and B ) Fluorescence microscopic visualization of KSHV-infected cells for each KO clone in nonsenescent (+dc, A ) and senescent (–dc, B ) HuARLT cells. CAV1 , caveolin-1; ITGA2 , integrin-α 2 . Scale bar: 100 μm. ( C and D ) Flow cytometric analysis of KSHV-infected cells for each KO clone in nonsenescent (+dc, C ) and senescent (–dc, D ) HuARLT cells. At the indicated GFP infectious units (GIU), the percentage of KSHV-infected cells was compared among each group. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. *** P < 0.001, Dunnett’s test for multiple comparisons.

Techniques: Infection, Virus, Expressing, Fluorescence

( A ) Representative confocal images of KSHV virus particles in CAV1 -KO and CD109 -KO HuARLT cells. Scale bars: 10 μm. ( B ) Analysis of the number of KSHV particles that bind to the cell surface per cell in the images in A and . Data are representative of 10 independent experiments. Data are shown as mean ± SD. n = 10. *** P < 0.001, Dunnett’s test for multiple comparisons. ( C ) Quantification of the cell-surface–bound KSHV genome in the KSHV-infected cells by quantitative PCR. After 1 hour of KSHV infection, the cells were immediately scraped, and genomic DNA extracted after washing. The KSHV genome was quantified in the extracted DNA by quantitative PCR using primers for KSHV ORF26. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. ** P < 0.01; *** P < 0.001, Dunnett’s test for multiple comparisons.

Journal: The Journal of Clinical Investigation

Article Title: Senescence of endothelial cells increases susceptibility to Kaposi’s sarcoma–associated herpesvirus infection via CD109-mediated viral entry

doi: 10.1172/JCI183561

Figure Lengend Snippet: ( A ) Representative confocal images of KSHV virus particles in CAV1 -KO and CD109 -KO HuARLT cells. Scale bars: 10 μm. ( B ) Analysis of the number of KSHV particles that bind to the cell surface per cell in the images in A and . Data are representative of 10 independent experiments. Data are shown as mean ± SD. n = 10. *** P < 0.001, Dunnett’s test for multiple comparisons. ( C ) Quantification of the cell-surface–bound KSHV genome in the KSHV-infected cells by quantitative PCR. After 1 hour of KSHV infection, the cells were immediately scraped, and genomic DNA extracted after washing. The KSHV genome was quantified in the extracted DNA by quantitative PCR using primers for KSHV ORF26. Data are representative of 3 independent experiments. Data are shown as mean ± SD. n = 3. ** P < 0.01; *** P < 0.001, Dunnett’s test for multiple comparisons.

Techniques: Virus, Infection, Real-time Polymerase Chain Reaction

( A and B ) Three-dimensional confocal microscopy images of the colocalization of KSHV with CD109 ( A ) or caveolin-1 (Cav-1) ( B ). Senescent HuARLT cells infected with KSHV for 1 hour were stained with KSHV K8.1 antibody and target proteins, and Z -axis scanning was performed at 4 μm intervals, generating more than 10 scans. The bar-shaped images at the edges represent cross-sections, guided by white solid lines in the stacked image. ( C ) Quantitative analysis of the colocalization of KSHV with CD109 or caveolin-1 by Manders’ colocalization coefficient in KSHV-infected senescent HuARLT cells. n = 10. *** P < 0.001 ( D ) SPR analysis of KSHV binding to immobilized recombinant CD109. Data are representative of 3 independent experiments. ( E ) Neutralization of KSHV infectivity using a recombinant CD109 protein. Data are representative of 3 independent experiments. Data are presented as mean ± SD. n = 3. *** P < 0.001, Dunnett’s test for multiple comparisons.

Journal: The Journal of Clinical Investigation

Article Title: Senescence of endothelial cells increases susceptibility to Kaposi’s sarcoma–associated herpesvirus infection via CD109-mediated viral entry

doi: 10.1172/JCI183561

Figure Lengend Snippet: ( A and B ) Three-dimensional confocal microscopy images of the colocalization of KSHV with CD109 ( A ) or caveolin-1 (Cav-1) ( B ). Senescent HuARLT cells infected with KSHV for 1 hour were stained with KSHV K8.1 antibody and target proteins, and Z -axis scanning was performed at 4 μm intervals, generating more than 10 scans. The bar-shaped images at the edges represent cross-sections, guided by white solid lines in the stacked image. ( C ) Quantitative analysis of the colocalization of KSHV with CD109 or caveolin-1 by Manders’ colocalization coefficient in KSHV-infected senescent HuARLT cells. n = 10. *** P < 0.001 ( D ) SPR analysis of KSHV binding to immobilized recombinant CD109. Data are representative of 3 independent experiments. ( E ) Neutralization of KSHV infectivity using a recombinant CD109 protein. Data are representative of 3 independent experiments. Data are presented as mean ± SD. n = 3. *** P < 0.001, Dunnett’s test for multiple comparisons.

Techniques: Confocal Microscopy, Infection, Staining, Binding Assay, Recombinant, Neutralization

Co-IP analysis of CD109 with KSHV glycoproteins gB ( A ), gH/gL ( B ), and K8.1 ( C ). HEK-293T cells were cotransfected with the indicated plasmids for 24 hours, after which cell lysates were subjected to IP using anti-FLAG magnetic agarose beads. The resulting complexes were then analyzed by immunoblotting (IB) using the indicated antibodies. Data are representative of 3 independent experiments.

Journal: The Journal of Clinical Investigation

Article Title: Senescence of endothelial cells increases susceptibility to Kaposi’s sarcoma–associated herpesvirus infection via CD109-mediated viral entry

doi: 10.1172/JCI183561

Figure Lengend Snippet: Co-IP analysis of CD109 with KSHV glycoproteins gB ( A ), gH/gL ( B ), and K8.1 ( C ). HEK-293T cells were cotransfected with the indicated plasmids for 24 hours, after which cell lysates were subjected to IP using anti-FLAG magnetic agarose beads. The resulting complexes were then analyzed by immunoblotting (IB) using the indicated antibodies. Data are representative of 3 independent experiments.

Techniques: Co-Immunoprecipitation Assay, Western Blot

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