ire 1 inhibitor Search Results


4mu8c  (Bio-Techne corporation)
99
Bio-Techne corporation 4mu8c
4mu8c, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/4mu8c/product/Bio-Techne corporation
Average 99 stars, based on 1 article reviews
4mu8c - by Bioz Stars, 2026-06
99/100 stars
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ire1-specific inhibitor (mkc8866  (Mannkind Inc)
90
Mannkind Inc ire1-specific inhibitor (mkc8866
XBP splicing is required for TGF-β1-induced fibrosis in primary human IPF, but not non-IPF, fibroblasts. A: primary human non-IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of the IRE1α inhibitor <t>MKC8866</t> (10 μM) for the indicated time points. The representative immunoblot shows the abundance of collagen 1α2, fibronectin, and sXBP in 4 different primary non-IPF fibroblasts. B and C: densitometry analysis (n = 4) confirmed that MKC8866 did not significantly reduce TGF-β1-induced collagen 1α2 or fibronectin biosynthesis in non-IPF human fibroblasts. Data are shown in dot plots of from 4 individual experiments using different cell lines. The horizontal line in each column represents the mean, with error bars showing SE. NSP > 0.05, no significant difference. D: primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of <t>IRE1</t> inhibitor (10 μM) for the indicated time points. Immunoblots are arranged to show expression of collagen 1α2, fibronectin and sXBP. The immunoblot is representative of experiments performed on 4 different primary IPF fibroblasts (n = 4). E and F: densitometry analysis confirmed that treatment of IPF fibroblasts with IRE1 inhibitor significantly reduced TGF-β1-induced collagen 1α2 and fibronectin biosynthesis. Data are shown in dot plots of from 4 individual experiments using different cell lines. The horizontal line in each column represents the mean, with error bars showing SE. ***P < 0.001; **P < 0.01. G: primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of IRE1 inhibitor (10 μM) for 96 h. For a baseline control, cells were maintained in serum- and TGF-β1-deficient media. Quantitative PCR showed that MKC8866 significantly inhibited TGF-β1-induced fibronectin mRNA accumulation in IPF fibroblasts. The experiments were performed in duplicate on 2 different primary IPF fibroblast cell lines. Data are shown in dot plots from each experiment. The horizontal line in each column represents the mean, with error bars showing SE. ***P < 0.001.
Ire1 Specific Inhibitor (Mkc8866, supplied by Mannkind Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ire1-specific inhibitor (mkc8866/product/Mannkind Inc
Average 90 stars, based on 1 article reviews
ire1-specific inhibitor (mkc8866 - by Bioz Stars, 2026-06
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ire1 inhibitor irestatin 9389  (Axon Medchem LLC)
90
Axon Medchem LLC ire1 inhibitor irestatin 9389
XBP splicing is required for TGF-β1-induced fibrosis in primary human IPF, but not non-IPF, fibroblasts. A: primary human non-IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of the IRE1α inhibitor <t>MKC8866</t> (10 μM) for the indicated time points. The representative immunoblot shows the abundance of collagen 1α2, fibronectin, and sXBP in 4 different primary non-IPF fibroblasts. B and C: densitometry analysis (n = 4) confirmed that MKC8866 did not significantly reduce TGF-β1-induced collagen 1α2 or fibronectin biosynthesis in non-IPF human fibroblasts. Data are shown in dot plots of from 4 individual experiments using different cell lines. The horizontal line in each column represents the mean, with error bars showing SE. NSP > 0.05, no significant difference. D: primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of <t>IRE1</t> inhibitor (10 μM) for the indicated time points. Immunoblots are arranged to show expression of collagen 1α2, fibronectin and sXBP. The immunoblot is representative of experiments performed on 4 different primary IPF fibroblasts (n = 4). E and F: densitometry analysis confirmed that treatment of IPF fibroblasts with IRE1 inhibitor significantly reduced TGF-β1-induced collagen 1α2 and fibronectin biosynthesis. Data are shown in dot plots of from 4 individual experiments using different cell lines. The horizontal line in each column represents the mean, with error bars showing SE. ***P < 0.001; **P < 0.01. G: primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of IRE1 inhibitor (10 μM) for 96 h. For a baseline control, cells were maintained in serum- and TGF-β1-deficient media. Quantitative PCR showed that MKC8866 significantly inhibited TGF-β1-induced fibronectin mRNA accumulation in IPF fibroblasts. The experiments were performed in duplicate on 2 different primary IPF fibroblast cell lines. Data are shown in dot plots from each experiment. The horizontal line in each column represents the mean, with error bars showing SE. ***P < 0.001.
Ire1 Inhibitor Irestatin 9389, supplied by Axon Medchem LLC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ire1 inhibitor irestatin 9389/product/Axon Medchem LLC
