rabbit polyclonal anti slc3a2 Search Results


mouse anti 4f2 lhx1 5  (Developmental Studies Hybridoma Bank)
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Developmental Studies Hybridoma Bank mouse anti 4f2 lhx1 5
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mouse anti lhx1  (Proteintech)
96
Proteintech mouse anti lhx1
Mouse Anti Lhx1, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti 4f2hc cd98  (Cell Signaling Technology Inc)
95
Cell Signaling Technology Inc anti 4f2hc cd98
Anti 4f2hc Cd98, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse anti cd98  (Santa Cruz Biotechnology)
93
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Mouse Anti Cd98, 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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anti slc3a2 antibody  (Cell Signaling Technology Inc)
95
Cell Signaling Technology Inc anti slc3a2 antibody
(A) Volcano plot of 4T1-P and Tyro3-OE differentially expressed genes. adj, adjusted. (B) <t>SLC3A2</t> expression in patients with melanoma with high (n = 52) and low (n = 19) TYRO3 expression levels who received anti–PD-1 therapy. ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (C) Relative lipid ROS in CD45− tumor cells. 4T1-P plus IgG versus 4T1-P plus anti–PD-1, *P = 0.037; Tyro3-OE plus IgG versus Tyro3-OE plus anti–PD-1, NS P = 0.92; and 4T1-P plus anti–PD-1 versus Tyro3-OE plus anti–PD-1, ***P = 0.0004, by 2-way ANOVA. (D) MFI of IFN-γ expression in CD8+ T cells from anti–PD-1–treated 4T1-P and Tyro3-OE tumors. NS P = 0.626, by 2-tailed, unpaired Student’s t test. (E) Percentage of 7-AAD+ cells in 4T1-P and Tyro3-OE cells treated with 2 μM erastin and/or 5 μM Fer-1 for 48 hours (n = 3). £P = 0.013, by 2-tailed, unpaired Student’s t test. (F) Relative lipid ROS in 4T1-P and Tyro3-OE cells treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). **P = 0.0013, by 2-tailed, unpaired Student’s t test. (G) Percentage of 7-AAD+ cells in 4T1-R and Tyro3−/− cells treated with 2 μM erastin and/or 5 μM Fer-1 for 24 hours (n = 3). ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (H) Relative lipid ROS in 4T1-R and Tyro3−/− cells treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). ****P < 0.0001, †††P = 0.000124, and ††P = 0.00125, by 2-tailed, unpaired Student’s t test. (I) A dual-luciferase reporter assay was performed by cotransfecting ARE-reporter-luciferase and pRL-TK with a TYRO3-OE plasmid, and cells were primed with 2 μM MK2206 for 24 hours (n = 3). ##P = 0.002 and NS P = 0.115, by 2-tailed, unpaired Student’s t test. (J) Relative lipid ROS in 4T1-P and Tyro3-OE cells primed with 2 μM MK2206 for 24 hours, and then treated with 10 μM erastin for 8 hours (n = 3). §P = 0.02, §§P = 0.003, NS P = 0.052, and NS P = 0.79, by 2-tailed, unpaired Student’s t test. (K) Relative lipid ROS in 4T1 cells primed with or without 200 nM Pros1 for 24 hours and then treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). ¶P = 0.013 and ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (L) Relative lipid ROS in 4T1 Tyro3−/− cells primed with or without 200 nM Pros1 for 24 hours and then treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). NS P = 0.059, NS P = 0.53, and NS P = 0.58, by 2-tailed, unpaired Student’s t test. Data are presented as the mean ± SD.
Anti Slc3a2 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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13180s  (Cell Signaling Technology Inc)
94
Cell Signaling Technology Inc 13180s
