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recombinant human il 1 α protein  (Bio-Techne corporation)


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    Bio-Techne corporation recombinant human il 1 α protein
    ASCT2 drives the proinflammatory SASP via <t>IL-1</t> α /NF- κ B feedback loop through interacting with precursor IL-1 α at Lys82 of senescent HSCs. (A) Protein of p31–IL-1 α and p16–IL-1 α was measured by Western blot analysis with 4-OHT ( n = 3 per group). (B) Detection of intracellular IL-1 α by ELISA with 4-OHT ( n = 3 per group). (C) mRNAs of proinflammatory SASP including IL1A , IL1B , IL6 and IL8 were measured by qPCR ( n = 5 per group). (D) Co-IP of ASCT2 with IL-1 α in LX2 cells, as detected by Western blot analysis ( n = 3 per group). (E) Schematic of fragments of IL-1 α that were fused to GST (top) and were transfection into 293T cells. Binding of ASCT2 to GST-IL-1 α proteins was detected by Western blot (bottom, n = 3 per group). FL: full length; F1: domain 1–112; F2: domain 112–271; F3: NLS domain (80–88) deletion; F4: K82N mutation. (F) rIL-1 <t>α</t> <t>protein</t> was added to senescent (ASCT2 depletion or etoposide treatment) LX2 cells, and IL1R1 signaling cascade indicators were analyzed by Western blotting ( n = 3 per group). (G) rIL-1 α protein was added to senescent (ASCT2 depletion or etoposide treatment) LX2 cells, and NF- κ B protein was measured in nuclear and cytoplasmic lysates by Western blot ( n = 3 per group). (H) Relative luciferase measurement of NF- κ B in indicated cells ( n = 5–6 per group). (I) ASCT2 depletion-senescent LX2 cells were treated with rIL-1 α protein and addressed in NF- κ B inhibitor PDTC, and the analysis of mRNAs of proinflammatory SASP IL1A , IL1B , IL6 and IL8 by qPCR ( n = 5–6 per group). Bars indicate mean ± SEM; ∗ P < 0.05, ∗∗ P < 0.01; ns, no significance.
    Recombinant Human Il 1 α Protein, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 95/100, based on 133 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant human il 1 α protein/product/Bio-Techne corporation
    Average 95 stars, based on 133 article reviews
    recombinant human il 1 α protein - by Bioz Stars, 2026-04
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    1) Product Images from "Inhibition of ASCT2 induces hepatic stellate cell senescence with modified proinflammatory secretome through an IL-1 α /NF- κ B feedback pathway to inhibit liver fibrosis"

    Article Title: Inhibition of ASCT2 induces hepatic stellate cell senescence with modified proinflammatory secretome through an IL-1 α /NF- κ B feedback pathway to inhibit liver fibrosis

    Journal: Acta Pharmaceutica Sinica. B

    doi: 10.1016/j.apsb.2022.03.014

    ASCT2 drives the proinflammatory SASP via IL-1 α /NF- κ B feedback loop through interacting with precursor IL-1 α at Lys82 of senescent HSCs. (A) Protein of p31–IL-1 α and p16–IL-1 α was measured by Western blot analysis with 4-OHT ( n = 3 per group). (B) Detection of intracellular IL-1 α by ELISA with 4-OHT ( n = 3 per group). (C) mRNAs of proinflammatory SASP including IL1A , IL1B , IL6 and IL8 were measured by qPCR ( n = 5 per group). (D) Co-IP of ASCT2 with IL-1 α in LX2 cells, as detected by Western blot analysis ( n = 3 per group). (E) Schematic of fragments of IL-1 α that were fused to GST (top) and were transfection into 293T cells. Binding of ASCT2 to GST-IL-1 α proteins was detected by Western blot (bottom, n = 3 per group). FL: full length; F1: domain 1–112; F2: domain 112–271; F3: NLS domain (80–88) deletion; F4: K82N mutation. (F) rIL-1 α protein was added to senescent (ASCT2 depletion or etoposide treatment) LX2 cells, and IL1R1 signaling cascade indicators were analyzed by Western blotting ( n = 3 per group). (G) rIL-1 α protein was added to senescent (ASCT2 depletion or etoposide treatment) LX2 cells, and NF- κ B protein was measured in nuclear and cytoplasmic lysates by Western blot ( n = 3 per group). (H) Relative luciferase measurement of NF- κ B in indicated cells ( n = 5–6 per group). (I) ASCT2 depletion-senescent LX2 cells were treated with rIL-1 α protein and addressed in NF- κ B inhibitor PDTC, and the analysis of mRNAs of proinflammatory SASP IL1A , IL1B , IL6 and IL8 by qPCR ( n = 5–6 per group). Bars indicate mean ± SEM; ∗ P < 0.05, ∗∗ P < 0.01; ns, no significance.
    Figure Legend Snippet: ASCT2 drives the proinflammatory SASP via IL-1 α /NF- κ B feedback loop through interacting with precursor IL-1 α at Lys82 of senescent HSCs. (A) Protein of p31–IL-1 α and p16–IL-1 α was measured by Western blot analysis with 4-OHT ( n = 3 per group). (B) Detection of intracellular IL-1 α by ELISA with 4-OHT ( n = 3 per group). (C) mRNAs of proinflammatory SASP including IL1A , IL1B , IL6 and IL8 were measured by qPCR ( n = 5 per group). (D) Co-IP of ASCT2 with IL-1 α in LX2 cells, as detected by Western blot analysis ( n = 3 per group). (E) Schematic of fragments of IL-1 α that were fused to GST (top) and were transfection into 293T cells. Binding of ASCT2 to GST-IL-1 α proteins was detected by Western blot (bottom, n = 3 per group). FL: full length; F1: domain 1–112; F2: domain 112–271; F3: NLS domain (80–88) deletion; F4: K82N mutation. (F) rIL-1 α protein was added to senescent (ASCT2 depletion or etoposide treatment) LX2 cells, and IL1R1 signaling cascade indicators were analyzed by Western blotting ( n = 3 per group). (G) rIL-1 α protein was added to senescent (ASCT2 depletion or etoposide treatment) LX2 cells, and NF- κ B protein was measured in nuclear and cytoplasmic lysates by Western blot ( n = 3 per group). (H) Relative luciferase measurement of NF- κ B in indicated cells ( n = 5–6 per group). (I) ASCT2 depletion-senescent LX2 cells were treated with rIL-1 α protein and addressed in NF- κ B inhibitor PDTC, and the analysis of mRNAs of proinflammatory SASP IL1A , IL1B , IL6 and IL8 by qPCR ( n = 5–6 per group). Bars indicate mean ± SEM; ∗ P < 0.05, ∗∗ P < 0.01; ns, no significance.

    Techniques Used: Western Blot, Enzyme-linked Immunosorbent Assay, Co-Immunoprecipitation Assay, Transfection, Binding Assay, Mutagenesis, Luciferase



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    ASCT2 drives the proinflammatory SASP via <t>IL-1</t> α /NF- κ B feedback loop through interacting with precursor IL-1 α at Lys82 of senescent HSCs. (A) Protein of p31–IL-1 α and p16–IL-1 α was measured by Western blot analysis with 4-OHT ( n = 3 per group). (B) Detection of intracellular IL-1 α by ELISA with 4-OHT ( n = 3 per group). (C) mRNAs of proinflammatory SASP including IL1A , IL1B , IL6 and IL8 were measured by qPCR ( n = 5 per group). (D) Co-IP of ASCT2 with IL-1 α in LX2 cells, as detected by Western blot analysis ( n = 3 per group). (E) Schematic of fragments of IL-1 α that were fused to GST (top) and were transfection into 293T cells. Binding of ASCT2 to GST-IL-1 α proteins was detected by Western blot (bottom, n = 3 per group). FL: full length; F1: domain 1–112; F2: domain 112–271; F3: NLS domain (80–88) deletion; F4: K82N mutation. (F) rIL-1 <t>α</t> <t>protein</t> was added to senescent (ASCT2 depletion or etoposide treatment) LX2 cells, and IL1R1 signaling cascade indicators were analyzed by Western blotting ( n = 3 per group). (G) rIL-1 α protein was added to senescent (ASCT2 depletion or etoposide treatment) LX2 cells, and NF- κ B protein was measured in nuclear and cytoplasmic lysates by Western blot ( n = 3 per group). (H) Relative luciferase measurement of NF- κ B in indicated cells ( n = 5–6 per group). (I) ASCT2 depletion-senescent LX2 cells were treated with rIL-1 α protein and addressed in NF- κ B inhibitor PDTC, and the analysis of mRNAs of proinflammatory SASP IL1A , IL1B , IL6 and IL8 by qPCR ( n = 5–6 per group). Bars indicate mean ± SEM; ∗ P < 0.05, ∗∗ P < 0.01; ns, no significance.
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    ASCT2 drives the proinflammatory SASP via IL-1 α /NF- κ B feedback loop through interacting with precursor IL-1 α at Lys82 of senescent HSCs. (A) Protein of p31–IL-1 α and p16–IL-1 α was measured by Western blot analysis with 4-OHT ( n = 3 per group). (B) Detection of intracellular IL-1 α by ELISA with 4-OHT ( n = 3 per group). (C) mRNAs of proinflammatory SASP including IL1A , IL1B , IL6 and IL8 were measured by qPCR ( n = 5 per group). (D) Co-IP of ASCT2 with IL-1 α in LX2 cells, as detected by Western blot analysis ( n = 3 per group). (E) Schematic of fragments of IL-1 α that were fused to GST (top) and were transfection into 293T cells. Binding of ASCT2 to GST-IL-1 α proteins was detected by Western blot (bottom, n = 3 per group). FL: full length; F1: domain 1–112; F2: domain 112–271; F3: NLS domain (80–88) deletion; F4: K82N mutation. (F) rIL-1 α protein was added to senescent (ASCT2 depletion or etoposide treatment) LX2 cells, and IL1R1 signaling cascade indicators were analyzed by Western blotting ( n = 3 per group). (G) rIL-1 α protein was added to senescent (ASCT2 depletion or etoposide treatment) LX2 cells, and NF- κ B protein was measured in nuclear and cytoplasmic lysates by Western blot ( n = 3 per group). (H) Relative luciferase measurement of NF- κ B in indicated cells ( n = 5–6 per group). (I) ASCT2 depletion-senescent LX2 cells were treated with rIL-1 α protein and addressed in NF- κ B inhibitor PDTC, and the analysis of mRNAs of proinflammatory SASP IL1A , IL1B , IL6 and IL8 by qPCR ( n = 5–6 per group). Bars indicate mean ± SEM; ∗ P < 0.05, ∗∗ P < 0.01; ns, no significance.

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: Inhibition of ASCT2 induces hepatic stellate cell senescence with modified proinflammatory secretome through an IL-1 α /NF- κ B feedback pathway to inhibit liver fibrosis

    doi: 10.1016/j.apsb.2022.03.014

    Figure Lengend Snippet: ASCT2 drives the proinflammatory SASP via IL-1 α /NF- κ B feedback loop through interacting with precursor IL-1 α at Lys82 of senescent HSCs. (A) Protein of p31–IL-1 α and p16–IL-1 α was measured by Western blot analysis with 4-OHT ( n = 3 per group). (B) Detection of intracellular IL-1 α by ELISA with 4-OHT ( n = 3 per group). (C) mRNAs of proinflammatory SASP including IL1A , IL1B , IL6 and IL8 were measured by qPCR ( n = 5 per group). (D) Co-IP of ASCT2 with IL-1 α in LX2 cells, as detected by Western blot analysis ( n = 3 per group). (E) Schematic of fragments of IL-1 α that were fused to GST (top) and were transfection into 293T cells. Binding of ASCT2 to GST-IL-1 α proteins was detected by Western blot (bottom, n = 3 per group). FL: full length; F1: domain 1–112; F2: domain 112–271; F3: NLS domain (80–88) deletion; F4: K82N mutation. (F) rIL-1 α protein was added to senescent (ASCT2 depletion or etoposide treatment) LX2 cells, and IL1R1 signaling cascade indicators were analyzed by Western blotting ( n = 3 per group). (G) rIL-1 α protein was added to senescent (ASCT2 depletion or etoposide treatment) LX2 cells, and NF- κ B protein was measured in nuclear and cytoplasmic lysates by Western blot ( n = 3 per group). (H) Relative luciferase measurement of NF- κ B in indicated cells ( n = 5–6 per group). (I) ASCT2 depletion-senescent LX2 cells were treated with rIL-1 α protein and addressed in NF- κ B inhibitor PDTC, and the analysis of mRNAs of proinflammatory SASP IL1A , IL1B , IL6 and IL8 by qPCR ( n = 5–6 per group). Bars indicate mean ± SEM; ∗ P < 0.05, ∗∗ P < 0.01; ns, no significance.

    Article Snippet: Recombinant human IL-1 α protein (200-LA, protein for addition of IL-1 α ) was purchased from Bio-Techne (R&D Systems, Shanghai, China), the concentration used is 20 ng/mL in vitro .

    Techniques: Western Blot, Enzyme-linked Immunosorbent Assay, Co-Immunoprecipitation Assay, Transfection, Binding Assay, Mutagenesis, Luciferase