Average 90 stars, based on 1 article reviews
ire1 inhibitor irestatin 9389 - by Bioz Stars, 2026-06
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ire1 α -specific inhibitor 4 μ 8c  (Topscience Co Ltd)
90
Topscience Co Ltd ire1 α -specific inhibitor 4 μ 8c
XBP splicing is required for TGF-β1-induced fibrosis in primary human IPF, but not non-IPF, fibroblasts. A: primary human non-IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of the IRE1α inhibitor <t>MKC8866</t> (10 μM) for the indicated time points. The representative immunoblot shows the abundance of collagen 1α2, fibronectin, and sXBP in 4 different primary non-IPF fibroblasts. B and C: densitometry analysis (n = 4) confirmed that MKC8866 did not significantly reduce TGF-β1-induced collagen 1α2 or fibronectin biosynthesis in non-IPF human fibroblasts. Data are shown in dot plots of from 4 individual experiments using different cell lines. The horizontal line in each column represents the mean, with error bars showing SE. NSP > 0.05, no significant difference. D: primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of <t>IRE1</t> inhibitor (10 μM) for the indicated time points. Immunoblots are arranged to show expression of collagen 1α2, fibronectin and sXBP. The immunoblot is representative of experiments performed on 4 different primary IPF fibroblasts (n = 4). E and F: densitometry analysis confirmed that treatment of IPF fibroblasts with IRE1 inhibitor significantly reduced TGF-β1-induced collagen 1α2 and fibronectin biosynthesis. Data are shown in dot plots of from 4 individual experiments using different cell lines. The horizontal line in each column represents the mean, with error bars showing SE. ***P < 0.001; **P < 0.01. G: primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of IRE1 inhibitor (10 μM) for 96 h. For a baseline control, cells were maintained in serum- and TGF-β1-deficient media. Quantitative PCR showed that MKC8866 significantly inhibited TGF-β1-induced fibronectin mRNA accumulation in IPF fibroblasts. The experiments were performed in duplicate on 2 different primary IPF fibroblast cell lines. Data are shown in dot plots from each experiment. The horizontal line in each column represents the mean, with error bars showing SE. ***P < 0.001.
Ire1 α Specific Inhibitor 4 μ 8c, supplied by Topscience Co Ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ire1 α -specific inhibitor 4 μ 8c/product/Topscience Co Ltd
Average 90 stars, based on 1 article reviews
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ire1 inhibitor mkc8866  (Amgen)
86
Amgen ire1 inhibitor mkc8866
XBP splicing is required for TGF-β1-induced fibrosis in primary human IPF, but not non-IPF, fibroblasts. A: primary human non-IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of the IRE1α inhibitor <t>MKC8866</t> (10 μM) for the indicated time points. The representative immunoblot shows the abundance of collagen 1α2, fibronectin, and sXBP in 4 different primary non-IPF fibroblasts. B and C: densitometry analysis (n = 4) confirmed that MKC8866 did not significantly reduce TGF-β1-induced collagen 1α2 or fibronectin biosynthesis in non-IPF human fibroblasts. Data are shown in dot plots of from 4 individual experiments using different cell lines. The horizontal line in each column represents the mean, with error bars showing SE. NSP > 0.05, no significant difference. D: primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of <t>IRE1</t> inhibitor (10 μM) for the indicated time points. Immunoblots are arranged to show expression of collagen 1α2, fibronectin and sXBP. The immunoblot is representative of experiments performed on 4 different primary IPF fibroblasts (n = 4). E and F: densitometry analysis confirmed that treatment of IPF fibroblasts with IRE1 inhibitor significantly reduced TGF-β1-induced collagen 1α2 and fibronectin biosynthesis. Data are shown in dot plots of from 4 individual experiments using different cell lines. The horizontal line in each column represents the mean, with error bars showing SE. ***P < 0.001; **P < 0.01. G: primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of IRE1 inhibitor (10 μM) for 96 h. For a baseline control, cells were maintained in serum- and TGF-β1-deficient media. Quantitative PCR showed that MKC8866 significantly inhibited TGF-β1-induced fibronectin mRNA accumulation in IPF fibroblasts. The experiments were performed in duplicate on 2 different primary IPF fibroblast cell lines. Data are shown in dot plots from each experiment. The horizontal line in each column represents the mean, with error bars showing SE. ***P < 0.001.
Ire1 Inhibitor Mkc8866, supplied by Amgen, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ire1 inhibitor mkc8866/product/Amgen
Average 86 stars, based on 1 article reviews
ire1 inhibitor mkc8866 - by Bioz Stars, 2026-06
86/100 stars
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amgen ire1± inhibitor  (Biosynth Carbosynth)
N/A
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Image Search Results


XBP splicing is required for TGF-β1-induced fibrosis in primary human IPF, but not non-IPF, fibroblasts. A: primary human non-IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of the IRE1α inhibitor MKC8866 (10 μM) for the indicated time points. The representative immunoblot shows the abundance of collagen 1α2, fibronectin, and sXBP in 4 different primary non-IPF fibroblasts. B and C: densitometry analysis (n = 4) confirmed that MKC8866 did not significantly reduce TGF-β1-induced collagen 1α2 or fibronectin biosynthesis in non-IPF human fibroblasts. Data are shown in dot plots of from 4 individual experiments using different cell lines. The horizontal line in each column represents the mean, with error bars showing SE. NSP > 0.05, no significant difference. D: primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of IRE1 inhibitor (10 μM) for the indicated time points. Immunoblots are arranged to show expression of collagen 1α2, fibronectin and sXBP. The immunoblot is representative of experiments performed on 4 different primary IPF fibroblasts (n = 4). E and F: densitometry analysis confirmed that treatment of IPF fibroblasts with IRE1 inhibitor significantly reduced TGF-β1-induced collagen 1α2 and fibronectin biosynthesis. Data are shown in dot plots of from 4 individual experiments using different cell lines. The horizontal line in each column represents the mean, with error bars showing SE. ***P < 0.001; **P < 0.01. G: primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of IRE1 inhibitor (10 μM) for 96 h. For a baseline control, cells were maintained in serum- and TGF-β1-deficient media. Quantitative PCR showed that MKC8866 significantly inhibited TGF-β1-induced fibronectin mRNA accumulation in IPF fibroblasts. The experiments were performed in duplicate on 2 different primary IPF fibroblast cell lines. Data are shown in dot plots from each experiment. The horizontal line in each column represents the mean, with error bars showing SE. ***P < 0.001.

Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

Article Title: Autophagy and the unfolded protein response promote profibrotic effects of TGF-β 1 in human lung fibroblasts

doi: 10.1152/ajplung.00372.2017

Figure Lengend Snippet: XBP splicing is required for TGF-β1-induced fibrosis in primary human IPF, but not non-IPF, fibroblasts. A: primary human non-IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of the IRE1α inhibitor MKC8866 (10 μM) for the indicated time points. The representative immunoblot shows the abundance of collagen 1α2, fibronectin, and sXBP in 4 different primary non-IPF fibroblasts. B and C: densitometry analysis (n = 4) confirmed that MKC8866 did not significantly reduce TGF-β1-induced collagen 1α2 or fibronectin biosynthesis in non-IPF human fibroblasts. Data are shown in dot plots of from 4 individual experiments using different cell lines. The horizontal line in each column represents the mean, with error bars showing SE. NSP > 0.05, no significant difference. D: primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of IRE1 inhibitor (10 μM) for the indicated time points. Immunoblots are arranged to show expression of collagen 1α2, fibronectin and sXBP. The immunoblot is representative of experiments performed on 4 different primary IPF fibroblasts (n = 4). E and F: densitometry analysis confirmed that treatment of IPF fibroblasts with IRE1 inhibitor significantly reduced TGF-β1-induced collagen 1α2 and fibronectin biosynthesis. Data are shown in dot plots of from 4 individual experiments using different cell lines. The horizontal line in each column represents the mean, with error bars showing SE. ***P < 0.001; **P < 0.01. G: primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of IRE1 inhibitor (10 μM) for 96 h. For a baseline control, cells were maintained in serum- and TGF-β1-deficient media. Quantitative PCR showed that MKC8866 significantly inhibited TGF-β1-induced fibronectin mRNA accumulation in IPF fibroblasts. The experiments were performed in duplicate on 2 different primary IPF fibroblast cell lines. Data are shown in dot plots from each experiment. The horizontal line in each column represents the mean, with error bars showing SE. ***P < 0.001.

Article Snippet: Bafilomycin-A1 (Baf-A1), rabbit anti-human/mouse/rat LC3βII (L8918, 1:3,000), anti-mouse IgG (A8924, 1:3,000), and anti-rabbit IgG (A6154, 1:5,000) were obtained from Sigma-Aldrich (Oakville, CA).The IRE1-specific inhibitor (MKC8866), which inhibits both basal and thapsigargin induced splicing of XBP1 mRNA ( 47 ), was provided by Mannkind (Westlake Village, CA).

Techniques: Western Blot, Expressing, Real-time Polymerase Chain Reaction

Autophagy flux inhibition and IRE1α inhibition modulates UPR and autophagy in IPF fibroblasts. Primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of bafilomycin-A1 (10 nM) or IRE1 inhibitor MKC8866 (10 μM) for 48 or 96 h. Immunoblots show abundance of autophagy (LC3βII, p62) and UPR (BIP) markers. The blot shown is representative of experiments performed on 2 different primary IPF fibroblast cell lines.

Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

Article Title: Autophagy and the unfolded protein response promote profibrotic effects of TGF-β 1 in human lung fibroblasts

doi: 10.1152/ajplung.00372.2017

Figure Lengend Snippet: Autophagy flux inhibition and IRE1α inhibition modulates UPR and autophagy in IPF fibroblasts. Primary human IPF fibroblasts were stimulated with TGF-β1 (2.5 ng/ml) in the presence or absence of bafilomycin-A1 (10 nM) or IRE1 inhibitor MKC8866 (10 μM) for 48 or 96 h. Immunoblots show abundance of autophagy (LC3βII, p62) and UPR (BIP) markers. The blot shown is representative of experiments performed on 2 different primary IPF fibroblast cell lines.

Article Snippet: Bafilomycin-A1 (Baf-A1), rabbit anti-human/mouse/rat LC3βII (L8918, 1:3,000), anti-mouse IgG (A8924, 1:3,000), and anti-rabbit IgG (A6154, 1:5,000) were obtained from Sigma-Aldrich (Oakville, CA).The IRE1-specific inhibitor (MKC8866), which inhibits both basal and thapsigargin induced splicing of XBP1 mRNA ( 47 ), was provided by Mannkind (Westlake Village, CA).

Techniques: Inhibition, Western Blot