(A) Volcano plot of 4T1-P and Tyro3-OE differentially expressed genes. adj, adjusted. (B) <t>SLC3A2</t> expression in patients with melanoma with high (n = 52) and low (n = 19) TYRO3 expression levels who received anti–PD-1 therapy. ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (C) Relative lipid ROS in CD45− tumor cells. 4T1-P plus IgG versus 4T1-P plus anti–PD-1, *P = 0.037; Tyro3-OE plus IgG versus Tyro3-OE plus anti–PD-1, NS P = 0.92; and 4T1-P plus anti–PD-1 versus Tyro3-OE plus anti–PD-1, ***P = 0.0004, by 2-way ANOVA. (D) MFI of IFN-γ expression in CD8+ T cells from anti–PD-1–treated 4T1-P and Tyro3-OE tumors. NS P = 0.626, by 2-tailed, unpaired Student’s t test. (E) Percentage of 7-AAD+ cells in 4T1-P and Tyro3-OE cells treated with 2 μM erastin and/or 5 μM Fer-1 for 48 hours (n = 3). £P = 0.013, by 2-tailed, unpaired Student’s t test. (F) Relative lipid ROS in 4T1-P and Tyro3-OE cells treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). **P = 0.0013, by 2-tailed, unpaired Student’s t test. (G) Percentage of 7-AAD+ cells in 4T1-R and Tyro3−/− cells treated with 2 μM erastin and/or 5 μM Fer-1 for 24 hours (n = 3). ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (H) Relative lipid ROS in 4T1-R and Tyro3−/− cells treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). ****P < 0.0001, †††P = 0.000124, and ††P = 0.00125, by 2-tailed, unpaired Student’s t test. (I) A dual-luciferase reporter assay was performed by cotransfecting ARE-reporter-luciferase and pRL-TK with a TYRO3-OE plasmid, and cells were primed with 2 μM MK2206 for 24 hours (n = 3). ##P = 0.002 and NS P = 0.115, by 2-tailed, unpaired Student’s t test. (J) Relative lipid ROS in 4T1-P and Tyro3-OE cells primed with 2 μM MK2206 for 24 hours, and then treated with 10 μM erastin for 8 hours (n = 3). §P = 0.02, §§P = 0.003, NS P = 0.052, and NS P = 0.79, by 2-tailed, unpaired Student’s t test. (K) Relative lipid ROS in 4T1 cells primed with or without 200 nM Pros1 for 24 hours and then treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). ¶P = 0.013 and ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (L) Relative lipid ROS in 4T1 Tyro3−/− cells primed with or without 200 nM Pros1 for 24 hours and then treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). NS P = 0.059, NS P = 0.53, and NS P = 0.58, by 2-tailed, unpaired Student’s t test. Data are presented as the mean ± SD.
13180s, supplied by Cell Signaling Technology Inc, 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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rabbit anti slc3a2  (Boster Bio)
92
Boster Bio rabbit anti slc3a2
(A) Volcano plot of 4T1-P and Tyro3-OE differentially expressed genes. adj, adjusted. (B) <t>SLC3A2</t> expression in patients with melanoma with high (n = 52) and low (n = 19) TYRO3 expression levels who received anti–PD-1 therapy. ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (C) Relative lipid ROS in CD45− tumor cells. 4T1-P plus IgG versus 4T1-P plus anti–PD-1, *P = 0.037; Tyro3-OE plus IgG versus Tyro3-OE plus anti–PD-1, NS P = 0.92; and 4T1-P plus anti–PD-1 versus Tyro3-OE plus anti–PD-1, ***P = 0.0004, by 2-way ANOVA. (D) MFI of IFN-γ expression in CD8+ T cells from anti–PD-1–treated 4T1-P and Tyro3-OE tumors. NS P = 0.626, by 2-tailed, unpaired Student’s t test. (E) Percentage of 7-AAD+ cells in 4T1-P and Tyro3-OE cells treated with 2 μM erastin and/or 5 μM Fer-1 for 48 hours (n = 3). £P = 0.013, by 2-tailed, unpaired Student’s t test. (F) Relative lipid ROS in 4T1-P and Tyro3-OE cells treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). **P = 0.0013, by 2-tailed, unpaired Student’s t test. (G) Percentage of 7-AAD+ cells in 4T1-R and Tyro3−/− cells treated with 2 μM erastin and/or 5 μM Fer-1 for 24 hours (n = 3). ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (H) Relative lipid ROS in 4T1-R and Tyro3−/− cells treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). ****P < 0.0001, †††P = 0.000124, and ††P = 0.00125, by 2-tailed, unpaired Student’s t test. (I) A dual-luciferase reporter assay was performed by cotransfecting ARE-reporter-luciferase and pRL-TK with a TYRO3-OE plasmid, and cells were primed with 2 μM MK2206 for 24 hours (n = 3). ##P = 0.002 and NS P = 0.115, by 2-tailed, unpaired Student’s t test. (J) Relative lipid ROS in 4T1-P and Tyro3-OE cells primed with 2 μM MK2206 for 24 hours, and then treated with 10 μM erastin for 8 hours (n = 3). §P = 0.02, §§P = 0.003, NS P = 0.052, and NS P = 0.79, by 2-tailed, unpaired Student’s t test. (K) Relative lipid ROS in 4T1 cells primed with or without 200 nM Pros1 for 24 hours and then treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). ¶P = 0.013 and ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (L) Relative lipid ROS in 4T1 Tyro3−/− cells primed with or without 200 nM Pros1 for 24 hours and then treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). NS P = 0.059, NS P = 0.53, and NS P = 0.58, by 2-tailed, unpaired Student’s t test. Data are presented as the mean ± SD.
