ll Search Results


ll97a  (ATCC)
93
ATCC ll97a
Ll97a, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ll37  (InvivoGen)
95
InvivoGen ll37
Fig. 3 <t>LL37/Poly(I:C)</t> complexes induce IL-36γ release from keratinocytes independent of inflammasome and GSDMD activity. A HPKs were primed with IL-17A (100 ng/ml) or left unprimed (medium control) for 6 h prior to stimulation with Poly(I:C), Poly(dA:dT), LL37/Poly(I:C) or LL37/Poly(dA:dT) complexes (all 5 μg/ml) for 18 h. Supernatants were analysed for IL-36γ release by ELISA. B, C GSDMD-deficient N/TERT-1 cells (sgGSDMD) were stimulated with IL-17A (100 ng/ml) for 6 h prior to stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or transfected with Poly(I:C) (1 μg/ml) for 18 h. Supernatants were analysed for D IL-36γ or E IL-1β levels by ELISA. D, E HPKs were stimulated with IL-17A (10 ng/ml) and TNF-α (5 ng/ml) for 5 h, followed by inhibitor treatment with SB 203580 (p38i, 20 μM), Belnacasan (Casp1i, 10 μM), or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or anisomycin (ANS, 1 μM) for 18 h. Supernatants were measured for D IL-36γ or E IL-1β by ELISA. F HPKs were primed with IL-17A for 5 h, followed by inhibitor treatment with MCC950 or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes for 18 h. Cells were treated with MCC950 1 h before stimulation. Supernatants were measured for IL-36γ release by ELISA. Data are presented (A–F) as the mean ±S.E.M. of 3 independent experiments and analysed with (A–C, F) two-way ANOVA and Šidák’s or (D, E) two-way ANOVA followed by Dunnett’s multiple comparisons test. *p < 0.05, **p < 0.01, ****p < 0.0001. ns non-significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.
Ll37, supplied by InvivoGen, 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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ccbd ll37  (Biosynth Carbosynth)
92
Biosynth Carbosynth ccbd ll37
Fig. 3 <t>LL37/Poly(I:C)</t> complexes induce IL-36γ release from keratinocytes independent of inflammasome and GSDMD activity. A HPKs were primed with IL-17A (100 ng/ml) or left unprimed (medium control) for 6 h prior to stimulation with Poly(I:C), Poly(dA:dT), LL37/Poly(I:C) or LL37/Poly(dA:dT) complexes (all 5 μg/ml) for 18 h. Supernatants were analysed for IL-36γ release by ELISA. B, C GSDMD-deficient N/TERT-1 cells (sgGSDMD) were stimulated with IL-17A (100 ng/ml) for 6 h prior to stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or transfected with Poly(I:C) (1 μg/ml) for 18 h. Supernatants were analysed for D IL-36γ or E IL-1β levels by ELISA. D, E HPKs were stimulated with IL-17A (10 ng/ml) and TNF-α (5 ng/ml) for 5 h, followed by inhibitor treatment with SB 203580 (p38i, 20 μM), Belnacasan (Casp1i, 10 μM), or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or anisomycin (ANS, 1 μM) for 18 h. Supernatants were measured for D IL-36γ or E IL-1β by ELISA. F HPKs were primed with IL-17A for 5 h, followed by inhibitor treatment with MCC950 or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes for 18 h. Cells were treated with MCC950 1 h before stimulation. Supernatants were measured for IL-36γ release by ELISA. Data are presented (A–F) as the mean ±S.E.M. of 3 independent experiments and analysed with (A–C, F) two-way ANOVA and Šidák’s or (D, E) two-way ANOVA followed by Dunnett’s multiple comparisons test. *p < 0.05, **p < 0.01, ****p < 0.0001. ns non-significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.
Ccbd Ll37, supplied by Biosynth Carbosynth, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ll 2 cell lines  (ATCC)
99
ATCC ll 2 cell lines
