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Novus Biologicals ctr1 antibody
Ctr1 Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/slc31a1+ctr1/SLC31A1%2FCTR1+Antibody+(5E6%2E1B4)+-+BSA+Free/10__1021_slash_cbmi__5c00237-285-0-5
Average 94 stars, based on 5 article reviews

ctr1 antibody - by Bioz Stars, 2026-10

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Article Title: Copper bioavailability is a KRAS-specific vulnerability in colorectal cancer.
Article Snippet: Primary antibodies targeted against Caspase-3 (1:100) and Ki-67 (1:100) are from Biocare Medical; CCS (H-7) (1:50) from Santa Cruz Biotechnology; SLC31A1/CTR1 (NBP100-402) (1:50) from Novus Biologicals; and (P)-ERK1/2 (E10) (1:400) (T202/Y204) from Cell Signaling Technologies.

Article Title: Copper bioavailability is a KRAS-specific vulnerability in colorectal cancer
Article Snippet: Primary antibodies targeted against Caspase-3 (1:100) and Ki-67 (1:100) are from Biocare Medical; CCS (H-7) (1:50) from Santa Cruz Biotechnology; SLC31A1/CTR1 (NBP100-402) (1:50) from Novus Biologicals; and (P)-ERK1/2 (E10) (1:400) (T202/Y204) from Cell Signaling Technologies.

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(a) Overview of the in vivo CRISPR screen. (b) CRISPR screen results. Grey dots represent genes in screen, black dots represent intergenic guideRNAs with linear regression and 99% confidence band overlaid. Red dots highlight notable genes from the screen. Axes represent mean log(2) fold change of the MAGeCK-normalized read counts of guides for each gene, relative to the mean read counts of the intergenic guides. (c) A scheme of the linked functions of SLC31A1, GSR and SDHA. (d) Experimental overview of in vivo competitive mixing experiments to validate single genes from the screen. (e-f) Change in %GFP+ cells compared to input, from mice at clinical endpoint that received intergenic or SLC31A1 -targeting sgRNA cells mixed with control mCherry-expressing cells. Maximal depletion is indicated by a dashed line at −50%. Data are normalized to the mean of the intergenic group, and are from either spleens of mice receiving cells by intravenous injection (e), or from the leptomeninges of mice receiving cells by intracisternal injection (f). Plotted data are mean ± SD, p-values from Šídák's multiple comparisons test. Each dot represents an individual mouse. (g) Kaplan-Meier survival curve of the top and bottom quartiles of patients from the MP2PRT-ALL cohort (n = 1,290 patients in total) or TARGET-ALL-P2 cohort (n = 374 patients in total) with available bone marrow mRNA-sequencing and overall survival (OS) data. Vertical dashes represent censored patients. Patients were sorted by MT1X expression in transcripts per million (TPM), and the survival data of the top (”high”) and bottom quartiles (”low”) were plotted. p-value from log-rank (Mantel-Cox) tests. HR = hazard ratio, FC = fold change, i.v. = intravenous, i.c. = intracisternal, sgRNA = single-guide RNA.

Journal: Nature cancer

Article Title: Copper depletion inhibits electron transport chain activity and nucleotide synthesis to boost leukemia therapy

doi: 10.1038/s43018-026-01177-4

Figure Lengend Snippet: (a) Overview of the in vivo CRISPR screen. (b) CRISPR screen results. Grey dots represent genes in screen, black dots represent intergenic guideRNAs with linear regression and 99% confidence band overlaid. Red dots highlight notable genes from the screen. Axes represent mean log(2) fold change of the MAGeCK-normalized read counts of guides for each gene, relative to the mean read counts of the intergenic guides. (c) A scheme of the linked functions of SLC31A1, GSR and SDHA. (d) Experimental overview of in vivo competitive mixing experiments to validate single genes from the screen. (e-f) Change in %GFP+ cells compared to input, from mice at clinical endpoint that received intergenic or SLC31A1 -targeting sgRNA cells mixed with control mCherry-expressing cells. Maximal depletion is indicated by a dashed line at −50%. Data are normalized to the mean of the intergenic group, and are from either spleens of mice receiving cells by intravenous injection (e), or from the leptomeninges of mice receiving cells by intracisternal injection (f). Plotted data are mean ± SD, p-values from Šídák's multiple comparisons test. Each dot represents an individual mouse. (g) Kaplan-Meier survival curve of the top and bottom quartiles of patients from the MP2PRT-ALL cohort (n = 1,290 patients in total) or TARGET-ALL-P2 cohort (n = 374 patients in total) with available bone marrow mRNA-sequencing and overall survival (OS) data. Vertical dashes represent censored patients. Patients were sorted by MT1X expression in transcripts per million (TPM), and the survival data of the top (”high”) and bottom quartiles (”low”) were plotted. p-value from log-rank (Mantel-Cox) tests. HR = hazard ratio, FC = fold change, i.v. = intravenous, i.c. = intracisternal, sgRNA = single-guide RNA.

Article Snippet: Immunoblotting was performed using the following primary antibodies: For reducing and denaturing western blot: vinculin (CST 13901; 1:2500) Beta actin (CST 8457; 1:2000) GAPDH (CST 2118L; 1:2000) MT-CO1/COX1 (abcam ab14705; 1:2000) COX4I1/COX4 (CST 4850; 1:1000) COX2 (Proteintech 55070–1-AP; 1:5000) DHODH (Santa Cruz E-8 sc-166348; 1:500) SDHA (CST 5839S; 1:1000) SLC31A1 (CST 13086S; 1:500) Beta tubulin (CST 2128P; 1:1000) Human Total OxPhos Cocktail (abcam ab110411; 1:1000) VDAC1/porin (abcam ab154856; 1:1000) Total ERK1/2 (CST 4696S; 1:1000) Phospho-ERK1/2 (CST 4370L; 1:1000) Primary antibodies were diluted in Signal Enhancer HIKARI Solution 1 (Nacalai USA NU00102).

Techniques: In Vivo, CRISPR, Knock-Out, Control, Expressing, Injection, Sequencing

(a-b) Seahorse MitoStress Test on (a) SEM cells or (b) NALM6 cells treated with BCS with or without CuCl 2 . (b) Blue-native (BN-PAGE) followed by western blot detection of COX1 in native complex IV in SEM cells or NALM6 cells treated with vehicle or BCS. Representative data of two biological replicates shown; an additional replicate can be found in Source Data. (c) Seahorse assay to measure OCR in permeabilized SEM or NALM6 cells following treatment with complex IV substrates. (d) Complex IV enzymatic activity in BCS-treated SEM or NALM6 measured colorimetrically by monitoring the oxidation of reduced cytochrome C over time from 5 μg of mitochondrial lysate immunocaptured on microplate wells coated with anti-Complex IV antibodies. (e) Schematic of AOX rescue of copper depletion by SLC31A1-KO or BCS treatment. (f) Relative cell number after four days of control or SLC31A1-KO SEM cells overexpressing RFP or AOX. n = 4 experimental repeats, each dot represents the mean of three technical replicates. (g) Doublings per day from days 5–11 (SEM and NALM6) or days 2–8 (MOLT16) of BCS treatment in the indicated cell lines overexpressing RFP or AOX. n = 3 biological replicates, doubling rate calculated as linear regression of growth over 2 passages. SEM cells were treated with BCS for 8 days and NALM6 cells were treated for 6 days prior to the indicated mitochondrial or Seahorse assays. For Seahorse assays, plotted data are mean±SD with 4–6 technical replicates (wells). BCS and CuCl 2 were used at 50 μM. All p-values from Šídák's multiple comparisons test. Other plotted values are mean±SD. BCS = bathocuproinedisulfonic acid, oligo = oligomycin, AA = antimycin A, rot = rotenone, FCCP = carbonyl cyanide-p-trifluoromethoxyphenylhydrazone, perm = XF Plasma Membrane Permeabilizer, ADP = adenosine diphosphate, TMPD = N,N,N,N-tetramethyl-p-phenylenediamine, asc = ascorbate, OD = optical density.

Journal: Nature cancer

Article Title: Copper depletion inhibits electron transport chain activity and nucleotide synthesis to boost leukemia therapy

doi: 10.1038/s43018-026-01177-4

Figure Lengend Snippet: (a-b) Seahorse MitoStress Test on (a) SEM cells or (b) NALM6 cells treated with BCS with or without CuCl 2 . (b) Blue-native (BN-PAGE) followed by western blot detection of COX1 in native complex IV in SEM cells or NALM6 cells treated with vehicle or BCS. Representative data of two biological replicates shown; an additional replicate can be found in Source Data. (c) Seahorse assay to measure OCR in permeabilized SEM or NALM6 cells following treatment with complex IV substrates. (d) Complex IV enzymatic activity in BCS-treated SEM or NALM6 measured colorimetrically by monitoring the oxidation of reduced cytochrome C over time from 5 μg of mitochondrial lysate immunocaptured on microplate wells coated with anti-Complex IV antibodies. (e) Schematic of AOX rescue of copper depletion by SLC31A1-KO or BCS treatment. (f) Relative cell number after four days of control or SLC31A1-KO SEM cells overexpressing RFP or AOX. n = 4 experimental repeats, each dot represents the mean of three technical replicates. (g) Doublings per day from days 5–11 (SEM and NALM6) or days 2–8 (MOLT16) of BCS treatment in the indicated cell lines overexpressing RFP or AOX. n = 3 biological replicates, doubling rate calculated as linear regression of growth over 2 passages. SEM cells were treated with BCS for 8 days and NALM6 cells were treated for 6 days prior to the indicated mitochondrial or Seahorse assays. For Seahorse assays, plotted data are mean±SD with 4–6 technical replicates (wells). BCS and CuCl 2 were used at 50 μM. All p-values from Šídák's multiple comparisons test. Other plotted values are mean±SD. BCS = bathocuproinedisulfonic acid, oligo = oligomycin, AA = antimycin A, rot = rotenone, FCCP = carbonyl cyanide-p-trifluoromethoxyphenylhydrazone, perm = XF Plasma Membrane Permeabilizer, ADP = adenosine diphosphate, TMPD = N,N,N,N-tetramethyl-p-phenylenediamine, asc = ascorbate, OD = optical density.

Techniques: Inhibition, Western Blot, Activity Assay, Control, Clinical Proteomics, Membrane

$(a) Volcano plot of changing metabolites between in day 14 BCS-treated SEM cells. n = 3 biological replicates. (b) Aspartate, carbamoyl aspartic acid (CAA) and dihydroorotate (DHO) levels in BCS or CuCl 2 treated SEM cells. (c) Nucleotide levels in BCS or CuCl 2 treated SEM cells. (d) Volcano plot depicting day 6 metabolite changes between BCS-treated and vehicle-treated NALM6 cells. n = 3 biological replicates. (e) Aspartate, carbamoyl aspartic acid (CAA) and dihydroorotate (DHO) levels in BCS or CuCl2 treated NALM6 cells. (f) Nucleotide levels in BCS or CuCl 2 treated NALM6 cells. (g) Isotopic labelling scheme of tracing 15 N-amide glutamine into pyrimidine synthesis and showing steps that can be inhibited by copper depletion. (h-i) Fractional labelling of metabolites in BCS and/or CuCl 2 treated SEM, NALM6 (h), and SEM, NALM6, and MOLT16 (i) cells pulsed for 4 hours with 15 N-amide glutamine. Labelling is expressed as a fraction of total unlabeled abundances measured in a parallel experiment for (h) DHO, and (i) CTP. n = 3 biological replicates. Cells were treated with BCS for: 14 days (SEM), 6 days (NALM6) or 8 days (MOLT16). (j) Scheme showing contribution of pyruvate and uridine to metabolic rescue following copper depletion. (k) Relative cell number after four days of control or SLC31A1-KO cells treated with vehicle or combination of pyruvate and uridine. n = 5–6 experimental replicates. (l) Doublings per day from days 6–10 (SEM cells) or 5–9 (NALM6 and MOLT16 cells) of BCS treatment and either vehicle or pyruvate and uridine. n = 3 biological replicates. Plotted data are mean ± SD, p-values from: (a, d) FDR-adjusted t-tests from MetaboAnalyst, (b, e, k, l) Šídák's multiple comparisons test, or (h, i) Tukey’s multiple comparison test. Cells were treated with uridine (400 μM), pyruvate (1 mM), BCS (50 μM) and CuCl 2 (50 μM). BCS = bathocuproinedisulfonic acid, CAA = carbamoyl aspartic acid, DHO = dihydroorotate, FC = fold change, CTP = cytidine triphosphate, OAA = oxaloacetate.$

Journal: Nature cancer

Article Title: Copper depletion inhibits electron transport chain activity and nucleotide synthesis to boost leukemia therapy

doi: 10.1038/s43018-026-01177-4

Figure Lengend Snippet: (a) Volcano plot of changing metabolites between in day 14 BCS-treated SEM cells. n = 3 biological replicates. (b) Aspartate, carbamoyl aspartic acid (CAA) and dihydroorotate (DHO) levels in BCS or CuCl 2 treated SEM cells. (c) Nucleotide levels in BCS or CuCl 2 treated SEM cells. (d) Volcano plot depicting day 6 metabolite changes between BCS-treated and vehicle-treated NALM6 cells. n = 3 biological replicates. (e) Aspartate, carbamoyl aspartic acid (CAA) and dihydroorotate (DHO) levels in BCS or CuCl2 treated NALM6 cells. (f) Nucleotide levels in BCS or CuCl 2 treated NALM6 cells. (g) Isotopic labelling scheme of tracing 15 N-amide glutamine into pyrimidine synthesis and showing steps that can be inhibited by copper depletion. (h-i) Fractional labelling of metabolites in BCS and/or CuCl 2 treated SEM, NALM6 (h), and SEM, NALM6, and MOLT16 (i) cells pulsed for 4 hours with 15 N-amide glutamine. Labelling is expressed as a fraction of total unlabeled abundances measured in a parallel experiment for (h) DHO, and (i) CTP. n = 3 biological replicates. Cells were treated with BCS for: 14 days (SEM), 6 days (NALM6) or 8 days (MOLT16). (j) Scheme showing contribution of pyruvate and uridine to metabolic rescue following copper depletion. (k) Relative cell number after four days of control or SLC31A1-KO cells treated with vehicle or combination of pyruvate and uridine. n = 5–6 experimental replicates. (l) Doublings per day from days 6–10 (SEM cells) or 5–9 (NALM6 and MOLT16 cells) of BCS treatment and either vehicle or pyruvate and uridine. n = 3 biological replicates. Plotted data are mean ± SD, p-values from: (a, d) FDR-adjusted t-tests from MetaboAnalyst, (b, e, k, l) Šídák's multiple comparisons test, or (h, i) Tukey’s multiple comparison test. Cells were treated with uridine (400 μM), pyruvate (1 mM), BCS (50 μM) and CuCl 2 (50 μM). BCS = bathocuproinedisulfonic acid, CAA = carbamoyl aspartic acid, DHO = dihydroorotate, FC = fold change, CTP = cytidine triphosphate, OAA = oxaloacetate.

Techniques: Inhibition, Isotopic Labeling, Control, Comparison

(a) Total copper levels in the plasma and cerebrospinal fluid (CSF) of untreated NOD-SCID mice as measured by inductively-coupled plasma mass spectrometry (ICP-MS). (b) flow cytometric assessment of SLC31A1 expression using indirect antibody staining in live SEM cells with knockout of SLC31A1 with GFP or CRISPR-resistant SLC31A1 rescue. (c) Western blot validation of SLC31A1 knockout. (d) Representative bioluminescent imaging (BLI) of mice 3 weeks after receiving luciferase-expressing SEM cells by either intravenous or intracisternal injection. (e) Hematoxylin and eosin staining of sections from skulls, spleens and femurs of terminal mice receiving luciferase-expressing SEM cells by intravenous or intracisternal injection. Scale bar for whole-skull images are 1cm, all other scale bars (including skull inset images) are 100 micrometers. Orange rectangles denote inset of skull images. (f) Change in %GFP+ cells compared to input, from CNS of mice at clinical endpoint that received intergenic or SLC31A1-KO sgRNA cells mixed with control mCherry-expressing cells by intravenous injection. Data are normalized to the mean of the intergenic group. (g) Quantitative real-time polymerase chain reaction (qRT-PCR) measurement of SLC31A1 mRNA knockdown following doxycycline-inducible sgRNA expression. mRNA was collected from cells after 9 days of doxycycline induction. Each group is normalized to the -doxycycline condition. (h) Experimental setup of in vivo mixing experiment in which doxycycline was administered via the drinking water starting at day 5 post engraftment. (i-j) Change in %GFP+ cells compared to input, from mice at clinical endpoint that received intergenic or SLC31A1-KO sgRNA cells mixed with control mCherry-expressing cells. Data are normalized to the mean of the intergenic group and are from the (i) spleen or (j) CNS of mice receiving cells by intravenous injection. Plotted data are mean ± SD. p-values from Šídák's multiple comparisons test. Each dot in bar graphs represents a biological replicate or mouse.

Journal: Nature cancer

Article Title: Copper depletion inhibits electron transport chain activity and nucleotide synthesis to boost leukemia therapy

doi: 10.1038/s43018-026-01177-4

Figure Lengend Snippet: (a) Total copper levels in the plasma and cerebrospinal fluid (CSF) of untreated NOD-SCID mice as measured by inductively-coupled plasma mass spectrometry (ICP-MS). (b) flow cytometric assessment of SLC31A1 expression using indirect antibody staining in live SEM cells with knockout of SLC31A1 with GFP or CRISPR-resistant SLC31A1 rescue. (c) Western blot validation of SLC31A1 knockout. (d) Representative bioluminescent imaging (BLI) of mice 3 weeks after receiving luciferase-expressing SEM cells by either intravenous or intracisternal injection. (e) Hematoxylin and eosin staining of sections from skulls, spleens and femurs of terminal mice receiving luciferase-expressing SEM cells by intravenous or intracisternal injection. Scale bar for whole-skull images are 1cm, all other scale bars (including skull inset images) are 100 micrometers. Orange rectangles denote inset of skull images. (f) Change in %GFP+ cells compared to input, from CNS of mice at clinical endpoint that received intergenic or SLC31A1-KO sgRNA cells mixed with control mCherry-expressing cells by intravenous injection. Data are normalized to the mean of the intergenic group. (g) Quantitative real-time polymerase chain reaction (qRT-PCR) measurement of SLC31A1 mRNA knockdown following doxycycline-inducible sgRNA expression. mRNA was collected from cells after 9 days of doxycycline induction. Each group is normalized to the -doxycycline condition. (h) Experimental setup of in vivo mixing experiment in which doxycycline was administered via the drinking water starting at day 5 post engraftment. (i-j) Change in %GFP+ cells compared to input, from mice at clinical endpoint that received intergenic or SLC31A1-KO sgRNA cells mixed with control mCherry-expressing cells. Data are normalized to the mean of the intergenic group and are from the (i) spleen or (j) CNS of mice receiving cells by intravenous injection. Plotted data are mean ± SD. p-values from Šídák's multiple comparisons test. Each dot in bar graphs represents a biological replicate or mouse.

Techniques: Knock-Out, In Vivo, Clinical Proteomics, Mass Spectrometry, Expressing, Staining, CRISPR, Western Blot, Biomarker Discovery, Imaging, Luciferase, Injection, H&E Stain, Control, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Knockdown

(a) qRT-PCR measurement of SLC31A1 or ATP7A mRNA levels in 8-day BCS or CuCl 2 treated SEM cells relative to vehicle treated cells. n=3 biological replicates. (b-g) Kaplan-Meier survival curves of patients from MPT2PRT-ALL or TARGET-ALL-P2 cohorts with available bone marrow mRNA-sequencing and overall survival (OS) data, vertical dashes represent censored patients. Patients were sorted by (b, e) ATP7A , (c ,f) SLC31A1 , or (d, g) log( SLC31A1/ATP7A ) expression in transcripts per million (TPM), and the survival data of the top (”high”) and bottom quartiles (”low”) were plotted. (h) qRT-PCR measurement of MT1X mRNA levels in 8-day BCS or CuCl 2 treated SEM cells relative to vehicle treated cells. n=3 biological replicates. (i-j) Kaplan-Meier survival curves of patients from (i) MPT2PRT-ALL or (j) TARGET-ALL-P2 cohorts sorted by COX17 expression with the top and bottom quartiles plotted. p-values from log-rank (Mantel-Cox) tests or (h) Dunnett’s multiple comparisons test.

Journal: Nature cancer

Article Title: Copper depletion inhibits electron transport chain activity and nucleotide synthesis to boost leukemia therapy

doi: 10.1038/s43018-026-01177-4

Figure Lengend Snippet: (a) qRT-PCR measurement of SLC31A1 or ATP7A mRNA levels in 8-day BCS or CuCl 2 treated SEM cells relative to vehicle treated cells. n=3 biological replicates. (b-g) Kaplan-Meier survival curves of patients from MPT2PRT-ALL or TARGET-ALL-P2 cohorts with available bone marrow mRNA-sequencing and overall survival (OS) data, vertical dashes represent censored patients. Patients were sorted by (b, e) ATP7A , (c ,f) SLC31A1 , or (d, g) log( SLC31A1/ATP7A ) expression in transcripts per million (TPM), and the survival data of the top (”high”) and bottom quartiles (”low”) were plotted. (h) qRT-PCR measurement of MT1X mRNA levels in 8-day BCS or CuCl 2 treated SEM cells relative to vehicle treated cells. n=3 biological replicates. (i-j) Kaplan-Meier survival curves of patients from (i) MPT2PRT-ALL or (j) TARGET-ALL-P2 cohorts sorted by COX17 expression with the top and bottom quartiles plotted. p-values from log-rank (Mantel-Cox) tests or (h) Dunnett’s multiple comparisons test.

Techniques: Analysis, Gene Expression, Quantitative RT-PCR, Sequencing, Expressing

(a) A scheme illustrating primary intracellular functions of copper ions. (b-c) NADP, NADPH levels and NADP/NADPH ratio, as well as oxidized and reduced glutathione levels as determined by LC-MS targetted metabolite profiling in (b) SLC31A1-KO SEM cells with or without genetic rescue, or (c) BCS-treated SEM cells (day 14), NALM6 (day 6), REH (day 8) or MOLT16 (day 8) with or without CuCl 2 rescue. Levels of reduced glutathione were determined by derivatization with Ellman’s reagent (see Supplementary Methods ). (d-e) Western blotting for total and phospho (p-)ERK1/2 levels in (d) SLC31A1-KO or (e) BCS treated SEM, NALM6, REH or MOLT16 cells. (f) Doublings per day normalized to vehicle-treated cells after either 4 days (NALM6) or 6 days of BCS treatment (SEM, REH, MOLT16, MOLT4, PF382). Doubling rate was calculated by taking the linear regression of cell number across at least 2 passages over 4 days. (g) MitoStress Seahorse Assay for indicated cell lines treated with BCS and/or CuCl 2 after 10 days of treatment. For Seahorse assays, plotted data are mean ± SD with 4–6 technical replicates (wells). All other plotted data are mean ± SD, p-values from Šídák's multiple comparisons test. Each dot represents a biological replicate. OE = overexpression, sgRNA = single guide RNA, oligo = oligomycin, AA = antimycin A, Rot = rotenone, FCCP = carbonyl cyanide-p-trifluoromethoxyphenylhydrazone.

Journal: Nature cancer

Article Title: Copper depletion inhibits electron transport chain activity and nucleotide synthesis to boost leukemia therapy

doi: 10.1038/s43018-026-01177-4

Figure Lengend Snippet: (a) A scheme illustrating primary intracellular functions of copper ions. (b-c) NADP, NADPH levels and NADP/NADPH ratio, as well as oxidized and reduced glutathione levels as determined by LC-MS targetted metabolite profiling in (b) SLC31A1-KO SEM cells with or without genetic rescue, or (c) BCS-treated SEM cells (day 14), NALM6 (day 6), REH (day 8) or MOLT16 (day 8) with or without CuCl 2 rescue. Levels of reduced glutathione were determined by derivatization with Ellman’s reagent (see Supplementary Methods ). (d-e) Western blotting for total and phospho (p-)ERK1/2 levels in (d) SLC31A1-KO or (e) BCS treated SEM, NALM6, REH or MOLT16 cells. (f) Doublings per day normalized to vehicle-treated cells after either 4 days (NALM6) or 6 days of BCS treatment (SEM, REH, MOLT16, MOLT4, PF382). Doubling rate was calculated by taking the linear regression of cell number across at least 2 passages over 4 days. (g) MitoStress Seahorse Assay for indicated cell lines treated with BCS and/or CuCl 2 after 10 days of treatment. For Seahorse assays, plotted data are mean ± SD with 4–6 technical replicates (wells). All other plotted data are mean ± SD, p-values from Šídák's multiple comparisons test. Each dot represents a biological replicate. OE = overexpression, sgRNA = single guide RNA, oligo = oligomycin, AA = antimycin A, Rot = rotenone, FCCP = carbonyl cyanide-p-trifluoromethoxyphenylhydrazone.

Techniques: In Vitro, Liquid Chromatography with Mass Spectroscopy, Profiling, Derivatization, Western Blot, Over Expression

(a) Western blot for COX2, COX1 and COX4 in BCS-treated SEM (day 8), NALM6 (day 6) and MOLT16 (day 8) cells. (b) Blue-native (BN-PAGE) followed by western blot detection of indicated subunits in native complex I-III in BCS treated SEM cells (day 8) or NALM6 cells (day 6). Representative data of two biological replicates shown. Additional replicate shown in Source Data. (c-d) Levels of NAD, NADH and the NAD/NADH ratio were determined by LC-MS targeted metabolite profiling in (c) SLC31A1-KO SEM cells or (d) BCS treated SEM (day 8), NALM6 (day 6) and MOLT16 (day 8) cells. (e) Levels of succinate, fumarate, and succinate/fumarate ratio in BCS treated SEM and NALM6 cells as determined by targeted LC-MS metabolite profiling. (f-g) Seahorse assay to measure OCR in permeabilized BCS-treated (f) SEM (day 8) or (g) NALM6 (day 6) cells following treatment with complex I or II substrates. (h-i) MitoStress Seahorse assay performed on SLC31A1-KO SEM cells with (h) eGFP or SLC31A1 rescue, or (i) 100 μM CuCl 2 pre-treatment for 24 hours. For Seahorse assays, plotted data are mean ± SD with 4–6 technical replicates (wells). Other plotted data are mean±SD, p-values from Šídák's multiple comparisons test. Each dot represents a biological replicate. BCS and CuCl 2 were used at 50 μM. OE = overexpression, BCS = bathocuproinedisulfonic acid, oligo = oligomycin, AA = antimycin A, rot = rotenone, FCCP = carbonyl cyanide-p-trifluoromethoxyphenylhydrazone, perm = XF Plasma Membrane Permeabilizer, pyr/mal = pyruvate and malate, succ = succinate.

Journal: Nature cancer

Article Title: Copper depletion inhibits electron transport chain activity and nucleotide synthesis to boost leukemia therapy

doi: 10.1038/s43018-026-01177-4

Figure Lengend Snippet: (a) Western blot for COX2, COX1 and COX4 in BCS-treated SEM (day 8), NALM6 (day 6) and MOLT16 (day 8) cells. (b) Blue-native (BN-PAGE) followed by western blot detection of indicated subunits in native complex I-III in BCS treated SEM cells (day 8) or NALM6 cells (day 6). Representative data of two biological replicates shown. Additional replicate shown in Source Data. (c-d) Levels of NAD, NADH and the NAD/NADH ratio were determined by LC-MS targeted metabolite profiling in (c) SLC31A1-KO SEM cells or (d) BCS treated SEM (day 8), NALM6 (day 6) and MOLT16 (day 8) cells. (e) Levels of succinate, fumarate, and succinate/fumarate ratio in BCS treated SEM and NALM6 cells as determined by targeted LC-MS metabolite profiling. (f-g) Seahorse assay to measure OCR in permeabilized BCS-treated (f) SEM (day 8) or (g) NALM6 (day 6) cells following treatment with complex I or II substrates. (h-i) MitoStress Seahorse assay performed on SLC31A1-KO SEM cells with (h) eGFP or SLC31A1 rescue, or (i) 100 μM CuCl 2 pre-treatment for 24 hours. For Seahorse assays, plotted data are mean ± SD with 4–6 technical replicates (wells). Other plotted data are mean±SD, p-values from Šídák's multiple comparisons test. Each dot represents a biological replicate. BCS and CuCl 2 were used at 50 μM. OE = overexpression, BCS = bathocuproinedisulfonic acid, oligo = oligomycin, AA = antimycin A, rot = rotenone, FCCP = carbonyl cyanide-p-trifluoromethoxyphenylhydrazone, perm = XF Plasma Membrane Permeabilizer, pyr/mal = pyruvate and malate, succ = succinate.

Techniques: Activity Assay, Western Blot, Liquid Chromatography with Mass Spectroscopy, Profiling, Over Expression, Clinical Proteomics, Membrane

(a) Relative cell number of SEM, NALM6 or MOLT16 cells expressing RFP or AOX and treated with vehicle or Antimycin A (5 nM) for 3 days. (c-c) Seahorse MitoStress Assay on (b) 6-day BCS-treated SEM cells overexpressing RFP or AOX, or (c) SLC31A1-KO SEM cells overexpressing RFP or AOX. Plotted data are mean ± SD with 5 technical replicates (wells) for Seahorse Assays. (d-e) Levels of NAD, NADH and NAD/NADH ratio were determined by LC-MS targeted metabolite profiling in (d) SLC31A1-KO SEM cells over expressing RFP or AOX, or (e) day 8 BCS-treated SEM cells over expressing RFP or AOX. (f) Flow cytometry histograms to measure mitochondrial mass (MitoSpy Green FM) and mitochondrial membrane potential (TMRM) in BCS-treated SEM (day 8), NALM6 (day 6), and MOLT16 (day 8) cells. Bar graphs depict the median TMRM/MitoSpy ratio for all recorded events. Cells were also gated for live cells using the Near IR Fixable LIVE/DEAD stain measured on the APC-Cy7 channel (APC-Cy7 negative). (g) Doublings per day from day 5–11 of BCS-treated AOX-overexpressing SEM or NALM6 cells also treated with MnTE-2-PyP (20 μM) or MnTBAP (50 μM). (h) Relative cell number of SEM, NALM6, or MOLT16 cells expressing RFP or NDI1 and treated with vehicle or Antimycin A (5 nM) for 3 days. (i) Doublings per day from day 5–11 of BCS treatment of SEM, NALM6, or MOLT16 cells overexpressing RFP or NDI1. Plotted data are mean±SD, p-values from Šídák's multiple comparisons test. Each dot represents a biological replicate. oligo = oligomycin, AA = antimycin A, Rot = rotenone, FCCP = = carbonyl cyanide-p-trifluoromethoxyphenylhydrazone, MnTE-2-PyP = manganese (III) meso-tetrakis (N-ethylpyridinium-2-yl) porphyrin, MnTBAP = manganese (III) tetrakis(4-benzoic acid) porphyrin chloride, AOX = alternative oxidase from Ciona intestinalis, NDI1 = yeast NADH-ubiquinone reductase.

Journal: Nature cancer

Article Title: Copper depletion inhibits electron transport chain activity and nucleotide synthesis to boost leukemia therapy

doi: 10.1038/s43018-026-01177-4

Figure Lengend Snippet: (a) Relative cell number of SEM, NALM6 or MOLT16 cells expressing RFP or AOX and treated with vehicle or Antimycin A (5 nM) for 3 days. (c-c) Seahorse MitoStress Assay on (b) 6-day BCS-treated SEM cells overexpressing RFP or AOX, or (c) SLC31A1-KO SEM cells overexpressing RFP or AOX. Plotted data are mean ± SD with 5 technical replicates (wells) for Seahorse Assays. (d-e) Levels of NAD, NADH and NAD/NADH ratio were determined by LC-MS targeted metabolite profiling in (d) SLC31A1-KO SEM cells over expressing RFP or AOX, or (e) day 8 BCS-treated SEM cells over expressing RFP or AOX. (f) Flow cytometry histograms to measure mitochondrial mass (MitoSpy Green FM) and mitochondrial membrane potential (TMRM) in BCS-treated SEM (day 8), NALM6 (day 6), and MOLT16 (day 8) cells. Bar graphs depict the median TMRM/MitoSpy ratio for all recorded events. Cells were also gated for live cells using the Near IR Fixable LIVE/DEAD stain measured on the APC-Cy7 channel (APC-Cy7 negative). (g) Doublings per day from day 5–11 of BCS-treated AOX-overexpressing SEM or NALM6 cells also treated with MnTE-2-PyP (20 μM) or MnTBAP (50 μM). (h) Relative cell number of SEM, NALM6, or MOLT16 cells expressing RFP or NDI1 and treated with vehicle or Antimycin A (5 nM) for 3 days. (i) Doublings per day from day 5–11 of BCS treatment of SEM, NALM6, or MOLT16 cells overexpressing RFP or NDI1. Plotted data are mean±SD, p-values from Šídák's multiple comparisons test. Each dot represents a biological replicate. oligo = oligomycin, AA = antimycin A, Rot = rotenone, FCCP = = carbonyl cyanide-p-trifluoromethoxyphenylhydrazone, MnTE-2-PyP = manganese (III) meso-tetrakis (N-ethylpyridinium-2-yl) porphyrin, MnTBAP = manganese (III) tetrakis(4-benzoic acid) porphyrin chloride, AOX = alternative oxidase from Ciona intestinalis, NDI1 = yeast NADH-ubiquinone reductase.

Techniques: Activity Assay, Over Expression, Expressing, Liquid Chromatography with Mass Spectroscopy, Profiling, Flow Cytometry, Membrane, Staining, Yeast

(a) Volcano plot of changing metabolites between SLC31A1-KO SEM cells and control cells. n = 3 biological replicates. (b) Aspartate and dihydroorotate (DHO) levels at baseline in SLC31A1-KO or control SEM cells with eGFP or SLC31A1 rescue. (c) Nucleotide levels in SLC31A1-KO SEM cells with eGFP or SLC31A1 rescue. (d) Volcano plot of changing metabolites between day 8 BCS-treated MOLT16 cells and control cells. n = 3 biological replicates. (e-f) Aspartate and (f) nucleotide levels in day 8 BCS-treated MOLT16 cells. (g-h) Volcano plot of significantly changing metabolites between day 14 BCS-treated (g) or SLC31A1-KO (h) SEM cells, with amino acids highlighted in pink. n = 3 biological replicates. (i) Western blot for DHODH levels in BCS-treated SEM (day 8), NALM6 (day 6) and MOLT16 cells (day 8); each lane represents an independent biological replicate. Actin is a loading control. . (j) Nucleotide levels in AOX-overexpressing SEM cells treated with BCS for 8 days. (k-l) Levels of aspartate, DHO, and IMP in (k) 14-day BCS-treated SEM cells overexpressing RFP or AOX, (l) or SLC31A1-KO SEM cells overexpressing RFP or AOX. DHO = dihydroorotate, CAA = carbamoyl aspartic acid, AOX = alternative oxidase, IMP = inosine monophosphate. Plotted data are mean ± SD. p-values from Šídák's multiple comparisons test.

Journal: Nature cancer

Article Title: Copper depletion inhibits electron transport chain activity and nucleotide synthesis to boost leukemia therapy

doi: 10.1038/s43018-026-01177-4

Figure Lengend Snippet: (a) Volcano plot of changing metabolites between SLC31A1-KO SEM cells and control cells. n = 3 biological replicates. (b) Aspartate and dihydroorotate (DHO) levels at baseline in SLC31A1-KO or control SEM cells with eGFP or SLC31A1 rescue. (c) Nucleotide levels in SLC31A1-KO SEM cells with eGFP or SLC31A1 rescue. (d) Volcano plot of changing metabolites between day 8 BCS-treated MOLT16 cells and control cells. n = 3 biological replicates. (e-f) Aspartate and (f) nucleotide levels in day 8 BCS-treated MOLT16 cells. (g-h) Volcano plot of significantly changing metabolites between day 14 BCS-treated (g) or SLC31A1-KO (h) SEM cells, with amino acids highlighted in pink. n = 3 biological replicates. (i) Western blot for DHODH levels in BCS-treated SEM (day 8), NALM6 (day 6) and MOLT16 cells (day 8); each lane represents an independent biological replicate. Actin is a loading control. . (j) Nucleotide levels in AOX-overexpressing SEM cells treated with BCS for 8 days. (k-l) Levels of aspartate, DHO, and IMP in (k) 14-day BCS-treated SEM cells overexpressing RFP or AOX, (l) or SLC31A1-KO SEM cells overexpressing RFP or AOX. DHO = dihydroorotate, CAA = carbamoyl aspartic acid, AOX = alternative oxidase, IMP = inosine monophosphate. Plotted data are mean ± SD. p-values from Šídák's multiple comparisons test.

Techniques: Control, Western Blot

(a) Cell number after 4 days of growth for SLC31A1-KO cells treated with pyruvate and/or uridine relative to vehicle-treated intergenic sgRNA-containing cells, all seeded at 0.1 million/mL. (b) Nucleotide levels in SEM cells treated with BCS and/or pyruvate and uridine for 8 days. (c-d) Whole cell NAD, NADH and NADH ratios in (c) SLC31A1-KO SEM cells with or without pyruvate and uridine treatment, or (d) 14-day BCS-treated SEM cells with or without concurrent pyruvate and uridine treatment. (e) Doublings per day from days 5–11 (SEM and NALM6) or days 2–8 (MOLT16) of cells treated with BCS and/or uridine and inosine (100 μM each). Doubling rate was calculated from the linear regression of cell number across at least 2 passages. (f) Levels of dihydroorotate (DHO), aspartate, or the NAD/NADH ratio in SEM and NALM6 cells after 8 days of treatment with BCS and/or inosine and uridine (Ino/Urid) relative to vehicle treated cells. CAA = carbamoyl aspartic acid. Plotted data are mean ± SD, p-values from Šídák's multiple comparisons test. Each dot represents a biological replicate.

Journal: Nature cancer

Article Title: Copper depletion inhibits electron transport chain activity and nucleotide synthesis to boost leukemia therapy

doi: 10.1038/s43018-026-01177-4

Figure Lengend Snippet: (a) Cell number after 4 days of growth for SLC31A1-KO cells treated with pyruvate and/or uridine relative to vehicle-treated intergenic sgRNA-containing cells, all seeded at 0.1 million/mL. (b) Nucleotide levels in SEM cells treated with BCS and/or pyruvate and uridine for 8 days. (c-d) Whole cell NAD, NADH and NADH ratios in (c) SLC31A1-KO SEM cells with or without pyruvate and uridine treatment, or (d) 14-day BCS-treated SEM cells with or without concurrent pyruvate and uridine treatment. (e) Doublings per day from days 5–11 (SEM and NALM6) or days 2–8 (MOLT16) of cells treated with BCS and/or uridine and inosine (100 μM each). Doubling rate was calculated from the linear regression of cell number across at least 2 passages. (f) Levels of dihydroorotate (DHO), aspartate, or the NAD/NADH ratio in SEM and NALM6 cells after 8 days of treatment with BCS and/or inosine and uridine (Ino/Urid) relative to vehicle treated cells. CAA = carbamoyl aspartic acid. Plotted data are mean ± SD, p-values from Šídák's multiple comparisons test. Each dot represents a biological replicate.

Techniques:

$(a) Experimental setup for copper depletion in leukemic mice. BLI = bioluminescent imaging. i.v. = intravenous, (b) Total photon flux from BLI at indicated timepoints expressed as fold change compared to day 14. n = 5 (CuR) or 6 (CuD). Plotted values represent mean +/− SEM. Representative BLI images shown on the right. (c) Principal component analysis (PCA) plot of targeted LC-MS metabolomics data of SEM cells. Cells were treated with 50 μM BCS for 8 days, 6-mercaptopurine (6-MP, 500 nM) for 24 hours, and/or methotrexate (MTX, 5 nM) for 24 hours. (d) Relative abundances of AICAR in MTX and BCS treated SEM and NALM6 cells, related to panel (c). (e) Dose-responsive curves of either SLC31A1-KO SEM cells or 8-day BCS-treated SEM cells treated with MTX for 3 days. Cells were plated in 96-well plates at a density of 0.25 million/mL. Relative luminescence was measured as a proxy for cell number using CellTiter-Glo. (f) Spleen weights at day 30 of mice from Main Figure 4c as a percentage of total body weight. (g-h) Quantification of mean intensity value for COX IV staining per whole image using ZEN for mouse (g) femurs and (h) spleens. 4–6 images were quantified per tissue per mouse. For femurs, n = 41 and 28 total images and for spleens, n = 41 and 31 images were quantified respectively. Lines indicate quartiles and median. (i) Example of per-cell quantification of COX IV staining intensity. Numbers in red indicate mean intensity value as reported from ZEN. All scale bars are 20 micrometers. (j) Relative unlabelled UTP and CTP levels in SEM leukemia cells harvested by MACS from the spleens of CuR+Vehicle or CuD+ZnAc treated mice. (k) m+1 13 C-labelled fraction of serine as measured from SEM leukemia cells harvested from the CNS or spleens of mice by MACS. (l) Ellman’s-derivatized glutathione (GSH) levels in SEM leukemia cells harvested from CNS or spleen. (m) Spleen weights from the endpoint of mice engrafted with PDX CBAB-62871 at week 7, related to Fig 5m - n . CuR = copper replete diet, CuD = copper depleted diet, AICAR = 5-aminoimidazole-4-carboxamide ribonucleotide, MACS = magnet-activated cell sorting. Plotted values are mean+/−SD unless otherwise specified. n.s. = not significant. p-values from Tukey’s multiple comparison tests (b and d), or unpaired t-tests (f-h, j-m).$

Journal: Nature cancer

Article Title: Copper depletion inhibits electron transport chain activity and nucleotide synthesis to boost leukemia therapy

doi: 10.1038/s43018-026-01177-4

Figure Lengend Snippet: (a) Experimental setup for copper depletion in leukemic mice. BLI = bioluminescent imaging. i.v. = intravenous, (b) Total photon flux from BLI at indicated timepoints expressed as fold change compared to day 14. n = 5 (CuR) or 6 (CuD). Plotted values represent mean +/− SEM. Representative BLI images shown on the right. (c) Principal component analysis (PCA) plot of targeted LC-MS metabolomics data of SEM cells. Cells were treated with 50 μM BCS for 8 days, 6-mercaptopurine (6-MP, 500 nM) for 24 hours, and/or methotrexate (MTX, 5 nM) for 24 hours. (d) Relative abundances of AICAR in MTX and BCS treated SEM and NALM6 cells, related to panel (c). (e) Dose-responsive curves of either SLC31A1-KO SEM cells or 8-day BCS-treated SEM cells treated with MTX for 3 days. Cells were plated in 96-well plates at a density of 0.25 million/mL. Relative luminescence was measured as a proxy for cell number using CellTiter-Glo. (f) Spleen weights at day 30 of mice from Main Figure 4c as a percentage of total body weight. (g-h) Quantification of mean intensity value for COX IV staining per whole image using ZEN for mouse (g) femurs and (h) spleens. 4–6 images were quantified per tissue per mouse. For femurs, n = 41 and 28 total images and for spleens, n = 41 and 31 images were quantified respectively. Lines indicate quartiles and median. (i) Example of per-cell quantification of COX IV staining intensity. Numbers in red indicate mean intensity value as reported from ZEN. All scale bars are 20 micrometers. (j) Relative unlabelled UTP and CTP levels in SEM leukemia cells harvested by MACS from the spleens of CuR+Vehicle or CuD+ZnAc treated mice. (k) m+1 13 C-labelled fraction of serine as measured from SEM leukemia cells harvested from the CNS or spleens of mice by MACS. (l) Ellman’s-derivatized glutathione (GSH) levels in SEM leukemia cells harvested from CNS or spleen. (m) Spleen weights from the endpoint of mice engrafted with PDX CBAB-62871 at week 7, related to Fig 5m - n . CuR = copper replete diet, CuD = copper depleted diet, AICAR = 5-aminoimidazole-4-carboxamide ribonucleotide, MACS = magnet-activated cell sorting. Plotted values are mean+/−SD unless otherwise specified. n.s. = not significant. p-values from Tukey’s multiple comparison tests (b and d), or unpaired t-tests (f-h, j-m).

Techniques: In Vivo, Imaging, Analysis, Liquid Chromatography with Mass Spectroscopy, 96 Well Plates, Staining, Tissue, FACS, Comparison

Transcriptomic analysis reveals tannic acid's anti-fibrotic mechanisms in injured rabbit corneas. ( A ) Volcano plot showing differentially expressed genes (DEGs) between TA-treated and control groups ( n = 3). ( B ) Gene Ontology (GO) enrichment analysis of DEGs, categorized into biological process (BP), cellular component (CC), and molecular function (MF). ( C ) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of DEGs. ( D ) Gene Set Enrichment Analysis (GSEA) based on REACTOME gene sets. ( E ) Heatmap displaying key DEGs associated with inflammatory response, redox homeostasis, and corneal scarring. ( F – K ) RT-qPCR validation of mRNA expression levels of representative genes in rabbit corneas at day 28 following different treatments ( n = 3), including F SOD2 , G ACTA2 , H IL1B , I LOX , J LOXL2 , and K SLC31A1 . * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Mean ± SD, 1-way ANOVA.

Journal: Investigative Ophthalmology & Visual Science

Article Title: Tannic Acid Achieves Rapid Scar-Free Corneal Healing by Chelating Excess Copper to Suppress Aberrant LOX-Mediated Fibrosis

doi: 10.1167/iovs.67.3.13

Figure Lengend Snippet: Transcriptomic analysis reveals tannic acid's anti-fibrotic mechanisms in injured rabbit corneas. ( A ) Volcano plot showing differentially expressed genes (DEGs) between TA-treated and control groups ( n = 3). ( B ) Gene Ontology (GO) enrichment analysis of DEGs, categorized into biological process (BP), cellular component (CC), and molecular function (MF). ( C ) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of DEGs. ( D ) Gene Set Enrichment Analysis (GSEA) based on REACTOME gene sets. ( E ) Heatmap displaying key DEGs associated with inflammatory response, redox homeostasis, and corneal scarring. ( F – K ) RT-qPCR validation of mRNA expression levels of representative genes in rabbit corneas at day 28 following different treatments ( n = 3), including F SOD2 , G ACTA2 , H IL1B , I LOX , J LOXL2 , and K SLC31A1 . * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Mean ± SD, 1-way ANOVA.

Article Snippet: After blocking, membranes were incubated with primary antibodies against LOX (1:1000, 17958-1-AP; Proteintech), LOXL2 (1:1000, GTX105085; GeneTex), CTR1 (1:5000, 67221-1-Ig; Proteintech), VIM (1:20000, 60330-1-Ig; Proteintech), α-SMA (1:5000, 14395-1-AP; Proteintech), IL-1β (1:1000, ab234437; Abcam), and β-actin (1:10000, AC026; ABclonal), followed by HRP-conjugated secondary antibodies (1:10000, SA00001-2; Proteintech).

Techniques: Control, Quantitative RT-PCR, Biomarker Discovery, Expressing

Tannic acid reduces fibrosis by chelating excess copper to inhibit lox expression and activity. ( A ) Quantitative analysis of copper concentration in corneal tissues following different treatments (FK = fungal keratitis; CED = corneal epithelial defect; n = 3). ( B ) Quantitative analysis of LOX enzymatic activity in corneal tissues following different treatments ( n = 3). ( C ) Quantitative analysis of central corneal thickness in TA-treated ALK model at day 56 compared with healthy controls ( n = 3). ( D ) Representative Western blot images of LOX, LOXL2, CTR1, VIM, α-SMA, IL-1β, and β-actin protein expression in rabbit corneas at day 28 and ( E – J ) corresponding quantitative analyses of E LOX, F LOXL2, G CTR1, H VIM, I α-SMA, and J IL-1β protein levels ( n = 3). ns, not significant, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Mean ± SD, 1-way ANOVA.

Journal: Investigative Ophthalmology & Visual Science

Article Title: Tannic Acid Achieves Rapid Scar-Free Corneal Healing by Chelating Excess Copper to Suppress Aberrant LOX-Mediated Fibrosis

doi: 10.1167/iovs.67.3.13

Figure Lengend Snippet: Tannic acid reduces fibrosis by chelating excess copper to inhibit lox expression and activity. ( A ) Quantitative analysis of copper concentration in corneal tissues following different treatments (FK = fungal keratitis; CED = corneal epithelial defect; n = 3). ( B ) Quantitative analysis of LOX enzymatic activity in corneal tissues following different treatments ( n = 3). ( C ) Quantitative analysis of central corneal thickness in TA-treated ALK model at day 56 compared with healthy controls ( n = 3). ( D ) Representative Western blot images of LOX, LOXL2, CTR1, VIM, α-SMA, IL-1β, and β-actin protein expression in rabbit corneas at day 28 and ( E – J ) corresponding quantitative analyses of E LOX, F LOXL2, G CTR1, H VIM, I α-SMA, and J IL-1β protein levels ( n = 3). ns, not significant, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Mean ± SD, 1-way ANOVA.

Techniques: Expressing, Activity Assay, Concentration Assay, Western Blot

Exogenous copper supplementation reverses tannic acid's anti-fibrotic effects. ( A ) Representative Western blot images of LOX, LOXL2, CTR1, VIM, α-SMA, and β-actin protein expression in rabbit corneas at day 28 following different treatments and ( B – F ) corresponding quantitative analyses of B LOX, C LOXL2, D CTR1, E VIM, and F α-SMA protein levels ( n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Mean ± SD, n = 3; 1-way ANOVA.

Journal: Investigative Ophthalmology & Visual Science

Article Title: Tannic Acid Achieves Rapid Scar-Free Corneal Healing by Chelating Excess Copper to Suppress Aberrant LOX-Mediated Fibrosis

doi: 10.1167/iovs.67.3.13

Figure Lengend Snippet: Exogenous copper supplementation reverses tannic acid's anti-fibrotic effects. ( A ) Representative Western blot images of LOX, LOXL2, CTR1, VIM, α-SMA, and β-actin protein expression in rabbit corneas at day 28 following different treatments and ( B – F ) corresponding quantitative analyses of B LOX, C LOXL2, D CTR1, E VIM, and F α-SMA protein levels ( n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Mean ± SD, n = 3; 1-way ANOVA.

Techniques: Western Blot, Expressing

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