Rabbit Anti Slc3a2, supplied by Boster Bio, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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12242 mouse anti β tubulin mab 4f2  (Cell Signaling Technology Inc)
98
Cell Signaling Technology Inc 12242 mouse anti β tubulin mab 4f2
(A) Volcano plot of 4T1-P and Tyro3-OE differentially expressed genes. adj, adjusted. (B) <t>SLC3A2</t> expression in patients with melanoma with high (n = 52) and low (n = 19) TYRO3 expression levels who received anti–PD-1 therapy. ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (C) Relative lipid ROS in CD45− tumor cells. 4T1-P plus IgG versus 4T1-P plus anti–PD-1, *P = 0.037; Tyro3-OE plus IgG versus Tyro3-OE plus anti–PD-1, NS P = 0.92; and 4T1-P plus anti–PD-1 versus Tyro3-OE plus anti–PD-1, ***P = 0.0004, by 2-way ANOVA. (D) MFI of IFN-γ expression in CD8+ T cells from anti–PD-1–treated 4T1-P and Tyro3-OE tumors. NS P = 0.626, by 2-tailed, unpaired Student’s t test. (E) Percentage of 7-AAD+ cells in 4T1-P and Tyro3-OE cells treated with 2 μM erastin and/or 5 μM Fer-1 for 48 hours (n = 3). £P = 0.013, by 2-tailed, unpaired Student’s t test. (F) Relative lipid ROS in 4T1-P and Tyro3-OE cells treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). **P = 0.0013, by 2-tailed, unpaired Student’s t test. (G) Percentage of 7-AAD+ cells in 4T1-R and Tyro3−/− cells treated with 2 μM erastin and/or 5 μM Fer-1 for 24 hours (n = 3). ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (H) Relative lipid ROS in 4T1-R and Tyro3−/− cells treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). ****P < 0.0001, †††P = 0.000124, and ††P = 0.00125, by 2-tailed, unpaired Student’s t test. (I) A dual-luciferase reporter assay was performed by cotransfecting ARE-reporter-luciferase and pRL-TK with a TYRO3-OE plasmid, and cells were primed with 2 μM MK2206 for 24 hours (n = 3). ##P = 0.002 and NS P = 0.115, by 2-tailed, unpaired Student’s t test. (J) Relative lipid ROS in 4T1-P and Tyro3-OE cells primed with 2 μM MK2206 for 24 hours, and then treated with 10 μM erastin for 8 hours (n = 3). §P = 0.02, §§P = 0.003, NS P = 0.052, and NS P = 0.79, by 2-tailed, unpaired Student’s t test. (K) Relative lipid ROS in 4T1 cells primed with or without 200 nM Pros1 for 24 hours and then treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). ¶P = 0.013 and ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (L) Relative lipid ROS in 4T1 Tyro3−/− cells primed with or without 200 nM Pros1 for 24 hours and then treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). NS P = 0.059, NS P = 0.53, and NS P = 0.58, by 2-tailed, unpaired Student’s t test. Data are presented as the mean ± SD.
12242 Mouse Anti β Tubulin Mab 4f2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rabbit anti-solute carrier family 3 member 2 (slc3a2  (ABclonal Biotechnology)
90
ABclonal Biotechnology rabbit anti-solute carrier family 3 member 2 (slc3a2
CGA regulates the relative expression level of ferroptosis proteins after HIBD in newborn mice. (A–F) Western blot of SLC7A11, FHC, FLC, <t>SLC3A2,</t> GLS2, and GSS expression in the cortex ( n = 4). β-Actin was used as an internal reference. (G) Cox-2 , Nrf2 , GSH and GPX4 mRNA levels in hippocampus tissue 24 hours after HIBD; GAPDH mRNA was used as a normalization control ( n = 3). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, vs . Sham + NS group; # P < 0.05, ## P < 0.01, vs . HI + NS group (one-way analysis of variance followed by Tukey’s post hoc test). CGA: Chlorogenic acid; COX2: cyclooxygenase-2; FHC: ferritin heavy chain; FLC: ferritin light chain; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GLS2: glutaminase 2; GSH: L-glutathione; GSS: glutathione synthase; HI or HIBD: hypoxic-ischemic brain injury; Nrf2: nuclear factor (erythroid-derived 2)-like 2; NS: normal saline; SLC3A2: solute carrier <t>family</t> <t>3</t> member 2; SLC7A11: solute carrier family 7 member 11.
