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( A ) <t>GAL8</t> staining in THP-1 macrophages stably expressing GFP-LC3B after Mtb WT infection (2.5 hpi, MOI: 2) under treatment with BAPTA-AM and EGTA-AM. ( B ) GAL8 and GAL3 staining in THP-1 macrophages after Mtb WT and Mtb ΔRD1 infection (2.5 hpi, MOI: 2) under indicated treatments. ( C ) Percentage of Mtb-LC3-TVS positive for GAL8 related to (A) and fig. S3D. n (number of infected cells) = 51 to 72; data points correspond to individual technical replicates from three independent experiments. ( D ) Percentage of infected cells with Mtb-GAL3 positive, Mtb-GAL8 positive, and Mtb-GAL3/GAL8 double positive compartments. n (number of infected cells) = 96 to 151; data points correspond to individual technical replicates from three independent experiments. ( E ) Percentage of infected cells showing the Mtb-GAL3 positive, Mtb-GAL8 positive, and Mtb-GAL3/GAL8 double positive structures at 2.5, 8, and 24 hpi. n (number of infected cells) = 101 to 151; data points correspond to individual technical replicates from three independent experiments. The datasets for 2.5 hpi matches data from (D). Scale bars, in (A) and (B): 10 μm (main images) and 1 μm (inserted area).

Gal8, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/gal8+af1305/pmc11939036-263-9-10?v=R%26D+Systems
Average 93 stars, based on 26 article reviews

gal8 - by Bioz Stars, 2026-07

93/100 stars

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1) Product Images from "Mycobacterium tuberculosis phagosome Ca 2+ leakage triggers multimembrane ATG8/LC3 lipidation to restrict damage in human macrophages"

Article Title: Mycobacterium tuberculosis phagosome Ca 2+ leakage triggers multimembrane ATG8/LC3 lipidation to restrict damage in human macrophages

Journal: Science Advances

doi: 10.1126/sciadv.adt3311

( A ) GAL8 staining in THP-1 macrophages stably expressing GFP-LC3B after Mtb WT infection (2.5 hpi, MOI: 2) under treatment with BAPTA-AM and EGTA-AM. ( B ) GAL8 and GAL3 staining in THP-1 macrophages after Mtb WT and Mtb ΔRD1 infection (2.5 hpi, MOI: 2) under indicated treatments. ( C ) Percentage of Mtb-LC3-TVS positive for GAL8 related to (A) and fig. S3D. n (number of infected cells) = 51 to 72; data points correspond to individual technical replicates from three independent experiments. ( D ) Percentage of infected cells with Mtb-GAL3 positive, Mtb-GAL8 positive, and Mtb-GAL3/GAL8 double positive compartments. n (number of infected cells) = 96 to 151; data points correspond to individual technical replicates from three independent experiments. ( E ) Percentage of infected cells showing the Mtb-GAL3 positive, Mtb-GAL8 positive, and Mtb-GAL3/GAL8 double positive structures at 2.5, 8, and 24 hpi. n (number of infected cells) = 101 to 151; data points correspond to individual technical replicates from three independent experiments. The datasets for 2.5 hpi matches data from (D). Scale bars, in (A) and (B): 10 μm (main images) and 1 μm (inserted area).

Figure Legend Snippet: ( A ) GAL8 staining in THP-1 macrophages stably expressing GFP-LC3B after Mtb WT infection (2.5 hpi, MOI: 2) under treatment with BAPTA-AM and EGTA-AM. ( B ) GAL8 and GAL3 staining in THP-1 macrophages after Mtb WT and Mtb ΔRD1 infection (2.5 hpi, MOI: 2) under indicated treatments. ( C ) Percentage of Mtb-LC3-TVS positive for GAL8 related to (A) and fig. S3D. n (number of infected cells) = 51 to 72; data points correspond to individual technical replicates from three independent experiments. ( D ) Percentage of infected cells with Mtb-GAL3 positive, Mtb-GAL8 positive, and Mtb-GAL3/GAL8 double positive compartments. n (number of infected cells) = 96 to 151; data points correspond to individual technical replicates from three independent experiments. ( E ) Percentage of infected cells showing the Mtb-GAL3 positive, Mtb-GAL8 positive, and Mtb-GAL3/GAL8 double positive structures at 2.5, 8, and 24 hpi. n (number of infected cells) = 101 to 151; data points correspond to individual technical replicates from three independent experiments. The datasets for 2.5 hpi matches data from (D). Scale bars, in (A) and (B): 10 μm (main images) and 1 μm (inserted area).

