the antibody against sod3 Search Results


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R&D Systems human sod3 ec sod affinity
Human Sod3 Ec Sod Affinity, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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R&D Systems sod3
Sod3, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology sod3 antibodies
Vascular endothelial growth factor C regulates <t>Sod3</t> expression in 66 cl4 mammary carcinoma cells. (A) Total RNA from 66 cl4-scramble and 66 cl4-VEGF-C KD2 cells was converted to cDNA and used to perform a mouse oxidative stress PCR array. Nine candidate genes of the eighty-four examined were identified in the PCR array with more than a twofold change in response to VEGF-C KD. (B) Sod3 mRNA expression was determined using a real-time PCR SYBR Green assay on 66 cl4-scram and 66 cl4-VEGF-C KD1 and KD2 cells (top). Western blot analysis of Sod3 expression in 66 cl4-scram and VEGF-C KD1 and KD2 cells (bottom). (C) Sod3 mRNA expression was determined by real-time PCR SYBR Green assay on three pairs of 66 cl4-scram and VEGF-C KD1 or KD2 tumors (each pair was derived from the same animal).
Sod3 Antibodies, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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R&D Systems anti sod3 polyclonal antibody af4817
Vascular endothelial growth factor C regulates <t>Sod3</t> expression in 66 cl4 mammary carcinoma cells. (A) Total RNA from 66 cl4-scramble and 66 cl4-VEGF-C KD2 cells was converted to cDNA and used to perform a mouse oxidative stress PCR array. Nine candidate genes of the eighty-four examined were identified in the PCR array with more than a twofold change in response to VEGF-C KD. (B) Sod3 mRNA expression was determined using a real-time PCR SYBR Green assay on 66 cl4-scram and 66 cl4-VEGF-C KD1 and KD2 cells (top). Western blot analysis of Sod3 expression in 66 cl4-scram and VEGF-C KD1 and KD2 cells (bottom). (C) Sod3 mRNA expression was determined by real-time PCR SYBR Green assay on three pairs of 66 cl4-scram and VEGF-C KD1 or KD2 tumors (each pair was derived from the same animal).
Anti Sod3 Polyclonal Antibody Af4817, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/the+antibody+against+sod3/Mouse+SOD3%2FEC-SOD+Antibody/pm41855087-55-0-7
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Santa Cruz Biotechnology anti sod3
Vascular endothelial growth factor C regulates <t>Sod3</t> expression in 66 cl4 mammary carcinoma cells. (A) Total RNA from 66 cl4-scramble and 66 cl4-VEGF-C KD2 cells was converted to cDNA and used to perform a mouse oxidative stress PCR array. Nine candidate genes of the eighty-four examined were identified in the PCR array with more than a twofold change in response to VEGF-C KD. (B) Sod3 mRNA expression was determined using a real-time PCR SYBR Green assay on 66 cl4-scram and 66 cl4-VEGF-C KD1 and KD2 cells (top). Western blot analysis of Sod3 expression in 66 cl4-scram and VEGF-C KD1 and KD2 cells (bottom). (C) Sod3 mRNA expression was determined by real-time PCR SYBR Green assay on three pairs of 66 cl4-scram and VEGF-C KD1 or KD2 tumors (each pair was derived from the same animal).
Anti Sod3, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/the+antibody+against+sod3/goat+anti-mouse+IgG-FITC/pm30008939-86-8-23
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Santa Cruz Biotechnology sod3
Vascular endothelial growth factor C regulates <t>Sod3</t> expression in 66 cl4 mammary carcinoma cells. (A) Total RNA from 66 cl4-scramble and 66 cl4-VEGF-C KD2 cells was converted to cDNA and used to perform a mouse oxidative stress PCR array. Nine candidate genes of the eighty-four examined were identified in the PCR array with more than a twofold change in response to VEGF-C KD. (B) Sod3 mRNA expression was determined using a real-time PCR SYBR Green assay on 66 cl4-scram and 66 cl4-VEGF-C KD1 and KD2 cells (top). Western blot analysis of Sod3 expression in 66 cl4-scram and VEGF-C KD1 and KD2 cells (bottom). (C) Sod3 mRNA expression was determined by real-time PCR SYBR Green assay on three pairs of 66 cl4-scram and VEGF-C KD1 or KD2 tumors (each pair was derived from the same animal).
Sod3, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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R&D Systems membranes
Vascular endothelial growth factor C regulates <t>Sod3</t> expression in 66 cl4 mammary carcinoma cells. (A) Total RNA from 66 cl4-scramble and 66 cl4-VEGF-C KD2 cells was converted to cDNA and used to perform a mouse oxidative stress PCR array. Nine candidate genes of the eighty-four examined were identified in the PCR array with more than a twofold change in response to VEGF-C KD. (B) Sod3 mRNA expression was determined using a real-time PCR SYBR Green assay on 66 cl4-scram and 66 cl4-VEGF-C KD1 and KD2 cells (top). Western blot analysis of Sod3 expression in 66 cl4-scram and VEGF-C KD1 and KD2 cells (bottom). (C) Sod3 mRNA expression was determined by real-time PCR SYBR Green assay on three pairs of 66 cl4-scram and VEGF-C KD1 or KD2 tumors (each pair was derived from the same animal).
Membranes, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Danaher Inc mouse monoclonal
Vascular endothelial growth factor C regulates <t>Sod3</t> expression in 66 cl4 mammary carcinoma cells. (A) Total RNA from 66 cl4-scramble and 66 cl4-VEGF-C KD2 cells was converted to cDNA and used to perform a mouse oxidative stress PCR array. Nine candidate genes of the eighty-four examined were identified in the PCR array with more than a twofold change in response to VEGF-C KD. (B) Sod3 mRNA expression was determined using a real-time PCR SYBR Green assay on 66 cl4-scram and 66 cl4-VEGF-C KD1 and KD2 cells (top). Western blot analysis of Sod3 expression in 66 cl4-scram and VEGF-C KD1 and KD2 cells (bottom). (C) Sod3 mRNA expression was determined by real-time PCR SYBR Green assay on three pairs of 66 cl4-scram and VEGF-C KD1 or KD2 tumors (each pair was derived from the same animal).
Mouse Monoclonal, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
Proteintech sod3 rabbit polyclonal antibody
( A ) The protein level of FOXM1, CPT1A, catalase (CAT), SOD1, SOD2, <t>SOD3</t> after knockout and overexpression of CPT1A. ( B ) The mRNA level of FOXM1, CAT, SOD1, SOD2, SOD3 after knockout and overexpression of CPT1A. ( C ) Venn diagram showing the potential transcription factor of SOD1, SOD2, and CAT. ( D ) The protein level of FOXM1, CPT1A, CAT, SOD1, SOD2 after overexpression of FOXM1 in HCT116-CPT1AKO cells. ( E ) Schematic diagram summarising our working model, namely, decreased CPT1A promotes the transcription factor activity of FOXM1, increasing the mRNA and protein level of CAT, SOD1, and SOD2, followed by increasing ROS scavenge after irradiation and therefore colorectal cancer (CRC) cells become radioresistance. ***p<0.001, **p<0.01, *p<0.05. Figure 6—source data 1. Original files for western blot analysis displayed in . Figure 6—source data 2. PDF file containing original western blots for .
Sod3 Rabbit Polyclonal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/the+antibody+against+sod3/SOD3+Antibody/pmc11604221-21-2-7
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Enzo Biochem antibody against sod3
( A ) The protein level of FOXM1, CPT1A, catalase (CAT), SOD1, SOD2, <t>SOD3</t> after knockout and overexpression of CPT1A. ( B ) The mRNA level of FOXM1, CAT, SOD1, SOD2, SOD3 after knockout and overexpression of CPT1A. ( C ) Venn diagram showing the potential transcription factor of SOD1, SOD2, and CAT. ( D ) The protein level of FOXM1, CPT1A, CAT, SOD1, SOD2 after overexpression of FOXM1 in HCT116-CPT1AKO cells. ( E ) Schematic diagram summarising our working model, namely, decreased CPT1A promotes the transcription factor activity of FOXM1, increasing the mRNA and protein level of CAT, SOD1, and SOD2, followed by increasing ROS scavenge after irradiation and therefore colorectal cancer (CRC) cells become radioresistance. ***p<0.001, **p<0.01, *p<0.05. Figure 6—source data 1. Original files for western blot analysis displayed in . Figure 6—source data 2. PDF file containing original western blots for .
Antibody Against Sod3, supplied by Enzo Biochem, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ABclonal Biotechnology sod3 rabbit pab

Sod3 Rabbit Pab, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Vascular endothelial growth factor C regulates Sod3 expression in 66 cl4 mammary carcinoma cells. (A) Total RNA from 66 cl4-scramble and 66 cl4-VEGF-C KD2 cells was converted to cDNA and used to perform a mouse oxidative stress PCR array. Nine candidate genes of the eighty-four examined were identified in the PCR array with more than a twofold change in response to VEGF-C KD. (B) Sod3 mRNA expression was determined using a real-time PCR SYBR Green assay on 66 cl4-scram and 66 cl4-VEGF-C KD1 and KD2 cells (top). Western blot analysis of Sod3 expression in 66 cl4-scram and VEGF-C KD1 and KD2 cells (bottom). (C) Sod3 mRNA expression was determined by real-time PCR SYBR Green assay on three pairs of 66 cl4-scram and VEGF-C KD1 or KD2 tumors (each pair was derived from the same animal).

Journal: Breast Cancer Research : BCR

Article Title: Vascular endothelial growth factor C promotes breast cancer progression via a novel antioxidant mechanism that involves regulation of superoxide dismutase 3

doi: 10.1186/s13058-014-0462-2

Figure Lengend Snippet: Vascular endothelial growth factor C regulates Sod3 expression in 66 cl4 mammary carcinoma cells. (A) Total RNA from 66 cl4-scramble and 66 cl4-VEGF-C KD2 cells was converted to cDNA and used to perform a mouse oxidative stress PCR array. Nine candidate genes of the eighty-four examined were identified in the PCR array with more than a twofold change in response to VEGF-C KD. (B) Sod3 mRNA expression was determined using a real-time PCR SYBR Green assay on 66 cl4-scram and 66 cl4-VEGF-C KD1 and KD2 cells (top). Western blot analysis of Sod3 expression in 66 cl4-scram and VEGF-C KD1 and KD2 cells (bottom). (C) Sod3 mRNA expression was determined by real-time PCR SYBR Green assay on three pairs of 66 cl4-scram and VEGF-C KD1 or KD2 tumors (each pair was derived from the same animal).

Article Snippet: VEGF-C and Sod3 antibodies (sc-25783 and sc-67089, respectively) were obtained from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Techniques: Expressing, Real-time Polymerase Chain Reaction, SYBR Green Assay, Western Blot, Derivative Assay

Restoration of Sod3 in 66 cl4-VEGF-C KD cells partially rescues resistance to oxidative stress and tumor progression. (A) Expression of Sod3 in 66 cl4-VEGF-C KD cells (KD2 in Figure ). Empty vector was also introduced into 66 cl4-scram and 66 cl4-VEGF-C KD2 cells as a control. Sod3 expression was assessed in each cell line using a real-time PCR SYBR Green assay (top). Expression of secreted Sod3 in the media of 66 cl4-scram, 66 cl4-VEGF-C KD and 66 cl4-VEGF-C KD + Sod3 cells was measured by Western blot analysis (bottom). (B) Flow cytometry was performed to measure cell death induced by H 2 O 2 under each condition shown. Three independent experiments were performed, and the data were combined for quantitation. (C) Cells from the 66 cl4-scram, VEGF-C KD and VEGF-C KD + Sod3 lines were injected into the fourth mammary fat pad of female BALB/c mice. Tumor growth in the mice was measured using calipers and calculated using the formula V = 1/2(W)(W)(L) (top). A representative picture of tumors from each group shows that restoration of Sod3 in VEGF-C KD cells partially rescues the size of tumors compared to scramble control tumors (bottom). (D) Representative in vivo image of 66 cl4-scram, VEGF-C KD and VEGF-C KD + Sod3 groups at day 60 after injection (top). Quantitation of bioluminescence imaging (in photons per second) emanating from the region surrounding the lungs (bottom). Mice that did not develop primary tumors were excluded from the quantitation. (E) Incidence of tumor formation and metastasis in the groups of mice injected with 66 cl4-scram, VEGF-C KD or VEGF-C KD + Sod3 cells. Restoration of Sod3 expression in the VEGF-C KD cells increased the number of mice that developed primary tumors and metastases, although not to the levels observed in the scramble control group. Fisher's exact test (two-sided) results indicated a significant increase in the number of mice that developed metastases when Sod3 expression was restored in the VEGF-C KD tumors.

Journal: Breast Cancer Research : BCR

Article Title: Vascular endothelial growth factor C promotes breast cancer progression via a novel antioxidant mechanism that involves regulation of superoxide dismutase 3

doi: 10.1186/s13058-014-0462-2

Figure Lengend Snippet: Restoration of Sod3 in 66 cl4-VEGF-C KD cells partially rescues resistance to oxidative stress and tumor progression. (A) Expression of Sod3 in 66 cl4-VEGF-C KD cells (KD2 in Figure ). Empty vector was also introduced into 66 cl4-scram and 66 cl4-VEGF-C KD2 cells as a control. Sod3 expression was assessed in each cell line using a real-time PCR SYBR Green assay (top). Expression of secreted Sod3 in the media of 66 cl4-scram, 66 cl4-VEGF-C KD and 66 cl4-VEGF-C KD + Sod3 cells was measured by Western blot analysis (bottom). (B) Flow cytometry was performed to measure cell death induced by H 2 O 2 under each condition shown. Three independent experiments were performed, and the data were combined for quantitation. (C) Cells from the 66 cl4-scram, VEGF-C KD and VEGF-C KD + Sod3 lines were injected into the fourth mammary fat pad of female BALB/c mice. Tumor growth in the mice was measured using calipers and calculated using the formula V = 1/2(W)(W)(L) (top). A representative picture of tumors from each group shows that restoration of Sod3 in VEGF-C KD cells partially rescues the size of tumors compared to scramble control tumors (bottom). (D) Representative in vivo image of 66 cl4-scram, VEGF-C KD and VEGF-C KD + Sod3 groups at day 60 after injection (top). Quantitation of bioluminescence imaging (in photons per second) emanating from the region surrounding the lungs (bottom). Mice that did not develop primary tumors were excluded from the quantitation. (E) Incidence of tumor formation and metastasis in the groups of mice injected with 66 cl4-scram, VEGF-C KD or VEGF-C KD + Sod3 cells. Restoration of Sod3 expression in the VEGF-C KD cells increased the number of mice that developed primary tumors and metastases, although not to the levels observed in the scramble control group. Fisher's exact test (two-sided) results indicated a significant increase in the number of mice that developed metastases when Sod3 expression was restored in the VEGF-C KD tumors.

Article Snippet: VEGF-C and Sod3 antibodies (sc-25783 and sc-67089, respectively) were obtained from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Techniques: Expressing, Plasmid Preparation, Control, Real-time Polymerase Chain Reaction, SYBR Green Assay, Western Blot, Flow Cytometry, Quantitation Assay, Injection, In Vivo, Imaging

Neuropilin 2-knockdown in 66 cl4 mouse mammary carcinoma cells decreases superoxide dismutase 3 expression and sensitizes cells to oxidative stress. (A) NRP2 and VEGFR3 mRNA expression in human breast cancer cell lines. Box plots of NRP2 (left) or VEGFR3 ( FLT4 ) (right) gene expression across 51 previously reported breast cancer cell lines grouped into basal A, basal B and luminal subgroups. NRP2 and VEGFR3 gene expression in human breast cancer cell lines was assessed using GOBO . (B) Two different short-hairpin RNAs (shRNAs 1 and 2) were used to knock down neuropilin 2 (Nrp2) in 66 cl4 cells. Expression of Nrp2 in 66 cl4-scram and 66 cl4-Nrp2 knockdown (KD) cells was determined by Western blot analysis (left). Decreased expression of superoxide dismutase 3 (Sod3) was observed in 66 cl4-Nrp2 KD cells compared to 66 cl4-scram cells (right). Whole-cell lysates (top) or media (bottom) from 66 cl4-scram and 66 cl4-Nrp2 KD cells were collected for the detection of Sod3 by Western blotting. (C) Viability of 66 cl4-scram and 66 cl4-Nrp2 KD cells treated with increasing doses of H 2 O 2 . A CellTiter-Glo assay was used to measure viable cells. Three independent experiments were performed and combined for quantification.

Journal: Breast Cancer Research : BCR

Article Title: Vascular endothelial growth factor C promotes breast cancer progression via a novel antioxidant mechanism that involves regulation of superoxide dismutase 3

doi: 10.1186/s13058-014-0462-2

Figure Lengend Snippet: Neuropilin 2-knockdown in 66 cl4 mouse mammary carcinoma cells decreases superoxide dismutase 3 expression and sensitizes cells to oxidative stress. (A) NRP2 and VEGFR3 mRNA expression in human breast cancer cell lines. Box plots of NRP2 (left) or VEGFR3 ( FLT4 ) (right) gene expression across 51 previously reported breast cancer cell lines grouped into basal A, basal B and luminal subgroups. NRP2 and VEGFR3 gene expression in human breast cancer cell lines was assessed using GOBO . (B) Two different short-hairpin RNAs (shRNAs 1 and 2) were used to knock down neuropilin 2 (Nrp2) in 66 cl4 cells. Expression of Nrp2 in 66 cl4-scram and 66 cl4-Nrp2 knockdown (KD) cells was determined by Western blot analysis (left). Decreased expression of superoxide dismutase 3 (Sod3) was observed in 66 cl4-Nrp2 KD cells compared to 66 cl4-scram cells (right). Whole-cell lysates (top) or media (bottom) from 66 cl4-scram and 66 cl4-Nrp2 KD cells were collected for the detection of Sod3 by Western blotting. (C) Viability of 66 cl4-scram and 66 cl4-Nrp2 KD cells treated with increasing doses of H 2 O 2 . A CellTiter-Glo assay was used to measure viable cells. Three independent experiments were performed and combined for quantification.

Article Snippet: VEGF-C and Sod3 antibodies (sc-25783 and sc-67089, respectively) were obtained from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Techniques: Knockdown, Expressing, Gene Expression, Western Blot, Glo Assay

Expression of VEGFC and SOD3 in human cancers. (A) VEGFC and SOD3 expression values were retrieved from an Oncomine microarray data set (as indicated in the figure) and were plotted by expression value. Statistical analysis was performed using Pearson r correlation (two-tailed). (B) Proposed model for the function of vascular endothelial growth factor C (VEGF-C) in breast cancer progression. Expression of VEGF-C in a subset of tumor cells confers the ability to resist oxidative stress generated during tumor growth, and this ability is partially mediated by Sod3. However, VEGF-C mediates other pathways that are important in conferring resistance to chemotherapies, thus contributing to tumor recurrence. Blocking VEGF-C signaling would therefore be expected to sensitize breast cancers to chemotherapies that induce oxidative stress, to contribute to a reduction in tumor-initiating cells (TICs) and to decrease lymphangiogenesis, thus likely improving survival and prevent recurrence.

Journal: Breast Cancer Research : BCR

Article Title: Vascular endothelial growth factor C promotes breast cancer progression via a novel antioxidant mechanism that involves regulation of superoxide dismutase 3

doi: 10.1186/s13058-014-0462-2

Figure Lengend Snippet: Expression of VEGFC and SOD3 in human cancers. (A) VEGFC and SOD3 expression values were retrieved from an Oncomine microarray data set (as indicated in the figure) and were plotted by expression value. Statistical analysis was performed using Pearson r correlation (two-tailed). (B) Proposed model for the function of vascular endothelial growth factor C (VEGF-C) in breast cancer progression. Expression of VEGF-C in a subset of tumor cells confers the ability to resist oxidative stress generated during tumor growth, and this ability is partially mediated by Sod3. However, VEGF-C mediates other pathways that are important in conferring resistance to chemotherapies, thus contributing to tumor recurrence. Blocking VEGF-C signaling would therefore be expected to sensitize breast cancers to chemotherapies that induce oxidative stress, to contribute to a reduction in tumor-initiating cells (TICs) and to decrease lymphangiogenesis, thus likely improving survival and prevent recurrence.

Article Snippet: VEGF-C and Sod3 antibodies (sc-25783 and sc-67089, respectively) were obtained from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Techniques: Expressing, Microarray, Two Tailed Test, Generated, Blocking Assay

( A ) The protein level of FOXM1, CPT1A, catalase (CAT), SOD1, SOD2, SOD3 after knockout and overexpression of CPT1A. ( B ) The mRNA level of FOXM1, CAT, SOD1, SOD2, SOD3 after knockout and overexpression of CPT1A. ( C ) Venn diagram showing the potential transcription factor of SOD1, SOD2, and CAT. ( D ) The protein level of FOXM1, CPT1A, CAT, SOD1, SOD2 after overexpression of FOXM1 in HCT116-CPT1AKO cells. ( E ) Schematic diagram summarising our working model, namely, decreased CPT1A promotes the transcription factor activity of FOXM1, increasing the mRNA and protein level of CAT, SOD1, and SOD2, followed by increasing ROS scavenge after irradiation and therefore colorectal cancer (CRC) cells become radioresistance. ***p<0.001, **p<0.01, *p<0.05. Figure 6—source data 1. Original files for western blot analysis displayed in . Figure 6—source data 2. PDF file containing original western blots for .

Journal: eLife

Article Title: CPT1A mediates radiation sensitivity in colorectal cancer

doi: 10.7554/eLife.97827

Figure Lengend Snippet: ( A ) The protein level of FOXM1, CPT1A, catalase (CAT), SOD1, SOD2, SOD3 after knockout and overexpression of CPT1A. ( B ) The mRNA level of FOXM1, CAT, SOD1, SOD2, SOD3 after knockout and overexpression of CPT1A. ( C ) Venn diagram showing the potential transcription factor of SOD1, SOD2, and CAT. ( D ) The protein level of FOXM1, CPT1A, CAT, SOD1, SOD2 after overexpression of FOXM1 in HCT116-CPT1AKO cells. ( E ) Schematic diagram summarising our working model, namely, decreased CPT1A promotes the transcription factor activity of FOXM1, increasing the mRNA and protein level of CAT, SOD1, and SOD2, followed by increasing ROS scavenge after irradiation and therefore colorectal cancer (CRC) cells become radioresistance. ***p<0.001, **p<0.01, *p<0.05. Figure 6—source data 1. Original files for western blot analysis displayed in . Figure 6—source data 2. PDF file containing original western blots for .

Article Snippet: Antibody , SOD3 Rabbit Polyclonal antibody , Proteintech (China) , 14316-1-AP , .

Techniques: Knock-Out, Over Expression, Activity Assay, Irradiation, Western Blot

Journal: eLife

Article Title: CPT1A mediates radiation sensitivity in colorectal cancer

doi: 10.7554/eLife.97827

Figure Lengend Snippet:

Article Snippet: Antibody , SOD3 Rabbit Polyclonal antibody , Proteintech (China) , 14316-1-AP , .

Techniques: Transfection, Construct, SYBR Green Assay, Protein Extraction, Single Cell Gel Electrophoresis, Activity Assay

Journal: iScience

Article Title: A pan-tissue multi-omics resource atlas of coordinated immune, metabolic, and fibrotic alterations in diet-induced MASH

doi: 10.1016/j.isci.2026.117139

Figure Lengend Snippet:

Article Snippet: SOD3 Rabbit pAb , ABclonal , Cat# A6984; RRID: AB_3542652.

Techniques: Recombinant, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Activity Assay, Transcriptomics, Mass Spectrometry, Reverse Transcription Polymerase Chain Reaction, Software