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lamp1 knockdown anti cd98 slc3a2 rabbit bethyl a304 331a  (Bethyl)
91
Bethyl lamp1 knockdown anti cd98 slc3a2 rabbit bethyl a304 331a
CGA regulates the relative expression level of ferroptosis proteins after HIBD in newborn mice. (A–F) Western blot of SLC7A11, FHC, FLC, <t>SLC3A2,</t> GLS2, and GSS expression in the cortex ( n = 4). β-Actin was used as an internal reference. (G) Cox-2 , Nrf2 , GSH and GPX4 mRNA levels in hippocampus tissue 24 hours after HIBD; GAPDH mRNA was used as a normalization control ( n = 3). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, vs . Sham + NS group; # P < 0.05, ## P < 0.01, vs . HI + NS group (one-way analysis of variance followed by Tukey’s post hoc test). CGA: Chlorogenic acid; COX2: cyclooxygenase-2; FHC: ferritin heavy chain; FLC: ferritin light chain; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GLS2: glutaminase 2; GSH: L-glutathione; GSS: glutathione synthase; HI or HIBD: hypoxic-ischemic brain injury; Nrf2: nuclear factor (erythroid-derived 2)-like 2; NS: normal saline; SLC3A2: solute carrier <t>family</t> <t>3</t> member 2; SLC7A11: solute carrier family 7 member 11.
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rabbit anti slc3a2  (Biosynth Carbosynth)
88
Biosynth Carbosynth rabbit anti slc3a2
CGA regulates the relative expression level of ferroptosis proteins after HIBD in newborn mice. (A–F) Western blot of SLC7A11, FHC, FLC, <t>SLC3A2,</t> GLS2, and GSS expression in the cortex ( n = 4). β-Actin was used as an internal reference. (G) Cox-2 , Nrf2 , GSH and GPX4 mRNA levels in hippocampus tissue 24 hours after HIBD; GAPDH mRNA was used as a normalization control ( n = 3). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, vs . Sham + NS group; # P < 0.05, ## P < 0.01, vs . HI + NS group (one-way analysis of variance followed by Tukey’s post hoc test). CGA: Chlorogenic acid; COX2: cyclooxygenase-2; FHC: ferritin heavy chain; FLC: ferritin light chain; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GLS2: glutaminase 2; GSH: L-glutathione; GSS: glutathione synthase; HI or HIBD: hypoxic-ischemic brain injury; Nrf2: nuclear factor (erythroid-derived 2)-like 2; NS: normal saline; SLC3A2: solute carrier <t>family</t> <t>3</t> member 2; SLC7A11: solute carrier family 7 member 11.
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rabbit polyclonal anti slc3a2 proteintech  (Proteintech)
96
Proteintech rabbit polyclonal anti slc3a2 proteintech
CGA regulates the relative expression level of ferroptosis proteins after HIBD in newborn mice. (A–F) Western blot of SLC7A11, FHC, FLC, <t>SLC3A2,</t> GLS2, and GSS expression in the cortex ( n = 4). β-Actin was used as an internal reference. (G) Cox-2 , Nrf2 , GSH and GPX4 mRNA levels in hippocampus tissue 24 hours after HIBD; GAPDH mRNA was used as a normalization control ( n = 3). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, vs . Sham + NS group; # P < 0.05, ## P < 0.01, vs . HI + NS group (one-way analysis of variance followed by Tukey’s post hoc test). CGA: Chlorogenic acid; COX2: cyclooxygenase-2; FHC: ferritin heavy chain; FLC: ferritin light chain; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GLS2: glutaminase 2; GSH: L-glutathione; GSS: glutathione synthase; HI or HIBD: hypoxic-ischemic brain injury; Nrf2: nuclear factor (erythroid-derived 2)-like 2; NS: normal saline; SLC3A2: solute carrier <t>family</t> <t>3</t> member 2; SLC7A11: solute carrier family 7 member 11.
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Image Search Results