Techniques Used: Staining, Stable Transfection, Expressing, Infection

( A ) Mtb infection (MOI: 2) in THP-1 macrophages stably expressing RFP-GFP-LC3B at 2.5 hpi under BafA1 and CQ treatment. ( B ) Percentage of infected cells showing Mtb-LC3-TVS under BafA1 and CQ treatment, related to (A). The dataset for control cells matches data from . Diagram shows endolysosome pH after BafA1and CQ treatment. n (number of infected cells) = 122 to 195; data points correspond to individual technical replicates from three independent experiments. ( C ) GAL8 staining in THP-1 macrophages stably expressing GFP-ATG16L1 at 2.5 hpi during Mtb infection (MOI: 2) under BafA1 treatment. ( D ) Quantification shows the percentage of Mtb-GAL8 positive structures positive for ATG16L1 under BafA1 treatment, related to (C). Diagram shows the function of BafA1 in blocking VATPase-ATG16L1 complex assembly. n (number of infected cells) = 178 and 202; data points correspond to individual technical replicates from 3 independent experiments. ( E ) ATP6V1D staining in THP-1 macrophages stably expressing GFP-ATG16L1 at 2.5 hpi during Mtb WT and Mtb ΔRD1 infection (MOI: 2) under indicated treatments. ( F and G ) Percentage of infected cells showing Mtb-ATP6V1D positive (F) and Mtb-ATG16L1 positive (G) structures under the indicated treatments, related to (E). n (number of infected cells) = 93 to 130; data points correspond to individual technical replicates from three independent experiments. ( H ) GAL8 and ATP6V1D staining in THP-1 macrophages infected with Mtb WT and Mtb ΔRD1 at 2.5 hpi. ( I ) Percentage of Mtb WT– and Mtb ΔRD1–infected cells showing the GAL8– and ATP6V1D–double positive structures, related to (H). n (number of infected cells) = 215 and 175; data points correspond to individual technical replicates from three independent experiments. Scale bars, 10 μm (main images) and 1 μm (inserted area).

Figure Legend Snippet: ( A ) Mtb infection (MOI: 2) in THP-1 macrophages stably expressing RFP-GFP-LC3B at 2.5 hpi under BafA1 and CQ treatment. ( B ) Percentage of infected cells showing Mtb-LC3-TVS under BafA1 and CQ treatment, related to (A). The dataset for control cells matches data from . Diagram shows endolysosome pH after BafA1and CQ treatment. n (number of infected cells) = 122 to 195; data points correspond to individual technical replicates from three independent experiments. ( C ) GAL8 staining in THP-1 macrophages stably expressing GFP-ATG16L1 at 2.5 hpi during Mtb infection (MOI: 2) under BafA1 treatment. ( D ) Quantification shows the percentage of Mtb-GAL8 positive structures positive for ATG16L1 under BafA1 treatment, related to (C). Diagram shows the function of BafA1 in blocking VATPase-ATG16L1 complex assembly. n (number of infected cells) = 178 and 202; data points correspond to individual technical replicates from 3 independent experiments. ( E ) ATP6V1D staining in THP-1 macrophages stably expressing GFP-ATG16L1 at 2.5 hpi during Mtb WT and Mtb ΔRD1 infection (MOI: 2) under indicated treatments. ( F and G ) Percentage of infected cells showing Mtb-ATP6V1D positive (F) and Mtb-ATG16L1 positive (G) structures under the indicated treatments, related to (E). n (number of infected cells) = 93 to 130; data points correspond to individual technical replicates from three independent experiments. ( H ) GAL8 and ATP6V1D staining in THP-1 macrophages infected with Mtb WT and Mtb ΔRD1 at 2.5 hpi. ( I ) Percentage of Mtb WT– and Mtb ΔRD1–infected cells showing the GAL8– and ATP6V1D–double positive structures, related to (H). n (number of infected cells) = 215 and 175; data points correspond to individual technical replicates from three independent experiments. Scale bars, 10 μm (main images) and 1 μm (inserted area).