Fig. 3 <t>LL37/Poly(I:C)</t> complexes induce IL-36γ release from keratinocytes independent of inflammasome and GSDMD activity. A HPKs were primed with IL-17A (100 ng/ml) or left unprimed (medium control) for 6 h prior to stimulation with Poly(I:C), Poly(dA:dT), LL37/Poly(I:C) or LL37/Poly(dA:dT) complexes (all 5 μg/ml) for 18 h. Supernatants were analysed for IL-36γ release by ELISA. B, C GSDMD-deficient N/TERT-1 cells (sgGSDMD) were stimulated with IL-17A (100 ng/ml) for 6 h prior to stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or transfected with Poly(I:C) (1 μg/ml) for 18 h. Supernatants were analysed for D IL-36γ or E IL-1β levels by ELISA. D, E HPKs were stimulated with IL-17A (10 ng/ml) and TNF-α (5 ng/ml) for 5 h, followed by inhibitor treatment with SB 203580 (p38i, 20 μM), Belnacasan (Casp1i, 10 μM), or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or anisomycin (ANS, 1 μM) for 18 h. Supernatants were measured for D IL-36γ or E IL-1β by ELISA. F HPKs were primed with IL-17A for 5 h, followed by inhibitor treatment with MCC950 or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes for 18 h. Cells were treated with MCC950 1 h before stimulation. Supernatants were measured for IL-36γ release by ELISA. Data are presented (A–F) as the mean ±S.E.M. of 3 independent experiments and analysed with (A–C, F) two-way ANOVA and Šidák’s or (D, E) two-way ANOVA followed by Dunnett’s multiple comparisons test. *p < 0.05, **p < 0.01, ****p < 0.0001. ns non-significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.
Ll 2 Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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tak1 inhibitor 5z 7 oxozeaenol  (MedChemExpress)
95
MedChemExpress tak1 inhibitor 5z 7 oxozeaenol
Fig. 3 <t>LL37/Poly(I:C)</t> complexes induce IL-36γ release from keratinocytes independent of inflammasome and GSDMD activity. A HPKs were primed with IL-17A (100 ng/ml) or left unprimed (medium control) for 6 h prior to stimulation with Poly(I:C), Poly(dA:dT), LL37/Poly(I:C) or LL37/Poly(dA:dT) complexes (all 5 μg/ml) for 18 h. Supernatants were analysed for IL-36γ release by ELISA. B, C GSDMD-deficient N/TERT-1 cells (sgGSDMD) were stimulated with IL-17A (100 ng/ml) for 6 h prior to stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or transfected with Poly(I:C) (1 μg/ml) for 18 h. Supernatants were analysed for D IL-36γ or E IL-1β levels by ELISA. D, E HPKs were stimulated with IL-17A (10 ng/ml) and TNF-α (5 ng/ml) for 5 h, followed by inhibitor treatment with SB 203580 (p38i, 20 μM), Belnacasan (Casp1i, 10 μM), or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or anisomycin (ANS, 1 μM) for 18 h. Supernatants were measured for D IL-36γ or E IL-1β by ELISA. F HPKs were primed with IL-17A for 5 h, followed by inhibitor treatment with MCC950 or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes for 18 h. Cells were treated with MCC950 1 h before stimulation. Supernatants were measured for IL-36γ release by ELISA. Data are presented (A–F) as the mean ±S.E.M. of 3 independent experiments and analysed with (A–C, F) two-way ANOVA and Šidák’s or (D, E) two-way ANOVA followed by Dunnett’s multiple comparisons test. *p < 0.05, **p < 0.01, ****p < 0.0001. ns non-significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.
Tak1 Inhibitor 5z 7 Oxozeaenol, supplied by MedChemExpress, 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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ll29 cells  (ATCC)
95
ATCC ll29 cells
Fig. 3 <t>LL37/Poly(I:C)</t> complexes induce IL-36γ release from keratinocytes independent of inflammasome and GSDMD activity. A HPKs were primed with IL-17A (100 ng/ml) or left unprimed (medium control) for 6 h prior to stimulation with Poly(I:C), Poly(dA:dT), LL37/Poly(I:C) or LL37/Poly(dA:dT) complexes (all 5 μg/ml) for 18 h. Supernatants were analysed for IL-36γ release by ELISA. B, C GSDMD-deficient N/TERT-1 cells (sgGSDMD) were stimulated with IL-17A (100 ng/ml) for 6 h prior to stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or transfected with Poly(I:C) (1 μg/ml) for 18 h. Supernatants were analysed for D IL-36γ or E IL-1β levels by ELISA. D, E HPKs were stimulated with IL-17A (10 ng/ml) and TNF-α (5 ng/ml) for 5 h, followed by inhibitor treatment with SB 203580 (p38i, 20 μM), Belnacasan (Casp1i, 10 μM), or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or anisomycin (ANS, 1 μM) for 18 h. Supernatants were measured for D IL-36γ or E IL-1β by ELISA. F HPKs were primed with IL-17A for 5 h, followed by inhibitor treatment with MCC950 or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes for 18 h. Cells were treated with MCC950 1 h before stimulation. Supernatants were measured for IL-36γ release by ELISA. Data are presented (A–F) as the mean ±S.E.M. of 3 independent experiments and analysed with (A–C, F) two-way ANOVA and Šidák’s or (D, E) two-way ANOVA followed by Dunnett’s multiple comparisons test. *p < 0.05, **p < 0.01, ****p < 0.0001. ns non-significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.