(A) Volcano plot of 4T1-P and Tyro3-OE differentially expressed genes. adj, adjusted. (B) SLC3A2 expression in patients with melanoma with high (n = 52) and low (n = 19) TYRO3 expression levels who received anti–PD-1 therapy. ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (C) Relative lipid ROS in CD45− tumor cells. 4T1-P plus IgG versus 4T1-P plus anti–PD-1, *P = 0.037; Tyro3-OE plus IgG versus Tyro3-OE plus anti–PD-1, NS P = 0.92; and 4T1-P plus anti–PD-1 versus Tyro3-OE plus anti–PD-1, ***P = 0.0004, by 2-way ANOVA. (D) MFI of IFN-γ expression in CD8+ T cells from anti–PD-1–treated 4T1-P and Tyro3-OE tumors. NS P = 0.626, by 2-tailed, unpaired Student’s t test. (E) Percentage of 7-AAD+ cells in 4T1-P and Tyro3-OE cells treated with 2 μM erastin and/or 5 μM Fer-1 for 48 hours (n = 3). £P = 0.013, by 2-tailed, unpaired Student’s t test. (F) Relative lipid ROS in 4T1-P and Tyro3-OE cells treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). **P = 0.0013, by 2-tailed, unpaired Student’s t test. (G) Percentage of 7-AAD+ cells in 4T1-R and Tyro3−/− cells treated with 2 μM erastin and/or 5 μM Fer-1 for 24 hours (n = 3). ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (H) Relative lipid ROS in 4T1-R and Tyro3−/− cells treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). ****P < 0.0001, †††P = 0.000124, and ††P = 0.00125, by 2-tailed, unpaired Student’s t test. (I) A dual-luciferase reporter assay was performed by cotransfecting ARE-reporter-luciferase and pRL-TK with a TYRO3-OE plasmid, and cells were primed with 2 μM MK2206 for 24 hours (n = 3). ##P = 0.002 and NS P = 0.115, by 2-tailed, unpaired Student’s t test. (J) Relative lipid ROS in 4T1-P and Tyro3-OE cells primed with 2 μM MK2206 for 24 hours, and then treated with 10 μM erastin for 8 hours (n = 3). §P = 0.02, §§P = 0.003, NS P = 0.052, and NS P = 0.79, by 2-tailed, unpaired Student’s t test. (K) Relative lipid ROS in 4T1 cells primed with or without 200 nM Pros1 for 24 hours and then treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). ¶P = 0.013 and ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (L) Relative lipid ROS in 4T1 Tyro3−/− cells primed with or without 200 nM Pros1 for 24 hours and then treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). NS P = 0.059, NS P = 0.53, and NS P = 0.58, by 2-tailed, unpaired Student’s t test. Data are presented as the mean ± SD.