Techniques Used: Infection, Stable Transfection, Expressing, Control, Staining, Blocking Assay

( A ) GAL8 and GAL3 staining in WT and ATG16L1 KO and FIP200 KO THP-1 macrophages after Mtb WT and Mtb ΔRD1 infection (2.5 hpi, MOI: 2). ( B and C ) Percentage of infected cells showing the Mtb-GAL8 positive and Mtb-GAL3 positive structures in WT and ATG7 KO, ATG16L1 KO, ATG13 KO, and FIP200 KO THP-1 macrophages related to (A) and fig. S5A. The datasets for WT cells are same as . n (number of infected cells) = 96 and 174; data points correspond to individual technical replicates from three independent experiments. ( D ) Representative micrographs at indicated time points of ATG16L1 KO and FIP200 KO THP-1 macrophages infected with Mtb WT (red) in the presence of PI+ necrotic cells (yellow). Bright-field images show the localization of macrophages. Data are representative from one of three independent experiments. ( E ) Quantification shows the fold change of Mtb area at 70 hpi with WT Mtb in WT, ATG7 KO, ATG16L1 KO, and FIP200 KO THP-1 macrophages. Data are from three independent biological replicates, each of which represents the mean of three technical replicates. ( F ) Quantification shows the fold change in the number of PI-positive cells 70 hpi with WT Mtb, compared to noninfected cells, in WT, ATG7 KO, ATG16L1 KO, and FIP200 KO THP-1 macrophages. Data are from three independent biological replicates, each of which represents the mean of three technical replicates. Scale bars, in (A): 10 μm; in (D): 50 μm.

Figure Legend Snippet: ( A ) GAL8 and GAL3 staining in WT and ATG16L1 KO and FIP200 KO THP-1 macrophages after Mtb WT and Mtb ΔRD1 infection (2.5 hpi, MOI: 2). ( B and C ) Percentage of infected cells showing the Mtb-GAL8 positive and Mtb-GAL3 positive structures in WT and ATG7 KO, ATG16L1 KO, ATG13 KO, and FIP200 KO THP-1 macrophages related to (A) and fig. S5A. The datasets for WT cells are same as . n (number of infected cells) = 96 and 174; data points correspond to individual technical replicates from three independent experiments. ( D ) Representative micrographs at indicated time points of ATG16L1 KO and FIP200 KO THP-1 macrophages infected with Mtb WT (red) in the presence of PI+ necrotic cells (yellow). Bright-field images show the localization of macrophages. Data are representative from one of three independent experiments. ( E ) Quantification shows the fold change of Mtb area at 70 hpi with WT Mtb in WT, ATG7 KO, ATG16L1 KO, and FIP200 KO THP-1 macrophages. Data are from three independent biological replicates, each of which represents the mean of three technical replicates. ( F ) Quantification shows the fold change in the number of PI-positive cells 70 hpi with WT Mtb, compared to noninfected cells, in WT, ATG7 KO, ATG16L1 KO, and FIP200 KO THP-1 macrophages. Data are from three independent biological replicates, each of which represents the mean of three technical replicates. Scale bars, in (A): 10 μm; in (D): 50 μm.