Ll29 Cells, supplied by ATCC, 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 ll 37  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology anti ll 37
Fig. 3 <t>LL37/Poly(I:C)</t> complexes induce IL-36γ release from keratinocytes independent of inflammasome and GSDMD activity. A HPKs were primed with IL-17A (100 ng/ml) or left unprimed (medium control) for 6 h prior to stimulation with Poly(I:C), Poly(dA:dT), LL37/Poly(I:C) or LL37/Poly(dA:dT) complexes (all 5 μg/ml) for 18 h. Supernatants were analysed for IL-36γ release by ELISA. B, C GSDMD-deficient N/TERT-1 cells (sgGSDMD) were stimulated with IL-17A (100 ng/ml) for 6 h prior to stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or transfected with Poly(I:C) (1 μg/ml) for 18 h. Supernatants were analysed for D IL-36γ or E IL-1β levels by ELISA. D, E HPKs were stimulated with IL-17A (10 ng/ml) and TNF-α (5 ng/ml) for 5 h, followed by inhibitor treatment with SB 203580 (p38i, 20 μM), Belnacasan (Casp1i, 10 μM), or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or anisomycin (ANS, 1 μM) for 18 h. Supernatants were measured for D IL-36γ or E IL-1β by ELISA. F HPKs were primed with IL-17A for 5 h, followed by inhibitor treatment with MCC950 or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes for 18 h. Cells were treated with MCC950 1 h before stimulation. Supernatants were measured for IL-36γ release by ELISA. Data are presented (A–F) as the mean ±S.E.M. of 3 independent experiments and analysed with (A–C, F) two-way ANOVA and Šidák’s or (D, E) two-way ANOVA followed by Dunnett’s multiple comparisons test. *p < 0.05, **p < 0.01, ****p < 0.0001. ns non-significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.
Anti Ll 37, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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leupeptin  (TargetMol)
96
TargetMol leupeptin
Fig. 3 <t>LL37/Poly(I:C)</t> complexes induce IL-36γ release from keratinocytes independent of inflammasome and GSDMD activity. A HPKs were primed with IL-17A (100 ng/ml) or left unprimed (medium control) for 6 h prior to stimulation with Poly(I:C), Poly(dA:dT), LL37/Poly(I:C) or LL37/Poly(dA:dT) complexes (all 5 μg/ml) for 18 h. Supernatants were analysed for IL-36γ release by ELISA. B, C GSDMD-deficient N/TERT-1 cells (sgGSDMD) were stimulated with IL-17A (100 ng/ml) for 6 h prior to stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or transfected with Poly(I:C) (1 μg/ml) for 18 h. Supernatants were analysed for D IL-36γ or E IL-1β levels by ELISA. D, E HPKs were stimulated with IL-17A (10 ng/ml) and TNF-α (5 ng/ml) for 5 h, followed by inhibitor treatment with SB 203580 (p38i, 20 μM), Belnacasan (Casp1i, 10 μM), or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or anisomycin (ANS, 1 μM) for 18 h. Supernatants were measured for D IL-36γ or E IL-1β by ELISA. F HPKs were primed with IL-17A for 5 h, followed by inhibitor treatment with MCC950 or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes for 18 h. Cells were treated with MCC950 1 h before stimulation. Supernatants were measured for IL-36γ release by ELISA. Data are presented (A–F) as the mean ±S.E.M. of 3 independent experiments and analysed with (A–C, F) two-way ANOVA and Šidák’s or (D, E) two-way ANOVA followed by Dunnett’s multiple comparisons test. *p < 0.05, **p < 0.01, ****p < 0.0001. ns non-significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.
Leupeptin, supplied by TargetMol, 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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ll47 mado cells  (ATCC)
92
ATCC ll47 mado cells
Fig. 3 <t>LL37/Poly(I:C)</t> complexes induce IL-36γ release from keratinocytes independent of inflammasome and GSDMD activity. A HPKs were primed with IL-17A (100 ng/ml) or left unprimed (medium control) for 6 h prior to stimulation with Poly(I:C), Poly(dA:dT), LL37/Poly(I:C) or LL37/Poly(dA:dT) complexes (all 5 μg/ml) for 18 h. Supernatants were analysed for IL-36γ release by ELISA. B, C GSDMD-deficient N/TERT-1 cells (sgGSDMD) were stimulated with IL-17A (100 ng/ml) for 6 h prior to stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or transfected with Poly(I:C) (1 μg/ml) for 18 h. Supernatants were analysed for D IL-36γ or E IL-1β levels by ELISA. D, E HPKs were stimulated with IL-17A (10 ng/ml) and TNF-α (5 ng/ml) for 5 h, followed by inhibitor treatment with SB 203580 (p38i, 20 μM), Belnacasan (Casp1i, 10 μM), or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or anisomycin (ANS, 1 μM) for 18 h. Supernatants were measured for D IL-36γ or E IL-1β by ELISA. F HPKs were primed with IL-17A for 5 h, followed by inhibitor treatment with MCC950 or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes for 18 h. Cells were treated with MCC950 1 h before stimulation. Supernatants were measured for IL-36γ release by ELISA. Data are presented (A–F) as the mean ±S.E.M. of 3 independent experiments and analysed with (A–C, F) two-way ANOVA and Šidák’s or (D, E) two-way ANOVA followed by Dunnett’s multiple comparisons test. *p < 0.05, **p < 0.01, ****p < 0.0001. ns non-significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.
Ll47 Mado Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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luciferase ll 2 llc1 luc2  (ATCC)
94
ATCC luciferase ll 2 llc1 luc2
Fig. 3 <t>LL37/Poly(I:C)</t> complexes induce IL-36γ release from keratinocytes independent of inflammasome and GSDMD activity. A HPKs were primed with IL-17A (100 ng/ml) or left unprimed (medium control) for 6 h prior to stimulation with Poly(I:C), Poly(dA:dT), LL37/Poly(I:C) or LL37/Poly(dA:dT) complexes (all 5 μg/ml) for 18 h. Supernatants were analysed for IL-36γ release by ELISA. B, C GSDMD-deficient N/TERT-1 cells (sgGSDMD) were stimulated with IL-17A (100 ng/ml) for 6 h prior to stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or transfected with Poly(I:C) (1 μg/ml) for 18 h. Supernatants were analysed for D IL-36γ or E IL-1β levels by ELISA. D, E HPKs were stimulated with IL-17A (10 ng/ml) and TNF-α (5 ng/ml) for 5 h, followed by inhibitor treatment with SB 203580 (p38i, 20 μM), Belnacasan (Casp1i, 10 μM), or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or anisomycin (ANS, 1 μM) for 18 h. Supernatants were measured for D IL-36γ or E IL-1β by ELISA. F HPKs were primed with IL-17A for 5 h, followed by inhibitor treatment with MCC950 or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes for 18 h. Cells were treated with MCC950 1 h before stimulation. Supernatants were measured for IL-36γ release by ELISA. Data are presented (A–F) as the mean ±S.E.M. of 3 independent experiments and analysed with (A–C, F) two-way ANOVA and Šidák’s or (D, E) two-way ANOVA followed by Dunnett’s multiple comparisons test. *p < 0.05, **p < 0.01, ****p < 0.0001. ns non-significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.
Luciferase Ll 2 Llc1 Luc2, supplied by ATCC, 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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well plate  (ATCC)
95
ATCC well plate
Fig. 3 <t>LL37/Poly(I:C)</t> complexes induce IL-36γ release from keratinocytes independent of inflammasome and GSDMD activity. A HPKs were primed with IL-17A (100 ng/ml) or left unprimed (medium control) for 6 h prior to stimulation with Poly(I:C), Poly(dA:dT), LL37/Poly(I:C) or LL37/Poly(dA:dT) complexes (all 5 μg/ml) for 18 h. Supernatants were analysed for IL-36γ release by ELISA. B, C GSDMD-deficient N/TERT-1 cells (sgGSDMD) were stimulated with IL-17A (100 ng/ml) for 6 h prior to stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or transfected with Poly(I:C) (1 μg/ml) for 18 h. Supernatants were analysed for D IL-36γ or E IL-1β levels by ELISA. D, E HPKs were stimulated with IL-17A (10 ng/ml) and TNF-α (5 ng/ml) for 5 h, followed by inhibitor treatment with SB 203580 (p38i, 20 μM), Belnacasan (Casp1i, 10 μM), or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or anisomycin (ANS, 1 μM) for 18 h. Supernatants were measured for D IL-36γ or E IL-1β by ELISA. F HPKs were primed with IL-17A for 5 h, followed by inhibitor treatment with MCC950 or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes for 18 h. Cells were treated with MCC950 1 h before stimulation. Supernatants were measured for IL-36γ release by ELISA. Data are presented (A–F) as the mean ±S.E.M. of 3 independent experiments and analysed with (A–C, F) two-way ANOVA and Šidák’s or (D, E) two-way ANOVA followed by Dunnett’s multiple comparisons test. *p < 0.05, **p < 0.01, ****p < 0.0001. ns non-significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.
Well Plate, supplied by ATCC, 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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human ll37 cap18  (Hycult Biotech)
92
Hycult Biotech human ll37 cap18
Fig. 3 <t>LL37/Poly(I:C)</t> complexes induce IL-36γ release from keratinocytes independent of inflammasome and GSDMD activity. A HPKs were primed with IL-17A (100 ng/ml) or left unprimed (medium control) for 6 h prior to stimulation with Poly(I:C), Poly(dA:dT), LL37/Poly(I:C) or LL37/Poly(dA:dT) complexes (all 5 μg/ml) for 18 h. Supernatants were analysed for IL-36γ release by ELISA. B, C GSDMD-deficient N/TERT-1 cells (sgGSDMD) were stimulated with IL-17A (100 ng/ml) for 6 h prior to stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or transfected with Poly(I:C) (1 μg/ml) for 18 h. Supernatants were analysed for D IL-36γ or E IL-1β levels by ELISA. D, E HPKs were stimulated with IL-17A (10 ng/ml) and TNF-α (5 ng/ml) for 5 h, followed by inhibitor treatment with SB 203580 (p38i, 20 μM), Belnacasan (Casp1i, 10 μM), or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or anisomycin (ANS, 1 μM) for 18 h. Supernatants were measured for D IL-36γ or E IL-1β by ELISA. F HPKs were primed with IL-17A for 5 h, followed by inhibitor treatment with MCC950 or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes for 18 h. Cells were treated with MCC950 1 h before stimulation. Supernatants were measured for IL-36γ release by ELISA. Data are presented (A–F) as the mean ±S.E.M. of 3 independent experiments and analysed with (A–C, F) two-way ANOVA and Šidák’s or (D, E) two-way ANOVA followed by Dunnett’s multiple comparisons test. *p < 0.05, **p < 0.01, ****p < 0.0001. ns non-significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.
Human Ll37 Cap18, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Fig. 3 LL37/Poly(I:C) complexes induce IL-36γ release from keratinocytes independent of inflammasome and GSDMD activity. A HPKs were primed with IL-17A (100 ng/ml) or left unprimed (medium control) for 6 h prior to stimulation with Poly(I:C), Poly(dA:dT), LL37/Poly(I:C) or LL37/Poly(dA:dT) complexes (all 5 μg/ml) for 18 h. Supernatants were analysed for IL-36γ release by ELISA. B, C GSDMD-deficient N/TERT-1 cells (sgGSDMD) were stimulated with IL-17A (100 ng/ml) for 6 h prior to stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or transfected with Poly(I:C) (1 μg/ml) for 18 h. Supernatants were analysed for D IL-36γ or E IL-1β levels by ELISA. D, E HPKs were stimulated with IL-17A (10 ng/ml) and TNF-α (5 ng/ml) for 5 h, followed by inhibitor treatment with SB 203580 (p38i, 20 μM), Belnacasan (Casp1i, 10 μM), or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or anisomycin (ANS, 1 μM) for 18 h. Supernatants were measured for D IL-36γ or E IL-1β by ELISA. F HPKs were primed with IL-17A for 5 h, followed by inhibitor treatment with MCC950 or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes for 18 h. Cells were treated with MCC950 1 h before stimulation. Supernatants were measured for IL-36γ release by ELISA. Data are presented (A–F) as the mean ±S.E.M. of 3 independent experiments and analysed with (A–C, F) two-way ANOVA and Šidák’s or (D, E) two-way ANOVA followed by Dunnett’s multiple comparisons test. *p < 0.05, **p < 0.01, ****p < 0.0001. ns non-significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.

Journal: Cell death & disease

Article Title: LL37 complexed to double-stranded RNA induces RIG-I-like receptor signalling and Gasdermin E activation facilitating IL-36γ release from keratinocytes.

doi: 10.1038/s41419-025-07537-9

Figure Lengend Snippet: Fig. 3 LL37/Poly(I:C) complexes induce IL-36γ release from keratinocytes independent of inflammasome and GSDMD activity. A HPKs were primed with IL-17A (100 ng/ml) or left unprimed (medium control) for 6 h prior to stimulation with Poly(I:C), Poly(dA:dT), LL37/Poly(I:C) or LL37/Poly(dA:dT) complexes (all 5 μg/ml) for 18 h. Supernatants were analysed for IL-36γ release by ELISA. B, C GSDMD-deficient N/TERT-1 cells (sgGSDMD) were stimulated with IL-17A (100 ng/ml) for 6 h prior to stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or transfected with Poly(I:C) (1 μg/ml) for 18 h. Supernatants were analysed for D IL-36γ or E IL-1β levels by ELISA. D, E HPKs were stimulated with IL-17A (10 ng/ml) and TNF-α (5 ng/ml) for 5 h, followed by inhibitor treatment with SB 203580 (p38i, 20 μM), Belnacasan (Casp1i, 10 μM), or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes (5 μg/ml), VbP (1 μM), or anisomycin (ANS, 1 μM) for 18 h. Supernatants were measured for D IL-36γ or E IL-1β by ELISA. F HPKs were primed with IL-17A for 5 h, followed by inhibitor treatment with MCC950 or DMSO for 1 h before stimulation with LL37/Poly(I:C) complexes for 18 h. Cells were treated with MCC950 1 h before stimulation. Supernatants were measured for IL-36γ release by ELISA. Data are presented (A–F) as the mean ±S.E.M. of 3 independent experiments and analysed with (A–C, F) two-way ANOVA and Šidák’s or (D, E) two-way ANOVA followed by Dunnett’s multiple comparisons test. *p < 0.05, **p < 0.01, ****p < 0.0001. ns non-significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.