Journal: The Journal of Clinical Investigation

Article Title: TYRO3 induces anti–PD-1/PD-L1 therapy resistance by limiting innate immunity and tumoral ferroptosis

doi: 10.1172/JCI139434

Figure Lengend Snippet: (A) Volcano plot of 4T1-P and Tyro3-OE differentially expressed genes. adj, adjusted. (B) SLC3A2 expression in patients with melanoma with high (n = 52) and low (n = 19) TYRO3 expression levels who received anti–PD-1 therapy. ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (C) Relative lipid ROS in CD45− tumor cells. 4T1-P plus IgG versus 4T1-P plus anti–PD-1, *P = 0.037; Tyro3-OE plus IgG versus Tyro3-OE plus anti–PD-1, NS P = 0.92; and 4T1-P plus anti–PD-1 versus Tyro3-OE plus anti–PD-1, ***P = 0.0004, by 2-way ANOVA. (D) MFI of IFN-γ expression in CD8+ T cells from anti–PD-1–treated 4T1-P and Tyro3-OE tumors. NS P = 0.626, by 2-tailed, unpaired Student’s t test. (E) Percentage of 7-AAD+ cells in 4T1-P and Tyro3-OE cells treated with 2 μM erastin and/or 5 μM Fer-1 for 48 hours (n = 3). £P = 0.013, by 2-tailed, unpaired Student’s t test. (F) Relative lipid ROS in 4T1-P and Tyro3-OE cells treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). **P = 0.0013, by 2-tailed, unpaired Student’s t test. (G) Percentage of 7-AAD+ cells in 4T1-R and Tyro3−/− cells treated with 2 μM erastin and/or 5 μM Fer-1 for 24 hours (n = 3). ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (H) Relative lipid ROS in 4T1-R and Tyro3−/− cells treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). ****P < 0.0001, †††P = 0.000124, and ††P = 0.00125, by 2-tailed, unpaired Student’s t test. (I) A dual-luciferase reporter assay was performed by cotransfecting ARE-reporter-luciferase and pRL-TK with a TYRO3-OE plasmid, and cells were primed with 2 μM MK2206 for 24 hours (n = 3). ##P = 0.002 and NS P = 0.115, by 2-tailed, unpaired Student’s t test. (J) Relative lipid ROS in 4T1-P and Tyro3-OE cells primed with 2 μM MK2206 for 24 hours, and then treated with 10 μM erastin for 8 hours (n = 3). §P = 0.02, §§P = 0.003, NS P = 0.052, and NS P = 0.79, by 2-tailed, unpaired Student’s t test. (K) Relative lipid ROS in 4T1 cells primed with or without 200 nM Pros1 for 24 hours and then treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). ¶P = 0.013 and ****P < 0.0001, by 2-tailed, unpaired Student’s t test. (L) Relative lipid ROS in 4T1 Tyro3−/− cells primed with or without 200 nM Pros1 for 24 hours and then treated with 10 μM erastin and/or 10 μM Fer-1 for 8 hours (n = 3). NS P = 0.059, NS P = 0.53, and NS P = 0.58, by 2-tailed, unpaired Student’s t test. Data are presented as the mean ± SD.

Article Snippet: Paraffin-embedded tissue array slides containing melanoma sections (ME804b, US Biomax) were pretreated using a Melanin Bleach Kit (24883-1, Polysciences) and stained with anti-SLC3A2 antibody (1:100; 47213S, Cell Signaling Technology) and anti-TYRO3 (1:100; OM223993, Omnimabs) as described above.

Techniques: Expressing, Luciferase, Reporter Assay, Plasmid Preparation

CGA regulates the relative expression level of ferroptosis proteins after HIBD in newborn mice. (A–F) Western blot of SLC7A11, FHC, FLC, SLC3A2, GLS2, and GSS expression in the cortex ( n = 4). β-Actin was used as an internal reference. (G) Cox-2 , Nrf2 , GSH and GPX4 mRNA levels in hippocampus tissue 24 hours after HIBD; GAPDH mRNA was used as a normalization control ( n = 3). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, vs . Sham + NS group; # P < 0.05, ## P < 0.01, vs . HI + NS group (one-way analysis of variance followed by Tukey’s post hoc test). CGA: Chlorogenic acid; COX2: cyclooxygenase-2; FHC: ferritin heavy chain; FLC: ferritin light chain; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GLS2: glutaminase 2; GSH: L-glutathione; GSS: glutathione synthase; HI or HIBD: hypoxic-ischemic brain injury; Nrf2: nuclear factor (erythroid-derived 2)-like 2; NS: normal saline; SLC3A2: solute carrier family 3 member 2; SLC7A11: solute carrier family 7 member 11.

