en2 Search Results


human en2 biotinylated antibody  (Bioss)
91
Bioss human en2 biotinylated antibody
Human En2 Biotinylated Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human en2 biotinylated antibody/product/Bioss
Average 91 stars, based on 1 article reviews
human en2 biotinylated antibody - by Bioz Stars, 2026-03
91/100 stars
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gene exp en2 mm00438710 m1  (Thermo Fisher)
85
Thermo Fisher gene exp en2 mm00438710 m1
(a,b) Representative immunofluorescence images are shown (NeuN+ neurons: red; cCASP3+: green; DAPI: blue). Dotted circles: cCASP3+/NeuN+ cell. Scale: 10 μm. (a) Quantification of cCASP3+ cells per cm 2 from 4mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or PLX-treated mice (striatum: mean=2.500, SEM=1.443; cerebellum: mean=119.2, SEM=20.02); p<0.0001, F=67.40; 14 cerebellum/striatum sections from n=4 mice/group. (b) Quantification of cCASP3+ cells per cm 2 from 4/5mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or Axl −/− Mertk −/− mice (striatum: mean=0, SEM=0; cerebellum: mean=33.17, SEM=8.355); p=0.0003, F=14.62;12 cerebellum/striatum sections from n=4 mice/group. Bar graphs with individual data points show mean ± SEM, one-way ANOVA with Tukey’s Multiple Comparison. (c) Horizontal bar graph shows relative expression (qPCR) of selected cbMg-enriched (orange) and stMg-enriched (purple) genes in microglia after 12 hours of exposure to vehicle or early apoptotic cells. Pparg (p=0.002, t 4 =7.144), Jdp2 (p<0.0001, t 4 =15.16), Rarg (p=0.001, t 4 =10.16), Tfec (p<0.0001, t 4 =11.47); Ahr (p=0.004, t 4 =6.033), <t>En2</t> (p=0.025, t 4 =3.493), Tead4 (p=0.002, t 4 =7.013), Anxa2 (p<0.0001, t 4 =36.96), Colec12 (p=0.002, t 4 =7.498), Lilrb4 (p<0.0001, t 4 =14.04), Apoe (p=0.002, t 4 =6.964), Cd74 (p=0.001, t 4 =8.070), Ptch1 (p=0.037, t 4 =3.066), Clec7a (p=0.015, t 4 =4.064), Msr1 (p=0.011, t 4 =4.448), Lyz2 (p=0.024, t 4 =3.529), Ptplad2 (p=0.009, t 4 =4.809), Kdm6b (p<0.0001, t 4 =15.33), Kdm6a (p=0.004, t 4 =5.871), Hhex (p=0.025, t 4 =3.501), Esr1 (p=0.018, t 4 =3.885), Irf8 (p=0.001, t 4 =9.580), Sall1 (p=0.139, t 4 =1.842), Sall3 (p=0.449, t 4 =0.8381), Slc2a5 (p<0.0001, t 4 =15.30), Asb2 (p<0.0001, t 4 =25.35), Tmem119 (p=0.003, t 4 =6.721), Fscn1 (p<0.0001, t 4 =18.93), P2ry12 (p=0.733, t 4 =0.3659), and Fcrls (p=0.001, t 4 =10.31). Bar graphs show mean ± SEM, two-tailed unpaired t-test, n=3 wells of primary microglia cultures obtained from four 3mo mice. Experiment was independently reproduced 4 times.
Gene Exp En2 Mm00438710 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 85 stars, based on 1 article reviews
gene exp en2 mm00438710 m1 - by Bioz Stars, 2026-03
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en2  (Bioss)
90
Bioss en2
(a,b) Representative immunofluorescence images are shown (NeuN+ neurons: red; cCASP3+: green; DAPI: blue). Dotted circles: cCASP3+/NeuN+ cell. Scale: 10 μm. (a) Quantification of cCASP3+ cells per cm 2 from 4mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or PLX-treated mice (striatum: mean=2.500, SEM=1.443; cerebellum: mean=119.2, SEM=20.02); p<0.0001, F=67.40; 14 cerebellum/striatum sections from n=4 mice/group. (b) Quantification of cCASP3+ cells per cm 2 from 4/5mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or Axl −/− Mertk −/− mice (striatum: mean=0, SEM=0; cerebellum: mean=33.17, SEM=8.355); p=0.0003, F=14.62;12 cerebellum/striatum sections from n=4 mice/group. Bar graphs with individual data points show mean ± SEM, one-way ANOVA with Tukey’s Multiple Comparison. (c) Horizontal bar graph shows relative expression (qPCR) of selected cbMg-enriched (orange) and stMg-enriched (purple) genes in microglia after 12 hours of exposure to vehicle or early apoptotic cells. Pparg (p=0.002, t 4 =7.144), Jdp2 (p<0.0001, t 4 =15.16), Rarg (p=0.001, t 4 =10.16), Tfec (p<0.0001, t 4 =11.47); Ahr (p=0.004, t 4 =6.033), <t>En2</t> (p=0.025, t 4 =3.493), Tead4 (p=0.002, t 4 =7.013), Anxa2 (p<0.0001, t 4 =36.96), Colec12 (p=0.002, t 4 =7.498), Lilrb4 (p<0.0001, t 4 =14.04), Apoe (p=0.002, t 4 =6.964), Cd74 (p=0.001, t 4 =8.070), Ptch1 (p=0.037, t 4 =3.066), Clec7a (p=0.015, t 4 =4.064), Msr1 (p=0.011, t 4 =4.448), Lyz2 (p=0.024, t 4 =3.529), Ptplad2 (p=0.009, t 4 =4.809), Kdm6b (p<0.0001, t 4 =15.33), Kdm6a (p=0.004, t 4 =5.871), Hhex (p=0.025, t 4 =3.501), Esr1 (p=0.018, t 4 =3.885), Irf8 (p=0.001, t 4 =9.580), Sall1 (p=0.139, t 4 =1.842), Sall3 (p=0.449, t 4 =0.8381), Slc2a5 (p<0.0001, t 4 =15.30), Asb2 (p<0.0001, t 4 =25.35), Tmem119 (p=0.003, t 4 =6.721), Fscn1 (p<0.0001, t 4 =18.93), P2ry12 (p=0.733, t 4 =0.3659), and Fcrls (p=0.001, t 4 =10.31). Bar graphs show mean ± SEM, two-tailed unpaired t-test, n=3 wells of primary microglia cultures obtained from four 3mo mice. Experiment was independently reproduced 4 times.
En2, supplied by Bioss, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
en2 - by Bioz Stars, 2026-03
90/100 stars
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ptx  (StressMarq)
93
StressMarq ptx
(a,b) Representative immunofluorescence images are shown (NeuN+ neurons: red; cCASP3+: green; DAPI: blue). Dotted circles: cCASP3+/NeuN+ cell. Scale: 10 μm. (a) Quantification of cCASP3+ cells per cm 2 from 4mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or PLX-treated mice (striatum: mean=2.500, SEM=1.443; cerebellum: mean=119.2, SEM=20.02); p<0.0001, F=67.40; 14 cerebellum/striatum sections from n=4 mice/group. (b) Quantification of cCASP3+ cells per cm 2 from 4/5mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or Axl −/− Mertk −/− mice (striatum: mean=0, SEM=0; cerebellum: mean=33.17, SEM=8.355); p=0.0003, F=14.62;12 cerebellum/striatum sections from n=4 mice/group. Bar graphs with individual data points show mean ± SEM, one-way ANOVA with Tukey’s Multiple Comparison. (c) Horizontal bar graph shows relative expression (qPCR) of selected cbMg-enriched (orange) and stMg-enriched (purple) genes in microglia after 12 hours of exposure to vehicle or early apoptotic cells. Pparg (p=0.002, t 4 =7.144), Jdp2 (p<0.0001, t 4 =15.16), Rarg (p=0.001, t 4 =10.16), Tfec (p<0.0001, t 4 =11.47); Ahr (p=0.004, t 4 =6.033), <t>En2</t> (p=0.025, t 4 =3.493), Tead4 (p=0.002, t 4 =7.013), Anxa2 (p<0.0001, t 4 =36.96), Colec12 (p=0.002, t 4 =7.498), Lilrb4 (p<0.0001, t 4 =14.04), Apoe (p=0.002, t 4 =6.964), Cd74 (p=0.001, t 4 =8.070), Ptch1 (p=0.037, t 4 =3.066), Clec7a (p=0.015, t 4 =4.064), Msr1 (p=0.011, t 4 =4.448), Lyz2 (p=0.024, t 4 =3.529), Ptplad2 (p=0.009, t 4 =4.809), Kdm6b (p<0.0001, t 4 =15.33), Kdm6a (p=0.004, t 4 =5.871), Hhex (p=0.025, t 4 =3.501), Esr1 (p=0.018, t 4 =3.885), Irf8 (p=0.001, t 4 =9.580), Sall1 (p=0.139, t 4 =1.842), Sall3 (p=0.449, t 4 =0.8381), Slc2a5 (p<0.0001, t 4 =15.30), Asb2 (p<0.0001, t 4 =25.35), Tmem119 (p=0.003, t 4 =6.721), Fscn1 (p<0.0001, t 4 =18.93), P2ry12 (p=0.733, t 4 =0.3659), and Fcrls (p=0.001, t 4 =10.31). Bar graphs show mean ± SEM, two-tailed unpaired t-test, n=3 wells of primary microglia cultures obtained from four 3mo mice. Experiment was independently reproduced 4 times.
Ptx, supplied by StressMarq, 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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Average 93 stars, based on 1 article reviews
ptx - by Bioz Stars, 2026-03
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potassium e trifluoro prop 1 en 1 yl borate  (Frontier Specialty Chemicals Inc)
90
Frontier Specialty Chemicals Inc potassium e trifluoro prop 1 en 1 yl borate
(a,b) Representative immunofluorescence images are shown (NeuN+ neurons: red; cCASP3+: green; DAPI: blue). Dotted circles: cCASP3+/NeuN+ cell. Scale: 10 μm. (a) Quantification of cCASP3+ cells per cm 2 from 4mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or PLX-treated mice (striatum: mean=2.500, SEM=1.443; cerebellum: mean=119.2, SEM=20.02); p<0.0001, F=67.40; 14 cerebellum/striatum sections from n=4 mice/group. (b) Quantification of cCASP3+ cells per cm 2 from 4/5mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or Axl −/− Mertk −/− mice (striatum: mean=0, SEM=0; cerebellum: mean=33.17, SEM=8.355); p=0.0003, F=14.62;12 cerebellum/striatum sections from n=4 mice/group. Bar graphs with individual data points show mean ± SEM, one-way ANOVA with Tukey’s Multiple Comparison. (c) Horizontal bar graph shows relative expression (qPCR) of selected cbMg-enriched (orange) and stMg-enriched (purple) genes in microglia after 12 hours of exposure to vehicle or early apoptotic cells. Pparg (p=0.002, t 4 =7.144), Jdp2 (p<0.0001, t 4 =15.16), Rarg (p=0.001, t 4 =10.16), Tfec (p<0.0001, t 4 =11.47); Ahr (p=0.004, t 4 =6.033), <t>En2</t> (p=0.025, t 4 =3.493), Tead4 (p=0.002, t 4 =7.013), Anxa2 (p<0.0001, t 4 =36.96), Colec12 (p=0.002, t 4 =7.498), Lilrb4 (p<0.0001, t 4 =14.04), Apoe (p=0.002, t 4 =6.964), Cd74 (p=0.001, t 4 =8.070), Ptch1 (p=0.037, t 4 =3.066), Clec7a (p=0.015, t 4 =4.064), Msr1 (p=0.011, t 4 =4.448), Lyz2 (p=0.024, t 4 =3.529), Ptplad2 (p=0.009, t 4 =4.809), Kdm6b (p<0.0001, t 4 =15.33), Kdm6a (p=0.004, t 4 =5.871), Hhex (p=0.025, t 4 =3.501), Esr1 (p=0.018, t 4 =3.885), Irf8 (p=0.001, t 4 =9.580), Sall1 (p=0.139, t 4 =1.842), Sall3 (p=0.449, t 4 =0.8381), Slc2a5 (p<0.0001, t 4 =15.30), Asb2 (p<0.0001, t 4 =25.35), Tmem119 (p=0.003, t 4 =6.721), Fscn1 (p<0.0001, t 4 =18.93), P2ry12 (p=0.733, t 4 =0.3659), and Fcrls (p=0.001, t 4 =10.31). Bar graphs show mean ± SEM, two-tailed unpaired t-test, n=3 wells of primary microglia cultures obtained from four 3mo mice. Experiment was independently reproduced 4 times.
Potassium E Trifluoro Prop 1 En 1 Yl Borate, supplied by Frontier Specialty Chemicals Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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gene exp en2 hs00171321 m1  (Thermo Fisher)
86
Thermo Fisher gene exp en2 hs00171321 m1
(a,b) Representative immunofluorescence images are shown (NeuN+ neurons: red; cCASP3+: green; DAPI: blue). Dotted circles: cCASP3+/NeuN+ cell. Scale: 10 μm. (a) Quantification of cCASP3+ cells per cm 2 from 4mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or PLX-treated mice (striatum: mean=2.500, SEM=1.443; cerebellum: mean=119.2, SEM=20.02); p<0.0001, F=67.40; 14 cerebellum/striatum sections from n=4 mice/group. (b) Quantification of cCASP3+ cells per cm 2 from 4/5mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or Axl −/− Mertk −/− mice (striatum: mean=0, SEM=0; cerebellum: mean=33.17, SEM=8.355); p=0.0003, F=14.62;12 cerebellum/striatum sections from n=4 mice/group. Bar graphs with individual data points show mean ± SEM, one-way ANOVA with Tukey’s Multiple Comparison. (c) Horizontal bar graph shows relative expression (qPCR) of selected cbMg-enriched (orange) and stMg-enriched (purple) genes in microglia after 12 hours of exposure to vehicle or early apoptotic cells. Pparg (p=0.002, t 4 =7.144), Jdp2 (p<0.0001, t 4 =15.16), Rarg (p=0.001, t 4 =10.16), Tfec (p<0.0001, t 4 =11.47); Ahr (p=0.004, t 4 =6.033), <t>En2</t> (p=0.025, t 4 =3.493), Tead4 (p=0.002, t 4 =7.013), Anxa2 (p<0.0001, t 4 =36.96), Colec12 (p=0.002, t 4 =7.498), Lilrb4 (p<0.0001, t 4 =14.04), Apoe (p=0.002, t 4 =6.964), Cd74 (p=0.001, t 4 =8.070), Ptch1 (p=0.037, t 4 =3.066), Clec7a (p=0.015, t 4 =4.064), Msr1 (p=0.011, t 4 =4.448), Lyz2 (p=0.024, t 4 =3.529), Ptplad2 (p=0.009, t 4 =4.809), Kdm6b (p<0.0001, t 4 =15.33), Kdm6a (p=0.004, t 4 =5.871), Hhex (p=0.025, t 4 =3.501), Esr1 (p=0.018, t 4 =3.885), Irf8 (p=0.001, t 4 =9.580), Sall1 (p=0.139, t 4 =1.842), Sall3 (p=0.449, t 4 =0.8381), Slc2a5 (p<0.0001, t 4 =15.30), Asb2 (p<0.0001, t 4 =25.35), Tmem119 (p=0.003, t 4 =6.721), Fscn1 (p<0.0001, t 4 =18.93), P2ry12 (p=0.733, t 4 =0.3659), and Fcrls (p=0.001, t 4 =10.31). Bar graphs show mean ± SEM, two-tailed unpaired t-test, n=3 wells of primary microglia cultures obtained from four 3mo mice. Experiment was independently reproduced 4 times.
Gene Exp En2 Hs00171321 M1, supplied by Thermo Fisher, 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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Average 86 stars, based on 1 article reviews
gene exp en2 hs00171321 m1 - by Bioz Stars, 2026-03
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s19 compound pa463  (Chem Impex International)
95
Chem Impex International s19 compound pa463
(a,b) Representative immunofluorescence images are shown (NeuN+ neurons: red; cCASP3+: green; DAPI: blue). Dotted circles: cCASP3+/NeuN+ cell. Scale: 10 μm. (a) Quantification of cCASP3+ cells per cm 2 from 4mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or PLX-treated mice (striatum: mean=2.500, SEM=1.443; cerebellum: mean=119.2, SEM=20.02); p<0.0001, F=67.40; 14 cerebellum/striatum sections from n=4 mice/group. (b) Quantification of cCASP3+ cells per cm 2 from 4/5mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or Axl −/− Mertk −/− mice (striatum: mean=0, SEM=0; cerebellum: mean=33.17, SEM=8.355); p=0.0003, F=14.62;12 cerebellum/striatum sections from n=4 mice/group. Bar graphs with individual data points show mean ± SEM, one-way ANOVA with Tukey’s Multiple Comparison. (c) Horizontal bar graph shows relative expression (qPCR) of selected cbMg-enriched (orange) and stMg-enriched (purple) genes in microglia after 12 hours of exposure to vehicle or early apoptotic cells. Pparg (p=0.002, t 4 =7.144), Jdp2 (p<0.0001, t 4 =15.16), Rarg (p=0.001, t 4 =10.16), Tfec (p<0.0001, t 4 =11.47); Ahr (p=0.004, t 4 =6.033), <t>En2</t> (p=0.025, t 4 =3.493), Tead4 (p=0.002, t 4 =7.013), Anxa2 (p<0.0001, t 4 =36.96), Colec12 (p=0.002, t 4 =7.498), Lilrb4 (p<0.0001, t 4 =14.04), Apoe (p=0.002, t 4 =6.964), Cd74 (p=0.001, t 4 =8.070), Ptch1 (p=0.037, t 4 =3.066), Clec7a (p=0.015, t 4 =4.064), Msr1 (p=0.011, t 4 =4.448), Lyz2 (p=0.024, t 4 =3.529), Ptplad2 (p=0.009, t 4 =4.809), Kdm6b (p<0.0001, t 4 =15.33), Kdm6a (p=0.004, t 4 =5.871), Hhex (p=0.025, t 4 =3.501), Esr1 (p=0.018, t 4 =3.885), Irf8 (p=0.001, t 4 =9.580), Sall1 (p=0.139, t 4 =1.842), Sall3 (p=0.449, t 4 =0.8381), Slc2a5 (p<0.0001, t 4 =15.30), Asb2 (p<0.0001, t 4 =25.35), Tmem119 (p=0.003, t 4 =6.721), Fscn1 (p<0.0001, t 4 =18.93), P2ry12 (p=0.733, t 4 =0.3659), and Fcrls (p=0.001, t 4 =10.31). Bar graphs show mean ± SEM, two-tailed unpaired t-test, n=3 wells of primary microglia cultures obtained from four 3mo mice. Experiment was independently reproduced 4 times.
S19 Compound Pa463, supplied by Chem Impex International, 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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lentiviral transduction particles  (Santa Cruz Biotechnology)
86
Santa Cruz Biotechnology lentiviral transduction particles
Figure 2. Aggregation of spectrin in Fas-associated death domain protein (FADD) knockdown (KnD) Jurkat T cells upon tumor necrosis factor-related apoptosis-inducing ligand (TRAIL-induced apoptosis). A. Level of FADD protein is decreased by 70% in FADD KnD cells, in comparison to control Jurkat T cells. shRNA <t>lentiviral</t> vector was used to establish stable FADD KnD cell-line. Level of FADD was analyzed by immunoblotting using mouse anti-FADD and rabbit anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1 in Material and methods, and evaluated by densitometry; B. Progression of TRAIL-induced apoptosis in FADD KnD cells was evaluated using an Annexin V-FITC Apoptotic Detection Kit with a flow cytometer. Note a statistically significant difference in the progres- sion of apoptosis in FADD KnD cells compared to control cells within 4 h of TRAIL treatment (100 ng/mL); *,** P ≤ 0.05 and P ≤ 0.01, respectively; C. Spectrin aggregates were observed later (90 min of TRAIL-treatment) in FADD KnD cells than in control cells (60 min of TRAIL-treatment). Analysis of spectrin aggregation in FADD KnD cells was performed by immunoblot analysis of detergent-insoluble fractions using mouse anti-spectrin and mouse anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1
Lentiviral Transduction Particles, supplied by Santa Cruz 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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hex 5 en 2 ol  (Biosynth Carbosynth)
91
Biosynth Carbosynth hex 5 en 2 ol
Figure 2. Aggregation of spectrin in Fas-associated death domain protein (FADD) knockdown (KnD) Jurkat T cells upon tumor necrosis factor-related apoptosis-inducing ligand (TRAIL-induced apoptosis). A. Level of FADD protein is decreased by 70% in FADD KnD cells, in comparison to control Jurkat T cells. shRNA <t>lentiviral</t> vector was used to establish stable FADD KnD cell-line. Level of FADD was analyzed by immunoblotting using mouse anti-FADD and rabbit anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1 in Material and methods, and evaluated by densitometry; B. Progression of TRAIL-induced apoptosis in FADD KnD cells was evaluated using an Annexin V-FITC Apoptotic Detection Kit with a flow cytometer. Note a statistically significant difference in the progres- sion of apoptosis in FADD KnD cells compared to control cells within 4 h of TRAIL treatment (100 ng/mL); *,** P ≤ 0.05 and P ≤ 0.01, respectively; C. Spectrin aggregates were observed later (90 min of TRAIL-treatment) in FADD KnD cells than in control cells (60 min of TRAIL-treatment). Analysis of spectrin aggregation in FADD KnD cells was performed by immunoblot analysis of detergent-insoluble fractions using mouse anti-spectrin and mouse anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1
Hex 5 En 2 Ol, supplied by Biosynth Carbosynth, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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copper ii acetylacetonate  (Chem Impex International)
96
Chem Impex International copper ii acetylacetonate
Figure 2. Aggregation of spectrin in Fas-associated death domain protein (FADD) knockdown (KnD) Jurkat T cells upon tumor necrosis factor-related apoptosis-inducing ligand (TRAIL-induced apoptosis). A. Level of FADD protein is decreased by 70% in FADD KnD cells, in comparison to control Jurkat T cells. shRNA <t>lentiviral</t> vector was used to establish stable FADD KnD cell-line. Level of FADD was analyzed by immunoblotting using mouse anti-FADD and rabbit anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1 in Material and methods, and evaluated by densitometry; B. Progression of TRAIL-induced apoptosis in FADD KnD cells was evaluated using an Annexin V-FITC Apoptotic Detection Kit with a flow cytometer. Note a statistically significant difference in the progres- sion of apoptosis in FADD KnD cells compared to control cells within 4 h of TRAIL treatment (100 ng/mL); *,** P ≤ 0.05 and P ≤ 0.01, respectively; C. Spectrin aggregates were observed later (90 min of TRAIL-treatment) in FADD KnD cells than in control cells (60 min of TRAIL-treatment). Analysis of spectrin aggregation in FADD KnD cells was performed by immunoblot analysis of detergent-insoluble fractions using mouse anti-spectrin and mouse anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1
Copper Ii Acetylacetonate, supplied by Chem Impex International, 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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2 17b amp  (Chem Impex International)
95
Chem Impex International 2 17b amp
Figure 2. Aggregation of spectrin in Fas-associated death domain protein (FADD) knockdown (KnD) Jurkat T cells upon tumor necrosis factor-related apoptosis-inducing ligand (TRAIL-induced apoptosis). A. Level of FADD protein is decreased by 70% in FADD KnD cells, in comparison to control Jurkat T cells. shRNA <t>lentiviral</t> vector was used to establish stable FADD KnD cell-line. Level of FADD was analyzed by immunoblotting using mouse anti-FADD and rabbit anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1 in Material and methods, and evaluated by densitometry; B. Progression of TRAIL-induced apoptosis in FADD KnD cells was evaluated using an Annexin V-FITC Apoptotic Detection Kit with a flow cytometer. Note a statistically significant difference in the progres- sion of apoptosis in FADD KnD cells compared to control cells within 4 h of TRAIL treatment (100 ng/mL); *,** P ≤ 0.05 and P ≤ 0.01, respectively; C. Spectrin aggregates were observed later (90 min of TRAIL-treatment) in FADD KnD cells than in control cells (60 min of TRAIL-treatment). Analysis of spectrin aggregation in FADD KnD cells was performed by immunoblot analysis of detergent-insoluble fractions using mouse anti-spectrin and mouse anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1
2 17b Amp, supplied by Chem Impex International, 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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en2  (Cusabio)
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Figure 2. Aggregation of spectrin in Fas-associated death domain protein (FADD) knockdown (KnD) Jurkat T cells upon tumor necrosis factor-related apoptosis-inducing ligand (TRAIL-induced apoptosis). A. Level of FADD protein is decreased by 70% in FADD KnD cells, in comparison to control Jurkat T cells. shRNA <t>lentiviral</t> vector was used to establish stable FADD KnD cell-line. Level of FADD was analyzed by immunoblotting using mouse anti-FADD and rabbit anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1 in Material and methods, and evaluated by densitometry; B. Progression of TRAIL-induced apoptosis in FADD KnD cells was evaluated using an Annexin V-FITC Apoptotic Detection Kit with a flow cytometer. Note a statistically significant difference in the progres- sion of apoptosis in FADD KnD cells compared to control cells within 4 h of TRAIL treatment (100 ng/mL); *,** P ≤ 0.05 and P ≤ 0.01, respectively; C. Spectrin aggregates were observed later (90 min of TRAIL-treatment) in FADD KnD cells than in control cells (60 min of TRAIL-treatment). Analysis of spectrin aggregation in FADD KnD cells was performed by immunoblot analysis of detergent-insoluble fractions using mouse anti-spectrin and mouse anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1
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Image Search Results


(a,b) Representative immunofluorescence images are shown (NeuN+ neurons: red; cCASP3+: green; DAPI: blue). Dotted circles: cCASP3+/NeuN+ cell. Scale: 10 μm. (a) Quantification of cCASP3+ cells per cm 2 from 4mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or PLX-treated mice (striatum: mean=2.500, SEM=1.443; cerebellum: mean=119.2, SEM=20.02); p<0.0001, F=67.40; 14 cerebellum/striatum sections from n=4 mice/group. (b) Quantification of cCASP3+ cells per cm 2 from 4/5mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or Axl −/− Mertk −/− mice (striatum: mean=0, SEM=0; cerebellum: mean=33.17, SEM=8.355); p=0.0003, F=14.62;12 cerebellum/striatum sections from n=4 mice/group. Bar graphs with individual data points show mean ± SEM, one-way ANOVA with Tukey’s Multiple Comparison. (c) Horizontal bar graph shows relative expression (qPCR) of selected cbMg-enriched (orange) and stMg-enriched (purple) genes in microglia after 12 hours of exposure to vehicle or early apoptotic cells. Pparg (p=0.002, t 4 =7.144), Jdp2 (p<0.0001, t 4 =15.16), Rarg (p=0.001, t 4 =10.16), Tfec (p<0.0001, t 4 =11.47); Ahr (p=0.004, t 4 =6.033), En2 (p=0.025, t 4 =3.493), Tead4 (p=0.002, t 4 =7.013), Anxa2 (p<0.0001, t 4 =36.96), Colec12 (p=0.002, t 4 =7.498), Lilrb4 (p<0.0001, t 4 =14.04), Apoe (p=0.002, t 4 =6.964), Cd74 (p=0.001, t 4 =8.070), Ptch1 (p=0.037, t 4 =3.066), Clec7a (p=0.015, t 4 =4.064), Msr1 (p=0.011, t 4 =4.448), Lyz2 (p=0.024, t 4 =3.529), Ptplad2 (p=0.009, t 4 =4.809), Kdm6b (p<0.0001, t 4 =15.33), Kdm6a (p=0.004, t 4 =5.871), Hhex (p=0.025, t 4 =3.501), Esr1 (p=0.018, t 4 =3.885), Irf8 (p=0.001, t 4 =9.580), Sall1 (p=0.139, t 4 =1.842), Sall3 (p=0.449, t 4 =0.8381), Slc2a5 (p<0.0001, t 4 =15.30), Asb2 (p<0.0001, t 4 =25.35), Tmem119 (p=0.003, t 4 =6.721), Fscn1 (p<0.0001, t 4 =18.93), P2ry12 (p=0.733, t 4 =0.3659), and Fcrls (p=0.001, t 4 =10.31). Bar graphs show mean ± SEM, two-tailed unpaired t-test, n=3 wells of primary microglia cultures obtained from four 3mo mice. Experiment was independently reproduced 4 times.

Journal: Nature neuroscience

Article Title: Epigenetic regulation of brain region-specific microglia clearance activity

doi: 10.1038/s41593-018-0192-3

Figure Lengend Snippet: (a,b) Representative immunofluorescence images are shown (NeuN+ neurons: red; cCASP3+: green; DAPI: blue). Dotted circles: cCASP3+/NeuN+ cell. Scale: 10 μm. (a) Quantification of cCASP3+ cells per cm 2 from 4mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or PLX-treated mice (striatum: mean=2.500, SEM=1.443; cerebellum: mean=119.2, SEM=20.02); p<0.0001, F=67.40; 14 cerebellum/striatum sections from n=4 mice/group. (b) Quantification of cCASP3+ cells per cm 2 from 4/5mo control (striatum: mean=0, SEM=0; cerebellum: mean=2.500, SEM=1.443) or Axl −/− Mertk −/− mice (striatum: mean=0, SEM=0; cerebellum: mean=33.17, SEM=8.355); p=0.0003, F=14.62;12 cerebellum/striatum sections from n=4 mice/group. Bar graphs with individual data points show mean ± SEM, one-way ANOVA with Tukey’s Multiple Comparison. (c) Horizontal bar graph shows relative expression (qPCR) of selected cbMg-enriched (orange) and stMg-enriched (purple) genes in microglia after 12 hours of exposure to vehicle or early apoptotic cells. Pparg (p=0.002, t 4 =7.144), Jdp2 (p<0.0001, t 4 =15.16), Rarg (p=0.001, t 4 =10.16), Tfec (p<0.0001, t 4 =11.47); Ahr (p=0.004, t 4 =6.033), En2 (p=0.025, t 4 =3.493), Tead4 (p=0.002, t 4 =7.013), Anxa2 (p<0.0001, t 4 =36.96), Colec12 (p=0.002, t 4 =7.498), Lilrb4 (p<0.0001, t 4 =14.04), Apoe (p=0.002, t 4 =6.964), Cd74 (p=0.001, t 4 =8.070), Ptch1 (p=0.037, t 4 =3.066), Clec7a (p=0.015, t 4 =4.064), Msr1 (p=0.011, t 4 =4.448), Lyz2 (p=0.024, t 4 =3.529), Ptplad2 (p=0.009, t 4 =4.809), Kdm6b (p<0.0001, t 4 =15.33), Kdm6a (p=0.004, t 4 =5.871), Hhex (p=0.025, t 4 =3.501), Esr1 (p=0.018, t 4 =3.885), Irf8 (p=0.001, t 4 =9.580), Sall1 (p=0.139, t 4 =1.842), Sall3 (p=0.449, t 4 =0.8381), Slc2a5 (p<0.0001, t 4 =15.30), Asb2 (p<0.0001, t 4 =25.35), Tmem119 (p=0.003, t 4 =6.721), Fscn1 (p<0.0001, t 4 =18.93), P2ry12 (p=0.733, t 4 =0.3659), and Fcrls (p=0.001, t 4 =10.31). Bar graphs show mean ± SEM, two-tailed unpaired t-test, n=3 wells of primary microglia cultures obtained from four 3mo mice. Experiment was independently reproduced 4 times.

Article Snippet: Probes used are Clec7a (Mm01183349_m1), Anxa2 (Mm01150673_m1), Lilrb4 (Mm01614371_m1), Msr1 (Mm00446214_m1), Cd74 (Mm01262765_g1), Apoe (Mm00437573_m1), Ptch1 (Mm00436026_m1), Ptplad2 (Mm01267670_m1), Lyz2 (Mm01612741_m1), Colec12 (Mm01236242_m1), Ahr (Mm00478932_m1), Jdp2 (Mm00473044_m1), Rarg (Mm00441091_m1), Pparg (Mm00440940_m1), Tfec (Mm01161234_m1), Tead4 (Mm01189836_m1), En2 (Mm00438710_m1), Asb2 (Mm01329892_m1), Irf8 (Mm00492567_m1), Hhex (Mm00433954_m1), Esr1 (Mm00433149_m1), Sall1 (Mm00491266_m1), Sall3 (Mm01265835_m1), Slc2a5 (Mm00600311_m1), Fscn1 (Mm00456046_m1), Fcrls (Mm01219431_m1), Tmem119 (Mm00525305_m1), P2ry12 (Mm01950543_s1), Ifnb1 (Mm00439552_s1), Mx1 (Mm00487796_m1), Ccl2 (Mm00441242_m1), Cxcl10 (Mm00445235_m1), Tnf (Mm00443258_m1), Kdm6b (Mm01332680_m1), Kdm6a (Mm00801998_m1), Gapdh (Mm99999915_g1).

Techniques: Immunofluorescence, Control, Comparison, Expressing, Two Tailed Test

Figure 2. Aggregation of spectrin in Fas-associated death domain protein (FADD) knockdown (KnD) Jurkat T cells upon tumor necrosis factor-related apoptosis-inducing ligand (TRAIL-induced apoptosis). A. Level of FADD protein is decreased by 70% in FADD KnD cells, in comparison to control Jurkat T cells. shRNA lentiviral vector was used to establish stable FADD KnD cell-line. Level of FADD was analyzed by immunoblotting using mouse anti-FADD and rabbit anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1 in Material and methods, and evaluated by densitometry; B. Progression of TRAIL-induced apoptosis in FADD KnD cells was evaluated using an Annexin V-FITC Apoptotic Detection Kit with a flow cytometer. Note a statistically significant difference in the progres- sion of apoptosis in FADD KnD cells compared to control cells within 4 h of TRAIL treatment (100 ng/mL); *,** P ≤ 0.05 and P ≤ 0.01, respectively; C. Spectrin aggregates were observed later (90 min of TRAIL-treatment) in FADD KnD cells than in control cells (60 min of TRAIL-treatment). Analysis of spectrin aggregation in FADD KnD cells was performed by immunoblot analysis of detergent-insoluble fractions using mouse anti-spectrin and mouse anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1

Journal: Folia Histochemica et Cytobiologica

Article Title: PKC-θ is a negative regulator of TRAIL-induced and FADD-mediated apoptotic spectrin aggregation

doi: 10.5603/fhc.a2016.0006

Figure Lengend Snippet: Figure 2. Aggregation of spectrin in Fas-associated death domain protein (FADD) knockdown (KnD) Jurkat T cells upon tumor necrosis factor-related apoptosis-inducing ligand (TRAIL-induced apoptosis). A. Level of FADD protein is decreased by 70% in FADD KnD cells, in comparison to control Jurkat T cells. shRNA lentiviral vector was used to establish stable FADD KnD cell-line. Level of FADD was analyzed by immunoblotting using mouse anti-FADD and rabbit anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1 in Material and methods, and evaluated by densitometry; B. Progression of TRAIL-induced apoptosis in FADD KnD cells was evaluated using an Annexin V-FITC Apoptotic Detection Kit with a flow cytometer. Note a statistically significant difference in the progres- sion of apoptosis in FADD KnD cells compared to control cells within 4 h of TRAIL treatment (100 ng/mL); *,** P ≤ 0.05 and P ≤ 0.01, respectively; C. Spectrin aggregates were observed later (90 min of TRAIL-treatment) in FADD KnD cells than in control cells (60 min of TRAIL-treatment). Analysis of spectrin aggregation in FADD KnD cells was performed by immunoblot analysis of detergent-insoluble fractions using mouse anti-spectrin and mouse anti-actin and developed by using appropriate secondary antibodies as detailed in Table 1

Article Snippet: Jurkat T cells (cells should be approximately 50% confluent) were incubated with the lentiviral transduction particles (20 μL) in the presence of 5 μg/mL of polibrene (Santa Cruz Biotechnology Inc.) for 16 h, then the medium was replaced with RPMI medium containing puromycin (Santa Cruz Biotechnology Inc.) at a final concentration of 2 μg/mL and cultured for additional 48 h. Detection of apoptosis by flow cytometry.

Techniques: Knockdown, Comparison, Control, shRNA, Plasmid Preparation, Western Blot, Flow Cytometry