Techniques Used: Staining, Infection

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Journal: Science Advances

Article Title: Mycobacterium tuberculosis phagosome Ca 2+ leakage triggers multimembrane ATG8/LC3 lipidation to restrict damage in human macrophages

doi: 10.1126/sciadv.adt3311

Figure Lengend Snippet: ( A ) GAL8 staining in THP-1 macrophages stably expressing GFP-LC3B after Mtb WT infection (2.5 hpi, MOI: 2) under treatment with BAPTA-AM and EGTA-AM. ( B ) GAL8 and GAL3 staining in THP-1 macrophages after Mtb WT and Mtb ΔRD1 infection (2.5 hpi, MOI: 2) under indicated treatments. ( C ) Percentage of Mtb-LC3-TVS positive for GAL8 related to (A) and fig. S3D. n (number of infected cells) = 51 to 72; data points correspond to individual technical replicates from three independent experiments. ( D ) Percentage of infected cells with Mtb-GAL3 positive, Mtb-GAL8 positive, and Mtb-GAL3/GAL8 double positive compartments. n (number of infected cells) = 96 to 151; data points correspond to individual technical replicates from three independent experiments. ( E ) Percentage of infected cells showing the Mtb-GAL3 positive, Mtb-GAL8 positive, and Mtb-GAL3/GAL8 double positive structures at 2.5, 8, and 24 hpi. n (number of infected cells) = 101 to 151; data points correspond to individual technical replicates from three independent experiments. The datasets for 2.5 hpi matches data from (D). Scale bars, in (A) and (B): 10 μm (main images) and 1 μm (inserted area).

Article Snippet: The antibodies used are as follows: GAL3 (BioLegend, 125410), GAL8 (R&D Systems, AF1305), LC3B (Sigma-Aldrich, L7543), p62 (CST, 88588), ATP6V1D (Abcam, ab157458), and CD63 (Abcam, ab217345).

Techniques: Staining, Stable Transfection, Expressing, Infection

Journal: Science Advances

Article Title: Mycobacterium tuberculosis phagosome Ca 2+ leakage triggers multimembrane ATG8/LC3 lipidation to restrict damage in human macrophages

doi: 10.1126/sciadv.adt3311

Figure Lengend Snippet: ( A ) Mtb infection (MOI: 2) in THP-1 macrophages stably expressing RFP-GFP-LC3B at 2.5 hpi under BafA1 and CQ treatment. ( B ) Percentage of infected cells showing Mtb-LC3-TVS under BafA1 and CQ treatment, related to (A). The dataset for control cells matches data from . Diagram shows endolysosome pH after BafA1and CQ treatment. n (number of infected cells) = 122 to 195; data points correspond to individual technical replicates from three independent experiments. ( C ) GAL8 staining in THP-1 macrophages stably expressing GFP-ATG16L1 at 2.5 hpi during Mtb infection (MOI: 2) under BafA1 treatment. ( D ) Quantification shows the percentage of Mtb-GAL8 positive structures positive for ATG16L1 under BafA1 treatment, related to (C). Diagram shows the function of BafA1 in blocking VATPase-ATG16L1 complex assembly. n (number of infected cells) = 178 and 202; data points correspond to individual technical replicates from 3 independent experiments. ( E ) ATP6V1D staining in THP-1 macrophages stably expressing GFP-ATG16L1 at 2.5 hpi during Mtb WT and Mtb ΔRD1 infection (MOI: 2) under indicated treatments. ( F and G ) Percentage of infected cells showing Mtb-ATP6V1D positive (F) and Mtb-ATG16L1 positive (G) structures under the indicated treatments, related to (E). n (number of infected cells) = 93 to 130; data points correspond to individual technical replicates from three independent experiments. ( H ) GAL8 and ATP6V1D staining in THP-1 macrophages infected with Mtb WT and Mtb ΔRD1 at 2.5 hpi. ( I ) Percentage of Mtb WT– and Mtb ΔRD1–infected cells showing the GAL8– and ATP6V1D–double positive structures, related to (H). n (number of infected cells) = 215 and 175; data points correspond to individual technical replicates from three independent experiments. Scale bars, 10 μm (main images) and 1 μm (inserted area).

Techniques: Infection, Stable Transfection, Expressing, Control, Staining, Blocking Assay

Journal: Science Advances

Article Title: Mycobacterium tuberculosis phagosome Ca 2+ leakage triggers multimembrane ATG8/LC3 lipidation to restrict damage in human macrophages

doi: 10.1126/sciadv.adt3311

Figure Lengend Snippet: ( A ) GAL8 and GAL3 staining in WT and ATG16L1 KO and FIP200 KO THP-1 macrophages after Mtb WT and Mtb ΔRD1 infection (2.5 hpi, MOI: 2). ( B and C ) Percentage of infected cells showing the Mtb-GAL8 positive and Mtb-GAL3 positive structures in WT and ATG7 KO, ATG16L1 KO, ATG13 KO, and FIP200 KO THP-1 macrophages related to (A) and fig. S5A. The datasets for WT cells are same as . n (number of infected cells) = 96 and 174; data points correspond to individual technical replicates from three independent experiments. ( D ) Representative micrographs at indicated time points of ATG16L1 KO and FIP200 KO THP-1 macrophages infected with Mtb WT (red) in the presence of PI+ necrotic cells (yellow). Bright-field images show the localization of macrophages. Data are representative from one of three independent experiments. ( E ) Quantification shows the fold change of Mtb area at 70 hpi with WT Mtb in WT, ATG7 KO, ATG16L1 KO, and FIP200 KO THP-1 macrophages. Data are from three independent biological replicates, each of which represents the mean of three technical replicates. ( F ) Quantification shows the fold change in the number of PI-positive cells 70 hpi with WT Mtb, compared to noninfected cells, in WT, ATG7 KO, ATG16L1 KO, and FIP200 KO THP-1 macrophages. Data are from three independent biological replicates, each of which represents the mean of three technical replicates. Scale bars, in (A): 10 μm; in (D): 50 μm.

Techniques: Staining, Infection

Figure 5. 3CLpro disrupts galectin-8 binding to Spike in antiviral-autophagy (A) Immunoblot of human galectin-8 (Gal8) in BEAS-2B cells in response to IFN-a, IFN-b, or vehicle. One way ANOVA and Dunnett’s posthoc test (mean ± SD, n = 3 each, *** p % 0.001, * p % 0.05). (B) MALDI-TOF-MS of intact versus 3CLpro-cleaved synthetic Gal8 P4–P4’ peptide. (C) SDS-PAGE and Edman sequencing of Gal8 incubated with 3CLpro+/ inhibitor GC376, or 3CLpro C145A (1:5 mol/mol, E:S). (D) Structural model of Gal8 docked onto 3CLpro. 3CLpro cleavage site identiﬁed by the neo-N-terminal peptide (red) in 9/9 independent TAILS analyses. (E) Gal8 immunoblots of lysates from primary HAECs incubated with 3CLpro or 3CLpro-C145A (1:200 w/w, E:S) for 18 h, 37C (N = 5). (F) Gal8 immunoblot of infected Calu-3 cells at 24 (n = 4) and 48 (n = 4) hpi (MOI 1.0, mock n = 3). b-actin and b-tubulin loading controls. (G) ELISA of SARS-CoV-2 Spike S1 protein binding intact Gal8 or 3CLpro-cleaved (DGal8) (mean ± SD, n = 2, N = 2, ****p % 0.0001, **p % 0.01, ns p > 0.05, two- way ANOVA with Sı´da´ k’s multiple comparison test). (legend continued on next page)

Journal: Cell reports

Article Title: Mechanistic insights into COVID-19 by global analysis of the SARS-CoV-2 3CL pro substrate degradome.