Journal: Neural Regeneration Research

Article Title: Chlorogenic acid alleviates hypoxic-ischemic brain injury in neonatal mice

doi: 10.4103/1673-5374.350203

Figure Lengend Snippet: CGA regulates the relative expression level of ferroptosis proteins after HIBD in newborn mice. (A–F) Western blot of SLC7A11, FHC, FLC, SLC3A2, GLS2, and GSS expression in the cortex ( n = 4). β-Actin was used as an internal reference. (G) Cox-2 , Nrf2 , GSH and GPX4 mRNA levels in hippocampus tissue 24 hours after HIBD; GAPDH mRNA was used as a normalization control ( n = 3). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, vs . Sham + NS group; # P < 0.05, ## P < 0.01, vs . HI + NS group (one-way analysis of variance followed by Tukey’s post hoc test). CGA: Chlorogenic acid; COX2: cyclooxygenase-2; FHC: ferritin heavy chain; FLC: ferritin light chain; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GLS2: glutaminase 2; GSH: L-glutathione; GSS: glutathione synthase; HI or HIBD: hypoxic-ischemic brain injury; Nrf2: nuclear factor (erythroid-derived 2)-like 2; NS: normal saline; SLC3A2: solute carrier family 3 member 2; SLC7A11: solute carrier family 7 member 11.

Article Snippet: The primary antibodies used included rabbit anti-4-hydroxynonenal (4-HNE; 1:2000, Abcam, Cat#ab46545, RRID: AB_722490), rabbit anti-glutathione peroxidase 4 (GPX4; 1:100, ABclonal, Wuhan, China, Cat# a1933, RRID:AB_2763960), rabbit anti-solute carrier family 3 member 2 (SLC3A2; 1:200, ABclonal, Cat# a5702, RRID:AB_2766461), rabbit anti-solute carrier family 7 member 11 (SLC7A11; 1:1000, ABclonal, Cat# a15604, RRID:AB_2763010), rabbit anti-glutaminase 2 (GLS2; 1:1000, ABclonal, Cat# a16029, RRID:AB_2763466), rabbit anti-glutathione synthase (GSS; 1:2000, ABclonal, Cat# a14535, RRID: AB_2861700), rabbit anti-ferritin light chain (FLC; 1:2000, Cat# a11241, ABclonal, RRID:AB_2861532), and rabbit anti-ferritin heavy chain (FHC; 1:2000, ABclonal, Cat# a1144, RRID: AB_2758562).

Techniques: Expressing, Western Blot, Derivative Assay

CGA exerts neuroprotection via the system Xc – /GPX4 axis. (A–D) Western blot analysis of SLC3A2, SLC7A11, GSS, and GPX4 in the cortex. β-Actin was used as an internal reference. (E–H) Quantitative analyses of SLC3A2, SLC7A11, GSS, and GPX4 expression normalized with β-actin in the cortex. (I) The MDA level in the cortex. Data are presented as mean ± SEM ( n = 4). * P < 0.05, ** P < 0.01 (one-way analysis of variance followed by Tukey’s post hoc test). CGA: Chlorogenic acid; GPX4: glutathione peroxidase 4; GSS: glutathione synthase; HI or HIBD: hypoxic-ischemic brain injury; MDA: malondialdehyde; SLC3A2: solute carrier family 3 member 2; SLC7A11: solute carrier family 7 member 11.

Journal: Neural Regeneration Research

Article Title: Chlorogenic acid alleviates hypoxic-ischemic brain injury in neonatal mice

doi: 10.4103/1673-5374.350203

Figure Lengend Snippet: CGA exerts neuroprotection via the system Xc – /GPX4 axis. (A–D) Western blot analysis of SLC3A2, SLC7A11, GSS, and GPX4 in the cortex. β-Actin was used as an internal reference. (E–H) Quantitative analyses of SLC3A2, SLC7A11, GSS, and GPX4 expression normalized with β-actin in the cortex. (I) The MDA level in the cortex. Data are presented as mean ± SEM ( n = 4). * P < 0.05, ** P < 0.01 (one-way analysis of variance followed by Tukey’s post hoc test). CGA: Chlorogenic acid; GPX4: glutathione peroxidase 4; GSS: glutathione synthase; HI or HIBD: hypoxic-ischemic brain injury; MDA: malondialdehyde; SLC3A2: solute carrier family 3 member 2; SLC7A11: solute carrier family 7 member 11.