Article Snippet: HPKs were transfected by the 1 μg/ml HMW Poly(I:C) coupled with biotin (Invivogen) using Lipofectamine 2000, or treated with 1 μg/ml LL37 with and without pre-incubation with 1 μg/ml HMW Poly(I:C) coupled with Biotin (Invivogen).

Techniques: Activity Assay, Control, Enzyme-linked Immunosorbent Assay, Transfection, Marker

Fig. 4 LL37/Poly(I:C) complexes activate Caspase-3 and GSDME cleavage in human primary keratinocytes. A, B HPKs were stimulated with LL37/Poly(I:C) complexes (5 μg/ml) or were transfected with Poly(I:C) (1 μg/ml) for indicated times control treatment (−) indicates Medium or Lipo, respectively. Supernatants and cell lysates were subjected to SDS-PAGE and immunoblotting with indicated antibodies. * indicates non- specific band (C, D) GSDME-deficient N/TERT-1 cells (sgGSDME) were (D) primed with IL-17A (100 ng/ml) or (C) left unprimed for 6 h prior to transfection with Lipo/Poly(I:C) (1 μg/ml), stimulation with LL37/Poly(I:C) complexes (5 μg/ml) or one UVB pulse (0.0875 J/cm2) for 18 h. Data are presented as a representative (A, B) of three independent experiments or are presented (C, D) as the mean ±S.E.M. of 3 independent experiments and analysed with two-way ANOVA and Šidák’s multiple comparisons test. **p < 0.01, ***p < 0.001, ****p < 0.0001. ns non- significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.

Journal: Cell death & disease

Article Title: LL37 complexed to double-stranded RNA induces RIG-I-like receptor signalling and Gasdermin E activation facilitating IL-36γ release from keratinocytes.

doi: 10.1038/s41419-025-07537-9

Figure Lengend Snippet: Fig. 4 LL37/Poly(I:C) complexes activate Caspase-3 and GSDME cleavage in human primary keratinocytes. A, B HPKs were stimulated with LL37/Poly(I:C) complexes (5 μg/ml) or were transfected with Poly(I:C) (1 μg/ml) for indicated times control treatment (−) indicates Medium or Lipo, respectively. Supernatants and cell lysates were subjected to SDS-PAGE and immunoblotting with indicated antibodies. * indicates non- specific band (C, D) GSDME-deficient N/TERT-1 cells (sgGSDME) were (D) primed with IL-17A (100 ng/ml) or (C) left unprimed for 6 h prior to transfection with Lipo/Poly(I:C) (1 μg/ml), stimulation with LL37/Poly(I:C) complexes (5 μg/ml) or one UVB pulse (0.0875 J/cm2) for 18 h. Data are presented as a representative (A, B) of three independent experiments or are presented (C, D) as the mean ±S.E.M. of 3 independent experiments and analysed with two-way ANOVA and Šidák’s multiple comparisons test. **p < 0.01, ***p < 0.001, ****p < 0.0001. ns non- significant, Lipo Lipofectamine 2000, M protein marker, sg single-guide RNA.

Article Snippet: HPKs were transfected by the 1 μg/ml HMW Poly(I:C) coupled with biotin (Invivogen) using Lipofectamine 2000, or treated with 1 μg/ml LL37 with and without pre-incubation with 1 μg/ml HMW Poly(I:C) coupled with Biotin (Invivogen).

Techniques: Transfection, Control, SDS Page, Western Blot, Marker