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anti slc3a2  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc anti slc3a2
    Anti Slc3a2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 845 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+slc3a2/HIF-1alpha+XP+Rabbit+mAb/pm41894392-381-15-16
    Average 97 stars, based on 845 article reviews
    anti slc3a2 - by Bioz Stars, 2026-11
    97/100 stars

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    Article Title: mTORC1 activity is supported by spatial association with focal adhesions
    Article Snippet: The following primary antibodies were used: rabbit anti–phospho-S6 Ser235/236 (1:200; 4856, Cell Signaling Technology), rabbit anti-S6 (1:1,000; 2217, Cell Signaling Technology), rabbit anti–phospho-4EBP1 Thr37/46 (1:200; 2855, Cell Signaling Technology), rabbit anti-mTOR (1:200; 2972, Cell Signaling Technology), rabbit anti-LAMP1 (1:1,000; ab24170, Abcam), mouse anti-LAMP1 (1:1,000; Developmental Studies Hybridoma Bank), mouse anti-paxillin (1:400; 610055, BD Biosciences, which was discontinued during the course of the project), mouse anti-paxillin (5H11) (1:1,000; AHO0492, Sigma-Aldrich), rabbit anti–phospho-EGFR Tyr1016 (1:1,000; STJ91037, St John’s), rabbit anti-EGFR (1:1,000; STJ96946, St John’s), rabbit anti–phospho-IGFR1 Tyr1165/1166 (1:1,000; STJ90299, St John’s), rabbit anti-SLC3A2 (1:200; 47213, Cell Signaling Technology), rabbit anti–phospho-AKT1 Thr308 (1:100; 2965, Cell Signaling Technology) and rat anti-LAMP1 (for mouse cells, 1:1,000; Developmental Studies Hybridoma Bank).

    Western Blot:

    Article Title: A synthetic agent ameliorates polycystic kidney disease by promoting apoptosis of cystic cells through increased oxidative stress
    Article Snippet: .. Immunoblotting Immunoblotting was performed in the renal tissues to deduce the extent of ferroptosis and inflammation using antibodies as follows: rabbit anti- FTH1 (1:1000, Cell Signal Technology, catalog no. 4393), rabbit anti- Slc7a11 (1:1000, Cell Signal Technology, catalog no. 12691), rabbit anti-Nrf2 (1:1000, Cell Signal Technology, catalog no. 12721), rabbit-keap1 (1:1000, Cell Signal Technology, catalog no. 8047), rabbit anti-Slc3a2 (1:1000, Cell Signal Technology, catalog no. 47213), and rabbit anti-IL1β (1:1000, Cell Signal Technology, catalog no. 31202). ..

    Cell-Signaling:

    Article Title: mTORC1 activity is supported by spatial association with focal adhesions
    Article Snippet: .. Then, cell bodies were removed with hydrodynamic force, and FAs were fixed and immunostained using mouse anti-paxillin (5H11; 1:1,000; AHO0492; Sigma-Aldrich), rabbit anti–phospho-EGFR Tyr1016 (1:1,000; STJ91037; St John’s), rabbit anti–phospho-IGFR1 Tyr1165/1166 (1:1,000; STJ90299; St John’s), and rabbit anti-SLC3A2 (1:200; 47213; Cell Signaling Technology) antibodies. .. Proximal associations of mTOR with paxillin were detected using Duolink in situ PLA technology (Sigma-Aldrich) following the manufacturer’s instructions.

    Article Title: mTORC1 activity is supported by spatial association with focal adhesions
    Article Snippet: .. The following primary antibodies were used: rabbit anti–phospho-S6 Ser235/236 (1:200; 4856; Cell Signaling Technology), rabbit anti-S6 (1:1,000; 2217; Cell Signaling Technology), rabbit anti-mTOR (1:200; 2972; Cell Signaling Technology), rabbit anti-LAMP1 (1:1,000; ab24170; Abcam), mouse anti-LAMP1 (1:1,000; Developmental Studies Hybridoma Bank), mouse anti-paxillin (1:400; 610055; BD Biosciences, which was discontinued during the course of the project), mouse anti-paxillin (5H11; 1:1,000; AHO0492; Sigma-Aldrich), rabbit anti–phospho-EGFR Tyr1016 (1:1,000; STJ91037; St John’s), rabbit anti-EGFR (1:1,000; STJ96946; St John’s), rabbit anti–phospho-IGFR1 Tyr1165/1166 (1:1,000; STJ90299; St John’s), rabbit anti-SLC3A2 (1:200; 47213; Cell Signaling Technology), and rat anti-LAMP1 (for mouse cells, 1:1,000; Developmental Studies Hybridoma Bank). .. Cells were washed and incubated with the appropriate secondary antibodies (1:1,000; Thermo Fisher Scientific) for 1 h at room temperature.



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    Derepression of ferroptosis decreases cell proliferation in PSC (A) Western blot showing the knockdown efficiency of <t>SLC3A2</t> and FTL in PLA-801D cells. (B) The cell proliferation of PLA-801D cells measured using CCK-8 assays following the knockdown of SLC3A2 (left) and FTL (right), respectively. (C) The cell proliferation of PLA-801D cells measured using colony formation assays following the knockdown of SLC3A2 (upper) and FTL (bottom), respectively. Following the knockdown of SLC3A2 or FTL , PLA-801D cells were plated and cultured for 14 days. All colonies were subsequently stained with crystal violet and quantified using ImageJ software. (D) The extracellular GSH concentration of PLA-801D cells was tested following the knockdown of SLC3A2 . (E) Following the knockdown of FTL , PLA-801D cells were stained by FerroOrange and quantified using the microplate reader, respectively. (F) The lysates of PLA-801D cells were immunoblotted with the indicated antibodies following the knockdown of FTL . (G) Following the knockdown of SLC3A2 , PLA-801D cells were treated with 10 μM ferrostatin-1 for 24 h. Afterward, the extracellular GSH concentration was tested. (H) Following the knockdown of FTL , PLA-801D cells were treated with 10 μM ferrostatin-1 for 24 h. Then the lysates of PLA-801D cells were immunoblotted with the indicated antibodies. (I) Following the knockdown of SLC3A2 (left) or FTL (right), PLA-801D cells were treated with DMSO or 10 μM ferrostatin-1 for 24 h. Then the cell proliferation of PLA-801D cells was detected by CCK-8 assays, respectively. (J and K) Following the knockdown of SLC3A2 (left) or FTL (right), PLA-801D cells were treated with DMSO or 10 μM ferrostatin-1 for 24 h. Then the fluorescent probes were added into the culture medium to test the relative level of ROS, respectively (J); the cell lysates were collected for bicinchoninic acid assay and the detection of lipid peroxidation MDA (K). (L) The graphic model of the repressed ferroptosis in PSC. NC, negative control; ns, not significant; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.
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    Derepression of ferroptosis decreases cell proliferation in PSC (A) Western blot showing the knockdown efficiency of <t>SLC3A2</t> and FTL in PLA-801D cells. (B) The cell proliferation of PLA-801D cells measured using CCK-8 assays following the knockdown of SLC3A2 (left) and FTL (right), respectively. (C) The cell proliferation of PLA-801D cells measured using colony formation assays following the knockdown of SLC3A2 (upper) and FTL (bottom), respectively. Following the knockdown of SLC3A2 or FTL , PLA-801D cells were plated and cultured for 14 days. All colonies were subsequently stained with crystal violet and quantified using ImageJ software. (D) The extracellular GSH concentration of PLA-801D cells was tested following the knockdown of SLC3A2 . (E) Following the knockdown of FTL , PLA-801D cells were stained by FerroOrange and quantified using the microplate reader, respectively. (F) The lysates of PLA-801D cells were immunoblotted with the indicated antibodies following the knockdown of FTL . (G) Following the knockdown of SLC3A2 , PLA-801D cells were treated with 10 μM ferrostatin-1 for 24 h. Afterward, the extracellular GSH concentration was tested. (H) Following the knockdown of FTL , PLA-801D cells were treated with 10 μM ferrostatin-1 for 24 h. Then the lysates of PLA-801D cells were immunoblotted with the indicated antibodies. (I) Following the knockdown of SLC3A2 (left) or FTL (right), PLA-801D cells were treated with DMSO or 10 μM ferrostatin-1 for 24 h. Then the cell proliferation of PLA-801D cells was detected by CCK-8 assays, respectively. (J and K) Following the knockdown of SLC3A2 (left) or FTL (right), PLA-801D cells were treated with DMSO or 10 μM ferrostatin-1 for 24 h. Then the fluorescent probes were added into the culture medium to test the relative level of ROS, respectively (J); the cell lysates were collected for bicinchoninic acid assay and the detection of lipid peroxidation MDA (K). (L) The graphic model of the repressed ferroptosis in PSC. NC, negative control; ns, not significant; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.
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    Derepression of ferroptosis decreases cell proliferation in PSC (A) Western blot showing the knockdown efficiency of <t>SLC3A2</t> and FTL in PLA-801D cells. (B) The cell proliferation of PLA-801D cells measured using CCK-8 assays following the knockdown of SLC3A2 (left) and FTL (right), respectively. (C) The cell proliferation of PLA-801D cells measured using colony formation assays following the knockdown of SLC3A2 (upper) and FTL (bottom), respectively. Following the knockdown of SLC3A2 or FTL , PLA-801D cells were plated and cultured for 14 days. All colonies were subsequently stained with crystal violet and quantified using ImageJ software. (D) The extracellular GSH concentration of PLA-801D cells was tested following the knockdown of SLC3A2 . (E) Following the knockdown of FTL , PLA-801D cells were stained by FerroOrange and quantified using the microplate reader, respectively. (F) The lysates of PLA-801D cells were immunoblotted with the indicated antibodies following the knockdown of FTL . (G) Following the knockdown of SLC3A2 , PLA-801D cells were treated with 10 μM ferrostatin-1 for 24 h. Afterward, the extracellular GSH concentration was tested. (H) Following the knockdown of FTL , PLA-801D cells were treated with 10 μM ferrostatin-1 for 24 h. Then the lysates of PLA-801D cells were immunoblotted with the indicated antibodies. (I) Following the knockdown of SLC3A2 (left) or FTL (right), PLA-801D cells were treated with DMSO or 10 μM ferrostatin-1 for 24 h. Then the cell proliferation of PLA-801D cells was detected by CCK-8 assays, respectively. (J and K) Following the knockdown of SLC3A2 (left) or FTL (right), PLA-801D cells were treated with DMSO or 10 μM ferrostatin-1 for 24 h. Then the fluorescent probes were added into the culture medium to test the relative level of ROS, respectively (J); the cell lysates were collected for bicinchoninic acid assay and the detection of lipid peroxidation MDA (K). (L) The graphic model of the repressed ferroptosis in PSC. NC, negative control; ns, not significant; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.
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    Image Search Results


    Derepression of ferroptosis decreases cell proliferation in PSC (A) Western blot showing the knockdown efficiency of SLC3A2 and FTL in PLA-801D cells. (B) The cell proliferation of PLA-801D cells measured using CCK-8 assays following the knockdown of SLC3A2 (left) and FTL (right), respectively. (C) The cell proliferation of PLA-801D cells measured using colony formation assays following the knockdown of SLC3A2 (upper) and FTL (bottom), respectively. Following the knockdown of SLC3A2 or FTL , PLA-801D cells were plated and cultured for 14 days. All colonies were subsequently stained with crystal violet and quantified using ImageJ software. (D) The extracellular GSH concentration of PLA-801D cells was tested following the knockdown of SLC3A2 . (E) Following the knockdown of FTL , PLA-801D cells were stained by FerroOrange and quantified using the microplate reader, respectively. (F) The lysates of PLA-801D cells were immunoblotted with the indicated antibodies following the knockdown of FTL . (G) Following the knockdown of SLC3A2 , PLA-801D cells were treated with 10 μM ferrostatin-1 for 24 h. Afterward, the extracellular GSH concentration was tested. (H) Following the knockdown of FTL , PLA-801D cells were treated with 10 μM ferrostatin-1 for 24 h. Then the lysates of PLA-801D cells were immunoblotted with the indicated antibodies. (I) Following the knockdown of SLC3A2 (left) or FTL (right), PLA-801D cells were treated with DMSO or 10 μM ferrostatin-1 for 24 h. Then the cell proliferation of PLA-801D cells was detected by CCK-8 assays, respectively. (J and K) Following the knockdown of SLC3A2 (left) or FTL (right), PLA-801D cells were treated with DMSO or 10 μM ferrostatin-1 for 24 h. Then the fluorescent probes were added into the culture medium to test the relative level of ROS, respectively (J); the cell lysates were collected for bicinchoninic acid assay and the detection of lipid peroxidation MDA (K). (L) The graphic model of the repressed ferroptosis in PSC. NC, negative control; ns, not significant; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.

    Journal: Cell Reports Medicine

    Article Title: Multi-omics profiling unveils biological and clinical insights into pulmonary sarcomatoid carcinoma

    doi: 10.1016/j.xcrm.2026.102887

    Figure Lengend Snippet: Derepression of ferroptosis decreases cell proliferation in PSC (A) Western blot showing the knockdown efficiency of SLC3A2 and FTL in PLA-801D cells. (B) The cell proliferation of PLA-801D cells measured using CCK-8 assays following the knockdown of SLC3A2 (left) and FTL (right), respectively. (C) The cell proliferation of PLA-801D cells measured using colony formation assays following the knockdown of SLC3A2 (upper) and FTL (bottom), respectively. Following the knockdown of SLC3A2 or FTL , PLA-801D cells were plated and cultured for 14 days. All colonies were subsequently stained with crystal violet and quantified using ImageJ software. (D) The extracellular GSH concentration of PLA-801D cells was tested following the knockdown of SLC3A2 . (E) Following the knockdown of FTL , PLA-801D cells were stained by FerroOrange and quantified using the microplate reader, respectively. (F) The lysates of PLA-801D cells were immunoblotted with the indicated antibodies following the knockdown of FTL . (G) Following the knockdown of SLC3A2 , PLA-801D cells were treated with 10 μM ferrostatin-1 for 24 h. Afterward, the extracellular GSH concentration was tested. (H) Following the knockdown of FTL , PLA-801D cells were treated with 10 μM ferrostatin-1 for 24 h. Then the lysates of PLA-801D cells were immunoblotted with the indicated antibodies. (I) Following the knockdown of SLC3A2 (left) or FTL (right), PLA-801D cells were treated with DMSO or 10 μM ferrostatin-1 for 24 h. Then the cell proliferation of PLA-801D cells was detected by CCK-8 assays, respectively. (J and K) Following the knockdown of SLC3A2 (left) or FTL (right), PLA-801D cells were treated with DMSO or 10 μM ferrostatin-1 for 24 h. Then the fluorescent probes were added into the culture medium to test the relative level of ROS, respectively (J); the cell lysates were collected for bicinchoninic acid assay and the detection of lipid peroxidation MDA (K). (L) The graphic model of the repressed ferroptosis in PSC. NC, negative control; ns, not significant; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.

    Article Snippet: Cells were lysed with 1% Triton X-100 buffer (Beyotime, ST1723) and then boiled in 5× loading buffer for 10 min. Each sample was electrophoresed on 10% PAGE gels, then transferred to PVDF membranes and immunoblotted with the antibodies targeting SLC3A2 (Abclonal, A24375), FTL (Abclonal, A11241), GPX4 (Abclonal, A1933) and β-Actin (Abclonal, AC004).

    Techniques: Western Blot, Knockdown, CCK-8 Assay, Cell Culture, Staining, Software, Concentration Assay, Acid Assay, Negative Control