Article Snippet: The primary antibodies used included rabbit anti-4-hydroxynonenal (4-HNE; 1:2000, Abcam, Cat#ab46545, RRID: AB_722490), rabbit anti-glutathione peroxidase 4 (GPX4; 1:100, ABclonal, Wuhan, China, Cat# a1933, RRID:AB_2763960), rabbit anti-solute carrier family 3 member 2 (SLC3A2; 1:200, ABclonal, Cat# a5702, RRID:AB_2766461), rabbit anti-solute carrier family 7 member 11 (SLC7A11; 1:1000, ABclonal, Cat# a15604, RRID:AB_2763010), rabbit anti-glutaminase 2 (GLS2; 1:1000, ABclonal, Cat# a16029, RRID:AB_2763466), rabbit anti-glutathione synthase (GSS; 1:2000, ABclonal, Cat# a14535, RRID: AB_2861700), rabbit anti-ferritin light chain (FLC; 1:2000, Cat# a11241, ABclonal, RRID:AB_2861532), and rabbit anti-ferritin heavy chain (FHC; 1:2000, ABclonal, Cat# a1144, RRID: AB_2758562).

Techniques: Western Blot, Expressing

Schematic model for the mechanism of CGA in HIE. CGA inhibits ferroptosis by activating the system Xc – /GPX4 axis after HI. CGA: Chlorogenic acid; GCL: glutamate cysteine ligase; GLS: glutaminase; GPX4: glutathione peroxidase 4; GSH: L-glutathione; GSS: glutathione synthase; GSSG: L-glutathione oxidized; HIE: hypoxic-ischemic encephalopathy; ROS: reactive oxygen species; SLC3A2: solute carrier family 3 member 2; SLC7A11: solute carrier family 7 member 11; Xc – : the glutamate/cystine antiporter.

Journal: Neural Regeneration Research

Article Title: Chlorogenic acid alleviates hypoxic-ischemic brain injury in neonatal mice

doi: 10.4103/1673-5374.350203

Figure Lengend Snippet: Schematic model for the mechanism of CGA in HIE. CGA inhibits ferroptosis by activating the system Xc – /GPX4 axis after HI. CGA: Chlorogenic acid; GCL: glutamate cysteine ligase; GLS: glutaminase; GPX4: glutathione peroxidase 4; GSH: L-glutathione; GSS: glutathione synthase; GSSG: L-glutathione oxidized; HIE: hypoxic-ischemic encephalopathy; ROS: reactive oxygen species; SLC3A2: solute carrier family 3 member 2; SLC7A11: solute carrier family 7 member 11; Xc – : the glutamate/cystine antiporter.

Article Snippet: The primary antibodies used included rabbit anti-4-hydroxynonenal (4-HNE; 1:2000, Abcam, Cat#ab46545, RRID: AB_722490), rabbit anti-glutathione peroxidase 4 (GPX4; 1:100, ABclonal, Wuhan, China, Cat# a1933, RRID:AB_2763960), rabbit anti-solute carrier family 3 member 2 (SLC3A2; 1:200, ABclonal, Cat# a5702, RRID:AB_2766461), rabbit anti-solute carrier family 7 member 11 (SLC7A11; 1:1000, ABclonal, Cat# a15604, RRID:AB_2763010), rabbit anti-glutaminase 2 (GLS2; 1:1000, ABclonal, Cat# a16029, RRID:AB_2763466), rabbit anti-glutathione synthase (GSS; 1:2000, ABclonal, Cat# a14535, RRID: AB_2861700), rabbit anti-ferritin light chain (FLC; 1:2000, Cat# a11241, ABclonal, RRID:AB_2861532), and rabbit anti-ferritin heavy chain (FHC; 1:2000, ABclonal, Cat# a1144, RRID: AB_2758562).

Techniques: