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tgfβr1 inhibitor galunisertib  (MedChemExpress)
97
MedChemExpress tgfβr1 inhibitor galunisertib
A The expression of total and surface ENO1 in human CRC cell lines was evaluated by immunoblotting and flow cytometry. B The expression of total and surface ENO1 in human BRCA cell lines was evaluated by immunoblotting and flow cytometry. C HT29 and LoVo cells were treated with different doses of recombinant human TGFβ1 protein (rhTGFβ1) for 24 hr, after which surface ENO1 expression was analyzed via flow cytometry. D HS578T and MDA-MB-468 cells were treated with different doses of the rhTGFβ1 protein for 24 hr, after which the surface ENO1 level was analyzed via flow cytometry. E LoVo cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) in combination with a PRMT5 inhibitor (AMG-193, 1 μM) or a PRMT6 inhibitor (EPZ020411 hydrochloride, 1 μM) for 24 hr. The surface ENO1 level was analyzed via flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). F HT29 cells were treated with rhTGFβ1 protein in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The surface ENO1 expression was analyzed via flow cytometry. ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). G LoVo shNC and LoVo shPRMT5 cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). H HT29 and LoVo cells were treated with LPS (1 μg/mL) and RT (5 Gy) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05 and ** p < 0.01. One-Way ANOVA test ( n = 3). I HT29 cells were treated with RT (5 Gy) in combination with a <t>TGFβR1</t> inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. *** p < 0.001. One-Way ANOVA test ( n = 3). J HT29 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05. One-Way ANOVA test ( n = 3). K MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). L MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05, and ** p < 0.01. One-Way ANOVA test ( n = 3). M HT29 cells were treated with RT (5 Gy) in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The level of surface-methylated ENO1 was evaluated by immunoprecipitation and immunoblotting.
Tgfβr1 Inhibitor Galunisertib, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tgf%CE%B2r1/Galunisertib/pmc12876979-35-1-5
Average 97 stars, based on 1 article reviews
tgfβr1 inhibitor galunisertib - by Bioz Stars, 2026-09
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tgfβr1  (Bioss)
94
Bioss tgfβr1
A The expression of total and surface ENO1 in human CRC cell lines was evaluated by immunoblotting and flow cytometry. B The expression of total and surface ENO1 in human BRCA cell lines was evaluated by immunoblotting and flow cytometry. C HT29 and LoVo cells were treated with different doses of recombinant human TGFβ1 protein (rhTGFβ1) for 24 hr, after which surface ENO1 expression was analyzed via flow cytometry. D HS578T and MDA-MB-468 cells were treated with different doses of the rhTGFβ1 protein for 24 hr, after which the surface ENO1 level was analyzed via flow cytometry. E LoVo cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) in combination with a PRMT5 inhibitor (AMG-193, 1 μM) or a PRMT6 inhibitor (EPZ020411 hydrochloride, 1 μM) for 24 hr. The surface ENO1 level was analyzed via flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). F HT29 cells were treated with rhTGFβ1 protein in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The surface ENO1 expression was analyzed via flow cytometry. ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). G LoVo shNC and LoVo shPRMT5 cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). H HT29 and LoVo cells were treated with LPS (1 μg/mL) and RT (5 Gy) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05 and ** p < 0.01. One-Way ANOVA test ( n = 3). I HT29 cells were treated with RT (5 Gy) in combination with a <t>TGFβR1</t> inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. *** p < 0.001. One-Way ANOVA test ( n = 3). J HT29 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05. One-Way ANOVA test ( n = 3). K MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). L MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05, and ** p < 0.01. One-Way ANOVA test ( n = 3). M HT29 cells were treated with RT (5 Gy) in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The level of surface-methylated ENO1 was evaluated by immunoprecipitation and immunoblotting.
Tgfβr1, supplied by Bioss, 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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antibodies against tgfβr1  (Huabio Inc)
86
Huabio Inc antibodies against tgfβr1
A The expression of total and surface ENO1 in human CRC cell lines was evaluated by immunoblotting and flow cytometry. B The expression of total and surface ENO1 in human BRCA cell lines was evaluated by immunoblotting and flow cytometry. C HT29 and LoVo cells were treated with different doses of recombinant human TGFβ1 protein (rhTGFβ1) for 24 hr, after which surface ENO1 expression was analyzed via flow cytometry. D HS578T and MDA-MB-468 cells were treated with different doses of the rhTGFβ1 protein for 24 hr, after which the surface ENO1 level was analyzed via flow cytometry. E LoVo cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) in combination with a PRMT5 inhibitor (AMG-193, 1 μM) or a PRMT6 inhibitor (EPZ020411 hydrochloride, 1 μM) for 24 hr. The surface ENO1 level was analyzed via flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). F HT29 cells were treated with rhTGFβ1 protein in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The surface ENO1 expression was analyzed via flow cytometry. ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). G LoVo shNC and LoVo shPRMT5 cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). H HT29 and LoVo cells were treated with LPS (1 μg/mL) and RT (5 Gy) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05 and ** p < 0.01. One-Way ANOVA test ( n = 3). I HT29 cells were treated with RT (5 Gy) in combination with a <t>TGFβR1</t> inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. *** p < 0.001. One-Way ANOVA test ( n = 3). J HT29 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05. One-Way ANOVA test ( n = 3). K MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). L MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05, and ** p < 0.01. One-Way ANOVA test ( n = 3). M HT29 cells were treated with RT (5 Gy) in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The level of surface-methylated ENO1 was evaluated by immunoprecipitation and immunoblotting.
Antibodies Against Tgfβr1, supplied by Huabio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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antibodies against tgfβr1 - by Bioz Stars, 2026-09
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tgfβr1  (Shanghai Korain Biotech Co Ltd)
94
Shanghai Korain Biotech Co Ltd tgfβr1
A The expression of total and surface ENO1 in human CRC cell lines was evaluated by immunoblotting and flow cytometry. B The expression of total and surface ENO1 in human BRCA cell lines was evaluated by immunoblotting and flow cytometry. C HT29 and LoVo cells were treated with different doses of recombinant human TGFβ1 protein (rhTGFβ1) for 24 hr, after which surface ENO1 expression was analyzed via flow cytometry. D HS578T and MDA-MB-468 cells were treated with different doses of the rhTGFβ1 protein for 24 hr, after which the surface ENO1 level was analyzed via flow cytometry. E LoVo cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) in combination with a PRMT5 inhibitor (AMG-193, 1 μM) or a PRMT6 inhibitor (EPZ020411 hydrochloride, 1 μM) for 24 hr. The surface ENO1 level was analyzed via flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). F HT29 cells were treated with rhTGFβ1 protein in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The surface ENO1 expression was analyzed via flow cytometry. ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). G LoVo shNC and LoVo shPRMT5 cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). H HT29 and LoVo cells were treated with LPS (1 μg/mL) and RT (5 Gy) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05 and ** p < 0.01. One-Way ANOVA test ( n = 3). I HT29 cells were treated with RT (5 Gy) in combination with a <t>TGFβR1</t> inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. *** p < 0.001. One-Way ANOVA test ( n = 3). J HT29 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05. One-Way ANOVA test ( n = 3). K MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). L MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05, and ** p < 0.01. One-Way ANOVA test ( n = 3). M HT29 cells were treated with RT (5 Gy) in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The level of surface-methylated ENO1 was evaluated by immunoprecipitation and immunoblotting.
Tgfβr1, supplied by Shanghai Korain Biotech Co Ltd, 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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anti tgfβr1  (Santa Cruz Biotechnology)
95
Santa Cruz Biotechnology anti tgfβr1
A The expression of total and surface ENO1 in human CRC cell lines was evaluated by immunoblotting and flow cytometry. B The expression of total and surface ENO1 in human BRCA cell lines was evaluated by immunoblotting and flow cytometry. C HT29 and LoVo cells were treated with different doses of recombinant human TGFβ1 protein (rhTGFβ1) for 24 hr, after which surface ENO1 expression was analyzed via flow cytometry. D HS578T and MDA-MB-468 cells were treated with different doses of the rhTGFβ1 protein for 24 hr, after which the surface ENO1 level was analyzed via flow cytometry. E LoVo cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) in combination with a PRMT5 inhibitor (AMG-193, 1 μM) or a PRMT6 inhibitor (EPZ020411 hydrochloride, 1 μM) for 24 hr. The surface ENO1 level was analyzed via flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). F HT29 cells were treated with rhTGFβ1 protein in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The surface ENO1 expression was analyzed via flow cytometry. ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). G LoVo shNC and LoVo shPRMT5 cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). H HT29 and LoVo cells were treated with LPS (1 μg/mL) and RT (5 Gy) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05 and ** p < 0.01. One-Way ANOVA test ( n = 3). I HT29 cells were treated with RT (5 Gy) in combination with a <t>TGFβR1</t> inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. *** p < 0.001. One-Way ANOVA test ( n = 3). J HT29 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05. One-Way ANOVA test ( n = 3). K MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). L MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05, and ** p < 0.01. One-Way ANOVA test ( n = 3). M HT29 cells were treated with RT (5 Gy) in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The level of surface-methylated ENO1 was evaluated by immunoprecipitation and immunoblotting.
Anti Tgfβr1, supplied by Santa Cruz Biotechnology, 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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anti tgfβr1 - by Bioz Stars, 2026-09
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tgfβr1 wuhan sanying  (Wuhan Sanying Biotechnology)
86
Wuhan Sanying Biotechnology tgfβr1 wuhan sanying
A The expression of total and surface ENO1 in human CRC cell lines was evaluated by immunoblotting and flow cytometry. B The expression of total and surface ENO1 in human BRCA cell lines was evaluated by immunoblotting and flow cytometry. C HT29 and LoVo cells were treated with different doses of recombinant human TGFβ1 protein (rhTGFβ1) for 24 hr, after which surface ENO1 expression was analyzed via flow cytometry. D HS578T and MDA-MB-468 cells were treated with different doses of the rhTGFβ1 protein for 24 hr, after which the surface ENO1 level was analyzed via flow cytometry. E LoVo cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) in combination with a PRMT5 inhibitor (AMG-193, 1 μM) or a PRMT6 inhibitor (EPZ020411 hydrochloride, 1 μM) for 24 hr. The surface ENO1 level was analyzed via flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). F HT29 cells were treated with rhTGFβ1 protein in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The surface ENO1 expression was analyzed via flow cytometry. ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). G LoVo shNC and LoVo shPRMT5 cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). H HT29 and LoVo cells were treated with LPS (1 μg/mL) and RT (5 Gy) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05 and ** p < 0.01. One-Way ANOVA test ( n = 3). I HT29 cells were treated with RT (5 Gy) in combination with a <t>TGFβR1</t> inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. *** p < 0.001. One-Way ANOVA test ( n = 3). J HT29 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05. One-Way ANOVA test ( n = 3). K MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). L MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05, and ** p < 0.01. One-Way ANOVA test ( n = 3). M HT29 cells were treated with RT (5 Gy) in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The level of surface-methylated ENO1 was evaluated by immunoprecipitation and immunoblotting.
Tgfβr1 Wuhan Sanying, supplied by Wuhan Sanying Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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tgfβr1 inhibitor  (MedChemExpress)
97
MedChemExpress tgfβr1 inhibitor
A The expression of total and surface ENO1 in human CRC cell lines was evaluated by immunoblotting and flow cytometry. B The expression of total and surface ENO1 in human BRCA cell lines was evaluated by immunoblotting and flow cytometry. C HT29 and LoVo cells were treated with different doses of recombinant human TGFβ1 protein (rhTGFβ1) for 24 hr, after which surface ENO1 expression was analyzed via flow cytometry. D HS578T and MDA-MB-468 cells were treated with different doses of the rhTGFβ1 protein for 24 hr, after which the surface ENO1 level was analyzed via flow cytometry. E LoVo cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) in combination with a PRMT5 inhibitor (AMG-193, 1 μM) or a PRMT6 inhibitor (EPZ020411 hydrochloride, 1 μM) for 24 hr. The surface ENO1 level was analyzed via flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). F HT29 cells were treated with rhTGFβ1 protein in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The surface ENO1 expression was analyzed via flow cytometry. ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). G LoVo shNC and LoVo shPRMT5 cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). H HT29 and LoVo cells were treated with LPS (1 μg/mL) and RT (5 Gy) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05 and ** p < 0.01. One-Way ANOVA test ( n = 3). I HT29 cells were treated with RT (5 Gy) in combination with a <t>TGFβR1</t> inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. *** p < 0.001. One-Way ANOVA test ( n = 3). J HT29 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05. One-Way ANOVA test ( n = 3). K MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). L MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05, and ** p < 0.01. One-Way ANOVA test ( n = 3). M HT29 cells were treated with RT (5 Gy) in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The level of surface-methylated ENO1 was evaluated by immunoprecipitation and immunoblotting.
Tgfβr1 Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tgf%CE%B2r1/Galunisertib/pmc12893420-93-6-9
Average 97 stars, based on 1 article reviews
tgfβr1 inhibitor - by Bioz Stars, 2026-09
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tgfβr1 inhibitor sb431542  (Selleck Chemicals)
96
Selleck Chemicals tgfβr1 inhibitor sb431542
TGFβ signaling blockade destabilizes human Treg cells. (A) A diagram of the gating strategy to isolate naïve Treg (nTreg, CD4 + CD25 + CD127 − CD45RO - ) cells and effector Treg (eTreg, CD4 + CD25 + CD127 − CD45RO + ) cells from CD25 beads enriched PMBC in healthy donors by FACS. The flow cytometry profiles are representative of more than three donors. (B) The expression of CD45RO and CD45RA in freshly isolated nTreg and eTreg cells were assessed by flow-cytometry. The flow cytometry profiles are representative of more than three donors. (C) Principal Component Analysis (PCA) of whole genome transcriptome data in nTreg and eTreg cells with (TGFβi) or without (NT) <t>TGFβR1</t> inhibitor treatment. n = 3 replicates of one donor. (D, F, G) Gene set enrichment analysis (GSEA) was performed on the indicated sample groups and gene collections. Normalized Enrichment Scores (NES), and p-values were calculated using permutation tests and are labeled accordingly. (E) The expression of TGFBR2 in freshly isolated nTreg and eTreg cells were assessed by flow-cytometry (Left panel). The flow cytometry profiles are representative of three donors. Quantifications of MFI of TGFBR2 level in nTreg and eTreg cells (Right panel). Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. n = 3 replicates of one donor. This data is representative of experiments conducted in three donors. (H) A scatter plot illustrates gene expression levels of the indicated genes from whole genome transcriptome dataset. Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. n = 3 replicates of one donor. (I) Representative flow cytometry profiles showing FOXP3 and HELIOS levels in the nTreg and eTreg cells with (TGFβi) or without (NT) TGFβR1 inhibitor treatment for five weeks. This data is representative of experiments conducted in three donors. (J) Line charts summarizing the percentage of FOXP3 + population in nTreg and eTreg cells at indicated time points. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors.
Tgfβr1 Inhibitor Sb431542, supplied by Selleck Chemicals, 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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Average 96 stars, based on 1 article reviews
tgfβr1 inhibitor sb431542 - by Bioz Stars, 2026-09
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adp-glo kinase assay and tgfβr1 kinase enzyme system kit  (Promega)
90
Promega adp-glo kinase assay and tgfβr1 kinase enzyme system kit
TGFβ signaling blockade destabilizes human Treg cells. (A) A diagram of the gating strategy to isolate naïve Treg (nTreg, CD4 + CD25 + CD127 − CD45RO - ) cells and effector Treg (eTreg, CD4 + CD25 + CD127 − CD45RO + ) cells from CD25 beads enriched PMBC in healthy donors by FACS. The flow cytometry profiles are representative of more than three donors. (B) The expression of CD45RO and CD45RA in freshly isolated nTreg and eTreg cells were assessed by flow-cytometry. The flow cytometry profiles are representative of more than three donors. (C) Principal Component Analysis (PCA) of whole genome transcriptome data in nTreg and eTreg cells with (TGFβi) or without (NT) <t>TGFβR1</t> inhibitor treatment. n = 3 replicates of one donor. (D, F, G) Gene set enrichment analysis (GSEA) was performed on the indicated sample groups and gene collections. Normalized Enrichment Scores (NES), and p-values were calculated using permutation tests and are labeled accordingly. (E) The expression of TGFBR2 in freshly isolated nTreg and eTreg cells were assessed by flow-cytometry (Left panel). The flow cytometry profiles are representative of three donors. Quantifications of MFI of TGFBR2 level in nTreg and eTreg cells (Right panel). Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. n = 3 replicates of one donor. This data is representative of experiments conducted in three donors. (H) A scatter plot illustrates gene expression levels of the indicated genes from whole genome transcriptome dataset. Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. n = 3 replicates of one donor. (I) Representative flow cytometry profiles showing FOXP3 and HELIOS levels in the nTreg and eTreg cells with (TGFβi) or without (NT) TGFβR1 inhibitor treatment for five weeks. This data is representative of experiments conducted in three donors. (J) Line charts summarizing the percentage of FOXP3 + population in nTreg and eTreg cells at indicated time points. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors.
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A The expression of total and surface ENO1 in human CRC cell lines was evaluated by immunoblotting and flow cytometry. B The expression of total and surface ENO1 in human BRCA cell lines was evaluated by immunoblotting and flow cytometry. C HT29 and LoVo cells were treated with different doses of recombinant human TGFβ1 protein (rhTGFβ1) for 24 hr, after which surface ENO1 expression was analyzed via flow cytometry. D HS578T and MDA-MB-468 cells were treated with different doses of the rhTGFβ1 protein for 24 hr, after which the surface ENO1 level was analyzed via flow cytometry. E LoVo cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) in combination with a PRMT5 inhibitor (AMG-193, 1 μM) or a PRMT6 inhibitor (EPZ020411 hydrochloride, 1 μM) for 24 hr. The surface ENO1 level was analyzed via flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). F HT29 cells were treated with rhTGFβ1 protein in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The surface ENO1 expression was analyzed via flow cytometry. ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). G LoVo shNC and LoVo shPRMT5 cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). H HT29 and LoVo cells were treated with LPS (1 μg/mL) and RT (5 Gy) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05 and ** p < 0.01. One-Way ANOVA test ( n = 3). I HT29 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. *** p < 0.001. One-Way ANOVA test ( n = 3). J HT29 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05. One-Way ANOVA test ( n = 3). K MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). L MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05, and ** p < 0.01. One-Way ANOVA test ( n = 3). M HT29 cells were treated with RT (5 Gy) in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The level of surface-methylated ENO1 was evaluated by immunoprecipitation and immunoblotting.

Journal: Cell Death & Disease

Article Title: Targeting ENO1 reprograms macrophage polarization to trigger antitumor immunity and improves the therapeutic effect of radiotherapy

doi: 10.1038/s41419-026-08416-7

Figure Lengend Snippet: A The expression of total and surface ENO1 in human CRC cell lines was evaluated by immunoblotting and flow cytometry. B The expression of total and surface ENO1 in human BRCA cell lines was evaluated by immunoblotting and flow cytometry. C HT29 and LoVo cells were treated with different doses of recombinant human TGFβ1 protein (rhTGFβ1) for 24 hr, after which surface ENO1 expression was analyzed via flow cytometry. D HS578T and MDA-MB-468 cells were treated with different doses of the rhTGFβ1 protein for 24 hr, after which the surface ENO1 level was analyzed via flow cytometry. E LoVo cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) in combination with a PRMT5 inhibitor (AMG-193, 1 μM) or a PRMT6 inhibitor (EPZ020411 hydrochloride, 1 μM) for 24 hr. The surface ENO1 level was analyzed via flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). F HT29 cells were treated with rhTGFβ1 protein in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The surface ENO1 expression was analyzed via flow cytometry. ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). G LoVo shNC and LoVo shPRMT5 cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). H HT29 and LoVo cells were treated with LPS (1 μg/mL) and RT (5 Gy) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05 and ** p < 0.01. One-Way ANOVA test ( n = 3). I HT29 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. *** p < 0.001. One-Way ANOVA test ( n = 3). J HT29 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05. One-Way ANOVA test ( n = 3). K MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). L MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05, and ** p < 0.01. One-Way ANOVA test ( n = 3). M HT29 cells were treated with RT (5 Gy) in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The level of surface-methylated ENO1 was evaluated by immunoprecipitation and immunoblotting.

Article Snippet: The TGFβR1 inhibitor galunisertib (HY-13226, MCE, USA) [ ], Smad3 inhibitor SIS3 (HY-13013, MCE, USA) and PRMT5 inhibitor EPZ015666 (HY-12727, MCE, USA) were dissolved in DMSO to a concentration of 10 mM.

Techniques: Expressing, Western Blot, Flow Cytometry, Recombinant, Activity Assay, Enzyme-linked Immunosorbent Assay, Methylation, Immunoprecipitation

TGFβ signaling blockade destabilizes human Treg cells. (A) A diagram of the gating strategy to isolate naïve Treg (nTreg, CD4 + CD25 + CD127 − CD45RO - ) cells and effector Treg (eTreg, CD4 + CD25 + CD127 − CD45RO + ) cells from CD25 beads enriched PMBC in healthy donors by FACS. The flow cytometry profiles are representative of more than three donors. (B) The expression of CD45RO and CD45RA in freshly isolated nTreg and eTreg cells were assessed by flow-cytometry. The flow cytometry profiles are representative of more than three donors. (C) Principal Component Analysis (PCA) of whole genome transcriptome data in nTreg and eTreg cells with (TGFβi) or without (NT) TGFβR1 inhibitor treatment. n = 3 replicates of one donor. (D, F, G) Gene set enrichment analysis (GSEA) was performed on the indicated sample groups and gene collections. Normalized Enrichment Scores (NES), and p-values were calculated using permutation tests and are labeled accordingly. (E) The expression of TGFBR2 in freshly isolated nTreg and eTreg cells were assessed by flow-cytometry (Left panel). The flow cytometry profiles are representative of three donors. Quantifications of MFI of TGFBR2 level in nTreg and eTreg cells (Right panel). Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. n = 3 replicates of one donor. This data is representative of experiments conducted in three donors. (H) A scatter plot illustrates gene expression levels of the indicated genes from whole genome transcriptome dataset. Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. n = 3 replicates of one donor. (I) Representative flow cytometry profiles showing FOXP3 and HELIOS levels in the nTreg and eTreg cells with (TGFβi) or without (NT) TGFβR1 inhibitor treatment for five weeks. This data is representative of experiments conducted in three donors. (J) Line charts summarizing the percentage of FOXP3 + population in nTreg and eTreg cells at indicated time points. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors.

Journal: Frontiers in Immunology

Article Title: Differential regulation of Treg stability in human naïve and effector Treg subsets by TGFβ-signaling via ARKADIA-SKI axis

doi: 10.3389/fimmu.2025.1636434

Figure Lengend Snippet: TGFβ signaling blockade destabilizes human Treg cells. (A) A diagram of the gating strategy to isolate naïve Treg (nTreg, CD4 + CD25 + CD127 − CD45RO - ) cells and effector Treg (eTreg, CD4 + CD25 + CD127 − CD45RO + ) cells from CD25 beads enriched PMBC in healthy donors by FACS. The flow cytometry profiles are representative of more than three donors. (B) The expression of CD45RO and CD45RA in freshly isolated nTreg and eTreg cells were assessed by flow-cytometry. The flow cytometry profiles are representative of more than three donors. (C) Principal Component Analysis (PCA) of whole genome transcriptome data in nTreg and eTreg cells with (TGFβi) or without (NT) TGFβR1 inhibitor treatment. n = 3 replicates of one donor. (D, F, G) Gene set enrichment analysis (GSEA) was performed on the indicated sample groups and gene collections. Normalized Enrichment Scores (NES), and p-values were calculated using permutation tests and are labeled accordingly. (E) The expression of TGFBR2 in freshly isolated nTreg and eTreg cells were assessed by flow-cytometry (Left panel). The flow cytometry profiles are representative of three donors. Quantifications of MFI of TGFBR2 level in nTreg and eTreg cells (Right panel). Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. n = 3 replicates of one donor. This data is representative of experiments conducted in three donors. (H) A scatter plot illustrates gene expression levels of the indicated genes from whole genome transcriptome dataset. Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. n = 3 replicates of one donor. (I) Representative flow cytometry profiles showing FOXP3 and HELIOS levels in the nTreg and eTreg cells with (TGFβi) or without (NT) TGFβR1 inhibitor treatment for five weeks. This data is representative of experiments conducted in three donors. (J) Line charts summarizing the percentage of FOXP3 + population in nTreg and eTreg cells at indicated time points. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors.

Article Snippet: TGFβR1 inhibitor treatments were done in the presence of 1nM TGFβR1 inhibitor SB431542 (Selleckchem, S1067), which was replaced every 3 days.

Techniques: Flow Cytometry, Expressing, Isolation, Labeling, Gene Expression

Overexpression of SKI destabilizes human Treg cells and further promotes TGFβi induced Treg destabilization. (A) The expression level of SKI protein in expanded naïve Treg (nTreg) cells and effector Treg (eTreg) cells analyzed by immunoblots with GAPDH as loading control. The blots are representative of three donors. Note: The endogenous SKI shows multiple bands due to post-translational modifications, a pattern previously reported before using the same antibody clone . (B) The expression level of SKI protein was quantitated and normalized to GAPDH to calculate normalized protein levels and then compared to nTreg cells to determine relative protein levels. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors. (C) The expression level of SKI and GAPDH protein in naïve Treg cells treated with (TGFβi) or without (NT) TGFβR1 inhibitor for 0 and 10 days, analyzed by immunoblots. Blots from the same gels are separated by dotted lines. The blots are representative of three donors. (D–I) Expanded nTreg and eTreg cells transduced with NGFR or SKI-T2A-NGFR (SKI) were treated with (TGFβi) or without (NT) TGFβR1 inhibitor for three weeks. Levels of FOXP3, HELIOS, and IFNγ within the NGFR + population were assessed weekly via flow cytometry. Representative flow cytometry profiles showing FOXP3 and HELIOS levels (D) and FOXP3 and IFNγ levels (G) are shown. The flow cytometry profiles are representative of experiments conducted in four donors. Line charts summarizing the percentage of FOXP3 + (E, H) and IFNγ - cells (H, I) within the NGFR + population in nTreg cells (E, H) and eTreg cells (F, I) at indicated time points are shown. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 4 donors. (J) nTreg or eTreg cells carrying SKI or the empty vector (NGFR) were treated with (TGFβi) or without (NT) TGFβR1 inhibitor for three weeks and then subjected to an in vitro suppression assay. Treg cells were cultured with Teff cells at a 2:1 ratio (Treg: Teff) for four days. Following incubation, Teff proliferation was assessed by CTV dilution and flow cytometry. Suppression efficiency was calculated as “% inhibition of Teff division,” determined by the percentage reduction in the division index of Teff cells compared to Teff cells cultured alone. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors.

Journal: Frontiers in Immunology

Article Title: Differential regulation of Treg stability in human naïve and effector Treg subsets by TGFβ-signaling via ARKADIA-SKI axis

doi: 10.3389/fimmu.2025.1636434

Figure Lengend Snippet: Overexpression of SKI destabilizes human Treg cells and further promotes TGFβi induced Treg destabilization. (A) The expression level of SKI protein in expanded naïve Treg (nTreg) cells and effector Treg (eTreg) cells analyzed by immunoblots with GAPDH as loading control. The blots are representative of three donors. Note: The endogenous SKI shows multiple bands due to post-translational modifications, a pattern previously reported before using the same antibody clone . (B) The expression level of SKI protein was quantitated and normalized to GAPDH to calculate normalized protein levels and then compared to nTreg cells to determine relative protein levels. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors. (C) The expression level of SKI and GAPDH protein in naïve Treg cells treated with (TGFβi) or without (NT) TGFβR1 inhibitor for 0 and 10 days, analyzed by immunoblots. Blots from the same gels are separated by dotted lines. The blots are representative of three donors. (D–I) Expanded nTreg and eTreg cells transduced with NGFR or SKI-T2A-NGFR (SKI) were treated with (TGFβi) or without (NT) TGFβR1 inhibitor for three weeks. Levels of FOXP3, HELIOS, and IFNγ within the NGFR + population were assessed weekly via flow cytometry. Representative flow cytometry profiles showing FOXP3 and HELIOS levels (D) and FOXP3 and IFNγ levels (G) are shown. The flow cytometry profiles are representative of experiments conducted in four donors. Line charts summarizing the percentage of FOXP3 + (E, H) and IFNγ - cells (H, I) within the NGFR + population in nTreg cells (E, H) and eTreg cells (F, I) at indicated time points are shown. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 4 donors. (J) nTreg or eTreg cells carrying SKI or the empty vector (NGFR) were treated with (TGFβi) or without (NT) TGFβR1 inhibitor for three weeks and then subjected to an in vitro suppression assay. Treg cells were cultured with Teff cells at a 2:1 ratio (Treg: Teff) for four days. Following incubation, Teff proliferation was assessed by CTV dilution and flow cytometry. Suppression efficiency was calculated as “% inhibition of Teff division,” determined by the percentage reduction in the division index of Teff cells compared to Teff cells cultured alone. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors.

Article Snippet: TGFβR1 inhibitor treatments were done in the presence of 1nM TGFβR1 inhibitor SB431542 (Selleckchem, S1067), which was replaced every 3 days.

Techniques: Over Expression, Expressing, Western Blot, Control, Transduction, Flow Cytometry, Plasmid Preparation, In Vitro, Suppression Assay, Cell Culture, Incubation, Inhibition

A degradation resistant SKI further destabilizes human Treg cells. (A, B) Naïve Treg cells transduced with SKI or (P35S) SKI were treated with (TGFβi) or without (NT) TGFβR1 inhibitor for three days, followed by immunoblots targeting SKI and GAPDH. (A) Representative immunoblots of three donors. (B) SKI levels were quantitated and normalized to GAPDH to calculate normalized protein levels and then compared to the NT-SKI samples to determine relative protein levels. Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. n = 3 donors. (C-E) Naïve Treg cells transduced with NGFR or SKI-T2A-NGFR (SKI) or (P35S)SKI-T2A-NGFR ((P35S)SKI) were treated with (TGFβi) or without (NT) TGFβR1 inhibitor for three weeks. (C) Levels of FOXP3 and HELIOS within the NGFR + population were assessed via flow cytometry. Representative flow cytometry profiles showing FOXP3 and HELIOS levels. n = 3 donors. (D) A bar graph summarizing the level of FOXP3 within the NGFR + population. Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. Data present n = 3 technical replicates from a single donor. This experiment was independently repeated with cells from three donors, yielding similar results. (E) These Treg cells were then subjected to an in vitro suppression assay and cultured with Teff cells at a 2:1 ratio (Treg: Teff) for four days. Following incubation, Teff proliferation was assessed by CTV dilution and flow cytometry. Suppression efficiency was calculated as “% inhibition of Teff division,” determined by the percentage reduction in the division index of Teff cells compared to Teff cells cultured alone. Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. n = 6 replicates from two donors.

Journal: Frontiers in Immunology

Article Title: Differential regulation of Treg stability in human naïve and effector Treg subsets by TGFβ-signaling via ARKADIA-SKI axis

doi: 10.3389/fimmu.2025.1636434

Figure Lengend Snippet: A degradation resistant SKI further destabilizes human Treg cells. (A, B) Naïve Treg cells transduced with SKI or (P35S) SKI were treated with (TGFβi) or without (NT) TGFβR1 inhibitor for three days, followed by immunoblots targeting SKI and GAPDH. (A) Representative immunoblots of three donors. (B) SKI levels were quantitated and normalized to GAPDH to calculate normalized protein levels and then compared to the NT-SKI samples to determine relative protein levels. Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. n = 3 donors. (C-E) Naïve Treg cells transduced with NGFR or SKI-T2A-NGFR (SKI) or (P35S)SKI-T2A-NGFR ((P35S)SKI) were treated with (TGFβi) or without (NT) TGFβR1 inhibitor for three weeks. (C) Levels of FOXP3 and HELIOS within the NGFR + population were assessed via flow cytometry. Representative flow cytometry profiles showing FOXP3 and HELIOS levels. n = 3 donors. (D) A bar graph summarizing the level of FOXP3 within the NGFR + population. Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. Data present n = 3 technical replicates from a single donor. This experiment was independently repeated with cells from three donors, yielding similar results. (E) These Treg cells were then subjected to an in vitro suppression assay and cultured with Teff cells at a 2:1 ratio (Treg: Teff) for four days. Following incubation, Teff proliferation was assessed by CTV dilution and flow cytometry. Suppression efficiency was calculated as “% inhibition of Teff division,” determined by the percentage reduction in the division index of Teff cells compared to Teff cells cultured alone. Data are presented as Mean ± SD. ∗ p < 0.05, two-sided t test. n = 6 replicates from two donors.

Article Snippet: TGFβR1 inhibitor treatments were done in the presence of 1nM TGFβR1 inhibitor SB431542 (Selleckchem, S1067), which was replaced every 3 days.

Techniques: Transduction, Western Blot, Flow Cytometry, In Vitro, Suppression Assay, Cell Culture, Incubation, Inhibition

ARKADIA prevents Treg destabilization upon TGFβ inhibition. (A, B) Naïve Treg cells carrying NGFR or ARKADIA-T2A-NGFR (ARKADIA) were cultured for seven days, followed by immunoblot targeting AKADIA, SKI, and GAPDH. (A) Representative immunoblots of three donors. Note: ARKADIA shows multiple bands due to truncation, a pattern previously reported using the same antibody clone . (B) ARKADIA and SKI levels were quantitated and normalized to GAPDH to calculate normalized protein levels and then compared to the NGFR samples to determine relative protein levels. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors. (C-H) Naïve Treg cells carrying NGFR or ARKADIA-T2A-NGFR (ARKADIA) were treated with (TGFβi) or without (NT) TGFβR1 inhibitor for three weeks. Levels of indicated proteins within the NGFR + population were assessed weekly via flow cytometry. Representative flow cytometry profiles showing FOXP3 and HELIOS levels (C) or FOXP3 and IFNγ levels (E) in transduced Treg cells after three weeks of treatment. The flow cytometry profiles are representative of experiments conducted in three donors. Line charts summarize the percentage of FOXP3 + cells (D) or IFNγ - cells (F) within the NGFR + population in the Treg cells. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors. After the three-week treatment, those Treg cells were subjected to an in vitro suppression assay by being cultured with Teff cells at a 2:1 ratio (Treg: Teff) (G) or 8:1 ratio (Treg: Teff) (H) for four days. Following incubation, Teff proliferation was assessed by CTV dilution and flow cytometry. Suppression efficiency was calculated as “% inhibition of Teff division,” determined by the percentage reduction in the division index of Teff cells compared to Teff cells cultured alone. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors.

Journal: Frontiers in Immunology

Article Title: Differential regulation of Treg stability in human naïve and effector Treg subsets by TGFβ-signaling via ARKADIA-SKI axis

doi: 10.3389/fimmu.2025.1636434

Figure Lengend Snippet: ARKADIA prevents Treg destabilization upon TGFβ inhibition. (A, B) Naïve Treg cells carrying NGFR or ARKADIA-T2A-NGFR (ARKADIA) were cultured for seven days, followed by immunoblot targeting AKADIA, SKI, and GAPDH. (A) Representative immunoblots of three donors. Note: ARKADIA shows multiple bands due to truncation, a pattern previously reported using the same antibody clone . (B) ARKADIA and SKI levels were quantitated and normalized to GAPDH to calculate normalized protein levels and then compared to the NGFR samples to determine relative protein levels. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors. (C-H) Naïve Treg cells carrying NGFR or ARKADIA-T2A-NGFR (ARKADIA) were treated with (TGFβi) or without (NT) TGFβR1 inhibitor for three weeks. Levels of indicated proteins within the NGFR + population were assessed weekly via flow cytometry. Representative flow cytometry profiles showing FOXP3 and HELIOS levels (C) or FOXP3 and IFNγ levels (E) in transduced Treg cells after three weeks of treatment. The flow cytometry profiles are representative of experiments conducted in three donors. Line charts summarize the percentage of FOXP3 + cells (D) or IFNγ - cells (F) within the NGFR + population in the Treg cells. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors. After the three-week treatment, those Treg cells were subjected to an in vitro suppression assay by being cultured with Teff cells at a 2:1 ratio (Treg: Teff) (G) or 8:1 ratio (Treg: Teff) (H) for four days. Following incubation, Teff proliferation was assessed by CTV dilution and flow cytometry. Suppression efficiency was calculated as “% inhibition of Teff division,” determined by the percentage reduction in the division index of Teff cells compared to Teff cells cultured alone. Data are presented as Mean ± SEM. ∗ p < 0.05, two-sided t test. n = 3 donors.

Article Snippet: TGFβR1 inhibitor treatments were done in the presence of 1nM TGFβR1 inhibitor SB431542 (Selleckchem, S1067), which was replaced every 3 days.

Techniques: Inhibition, Cell Culture, Western Blot, Flow Cytometry, In Vitro, Suppression Assay, Incubation