doi: 10.1016/j.celrep.2021.109892

Figure Lengend Snippet: Figure 5. 3CLpro disrupts galectin-8 binding to Spike in antiviral-autophagy (A) Immunoblot of human galectin-8 (Gal8) in BEAS-2B cells in response to IFN-a, IFN-b, or vehicle. One way ANOVA and Dunnett’s posthoc test (mean ± SD, n = 3 each, *** p % 0.001, * p % 0.05). (B) MALDI-TOF-MS of intact versus 3CLpro-cleaved synthetic Gal8 P4–P4’ peptide. (C) SDS-PAGE and Edman sequencing of Gal8 incubated with 3CLpro+/ inhibitor GC376, or 3CLpro C145A (1:5 mol/mol, E:S). (D) Structural model of Gal8 docked onto 3CLpro. 3CLpro cleavage site identiﬁed by the neo-N-terminal peptide (red) in 9/9 independent TAILS analyses. (E) Gal8 immunoblots of lysates from primary HAECs incubated with 3CLpro or 3CLpro-C145A (1:200 w/w, E:S) for 18 h, 37C (N = 5). (F) Gal8 immunoblot of infected Calu-3 cells at 24 (n = 4) and 48 (n = 4) hpi (MOI 1.0, mock n = 3). b-actin and b-tubulin loading controls. (G) ELISA of SARS-CoV-2 Spike S1 protein binding intact Gal8 or 3CLpro-cleaved (DGal8) (mean ± SD, n = 2, N = 2, ****p % 0.0001, **p % 0.01, ns p > 0.05, two- way ANOVA with Sı´da´ k’s multiple comparison test). (legend continued on next page)

Article Snippet: The primary antibodies and dilutions used were: mousemonoclonal anti-SARS-CoV-2 nucleocapsid antibody (1:1,000, Invitrogen, MA5-29981, RRID: AB_2785780); rabbit anti-SARS-CoV-1 3CLpro antibody (1:2000, Rockland, 200-401-A51, RRID: AB_828457); rabbit polyclonal anti-RPAP1 antibody (1:1,000, Proteintech, 15138-1-AP, RRID: AB_2301137); mouse monoclonal anti-PTBP1 antibody (1:500, Biolegend, 630101, 3H7, RRID: AB_2171285); rabbit polyclonal anti-MAP4K5 antibody (1:1,000, Cusabio, CSBPA013440DSR2HU, RRID: AB_2892084); rabbit polyclonal anti-CREB1 antibody (1:1,000, Abclonal, A11989, RRID: AB_2758916); rabbit polyclonal anti-YAP1 antibody (1:1,000, Abclonal, A11430, RRID: AB_2758556); rabbit polyclonal anti-FYCO1 antibody (1:1,000, Cusabio, CSB-PA866262LA01HU, RRID: AB_2892085); rabbit polyclonal anti-FAF1 antibody (1:1,000, Abclonal, A2921, RRID: AB_2764739); goat polyclonal anti-Gal8 antibody (1:400, R&D Systems, AF1305, RRID: AB_2137229); rabbit polyclonal anti-KPNA3 (IMA4) antibody (1:1,000, Abclonal, A8347, RRID: AB_2770124); rabbit polyclonal anti-NUP107 antibody (1:1,000, Abclonal, A13110, RRID: AB_2759959); mouse monoclonal anti-IRS2 antibody (1:300, R&D Systems, MAB6347, 676415, RRID: AB_10992928); mouse monoclonal anti-FLAG M2 antibody (1:10,000, Sigma, F3165, RRID: AB_259529); mouse monoclonal antib-tubulin antibody (1:2000, AbLab, 21-0018-00, clone BT7R); mouse monoclonal anti-b-actin antibody (1:1,000, Abcam, ab8226, RRID: AB_306371); rabbit monoclonal anti-b-actin antibody (1:200, Abcam, ab115777, RRID: AB_10899528).

Techniques: Binding Assay, Western Blot, SDS Page, Sequencing, Incubation, Infection, Enzyme-linked Immunosorbent Assay, Protein Binding, Comparison

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