e2f4 (a-20) rabbit polyclonal antibody Search Results


e2f4  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology e2f4
E2f4, 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
https://www.bioz.com/result/e2f4/product/Santa Cruz Biotechnology
Average 93 stars, based on 1 article reviews
e2f4 - by Bioz Stars, 2026-03
93/100 stars
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anti-e2f4  (Santa Cruz Biotechnology)
90
Santa Cruz Biotechnology anti-e2f4
Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, HDAC2, or <t>E2F4</t> separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.
Anti E2f4, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti-e2f4/product/Santa Cruz Biotechnology
Average 90 stars, based on 1 article reviews
anti-e2f4 - by Bioz Stars, 2026-03
90/100 stars
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antibody a-e2f4 c-20  (Santa Cruz Biotechnology)
90
Santa Cruz Biotechnology antibody a-e2f4 c-20
Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, HDAC2, or <t>E2F4</t> separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.
Antibody A E2f4 C 20, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/antibody a-e2f4 c-20/product/Santa Cruz Biotechnology
Average 90 stars, based on 1 article reviews
antibody a-e2f4 c-20 - by Bioz Stars, 2026-03
90/100 stars
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rabbit anti e2f4  (Santa Cruz Biotechnology)
94
Santa Cruz Biotechnology rabbit anti e2f4
Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, HDAC2, or <t>E2F4</t> separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.
Rabbit Anti E2f4, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit anti e2f4/product/Santa Cruz Biotechnology
Average 94 stars, based on 1 article reviews
rabbit anti e2f4 - by Bioz Stars, 2026-03
94/100 stars
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prb  (Becton Dickinson)
90
Becton Dickinson prb
Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, HDAC2, or <t>E2F4</t> separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.
Prb, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/prb/product/Becton Dickinson
Average 90 stars, based on 1 article reviews
prb - by Bioz Stars, 2026-03
90/100 stars
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protein or g-sepharose beads  (Thermo Fisher)
90
Thermo Fisher protein or g-sepharose beads
Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, HDAC2, or <t>E2F4</t> separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.
Protein Or G Sepharose Beads, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/protein or g-sepharose beads/product/Thermo Fisher
Average 90 stars, based on 1 article reviews
protein or g-sepharose beads - by Bioz Stars, 2026-03
90/100 stars
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anti-actin  (Millipore)
90
Millipore anti-actin
Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, HDAC2, or <t>E2F4</t> separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.
Anti Actin, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti-actin/product/Millipore
Average 90 stars, based on 1 article reviews
anti-actin - by Bioz Stars, 2026-03
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anti-hdac1  (Millipore)
90
Millipore anti-hdac1
Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against <t>HDAC1,</t> HDAC2, or E2F4 separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.
Anti Hdac1, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti-hdac1/product/Millipore
Average 90 stars, based on 1 article reviews
anti-hdac1 - by Bioz Stars, 2026-03
90/100 stars
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anti–α-tubulin  (Millipore)
90
Millipore anti–α-tubulin
Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against <t>HDAC1,</t> HDAC2, or E2F4 separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.
Anti–α Tubulin, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti–α-tubulin/product/Millipore
Average 90 stars, based on 1 article reviews
anti–α-tubulin - by Bioz Stars, 2026-03
90/100 stars
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anti-hdac2  (Millipore)
90
Millipore anti-hdac2
Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, <t>HDAC2,</t> or E2F4 separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.
Anti Hdac2, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti-hdac2/product/Millipore
Average 90 stars, based on 1 article reviews
anti-hdac2 - by Bioz Stars, 2026-03
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a-ha (mms-101) antibody  (Covance)
90
Covance a-ha (mms-101) antibody
Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, <t>HDAC2,</t> or E2F4 separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.
A Ha (Mms 101) Antibody, supplied by Covance, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/a-ha (mms-101) antibody/product/Covance
Average 90 stars, based on 1 article reviews
a-ha (mms-101) antibody - by Bioz Stars, 2026-03
90/100 stars
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cyclin d3 (ab-2  (Thermo Fisher)
90
Thermo Fisher cyclin d3 (ab-2
Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, <t>HDAC2,</t> or E2F4 separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.
Cyclin D3 (Ab 2, supplied by Thermo Fisher, 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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cyclin d3 (ab-2 - by Bioz Stars, 2026-03
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Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, HDAC2, or E2F4 separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.

Journal: The Journal of Experimental Medicine

Article Title: HDAC stimulates gene expression through BRD4 availability in response to IFN and in interferonopathies

doi: 10.1084/jem.20180520

Figure Lengend Snippet: Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, HDAC2, or E2F4 separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.

Article Snippet: Antibodies used were anti-IRF9 , anti-STAT1, anti-STAT2, anti-phospho-STAT1 and anti-phospho-STAT2 (Invitrogen), anti–α-tubulin (T9026; Sigma), anti-HDAC1 (clone 2E10, 05-614; Millipore Sigma), anti-HDAC2 (clone 3F3, 05-814; Millipore Sigma), anti-E2F4 (A-20, sc-1082; Santa Cruz Biotechnology), anti-Sin3B (AK-12; Santa Cruz Biotechnology), anti–NELF-E (H140; Santa Cruz Biotechnology), anti-Brd4 (A-301-985A100; Bethyl Laboratories), anti-actin (Clone C4, MAB1501; Millipore Sigma).

Techniques: Expressing, Quantitative RT-PCR, Transfection, Western Blot, Molecular Weight, Construct

Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, HDAC2, or E2F4 separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.

Journal: The Journal of Experimental Medicine

Article Title: HDAC stimulates gene expression through BRD4 availability in response to IFN and in interferonopathies

doi: 10.1084/jem.20180520

Figure Lengend Snippet: Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, HDAC2, or E2F4 separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.

Article Snippet: Antibodies used were anti-IRF9 , anti-STAT1, anti-STAT2, anti-phospho-STAT1 and anti-phospho-STAT2 (Invitrogen), anti–α-tubulin (T9026; Sigma), anti-HDAC1 (clone 2E10, 05-614; Millipore Sigma), anti-HDAC2 (clone 3F3, 05-814; Millipore Sigma), anti-E2F4 (A-20, sc-1082; Santa Cruz Biotechnology), anti-Sin3B (AK-12; Santa Cruz Biotechnology), anti–NELF-E (H140; Santa Cruz Biotechnology), anti-Brd4 (A-301-985A100; Bethyl Laboratories), anti-actin (Clone C4, MAB1501; Millipore Sigma).

Techniques: Expressing, Quantitative RT-PCR, Transfection, Western Blot, Molecular Weight, Construct

Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, HDAC2, or E2F4 separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.

Journal: The Journal of Experimental Medicine

Article Title: HDAC stimulates gene expression through BRD4 availability in response to IFN and in interferonopathies

doi: 10.1084/jem.20180520

Figure Lengend Snippet: Class I HDAC mediates ISG expression. (A and B) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of Romidepsin or TSA, as indicated. RNA was quantified by real-time RT-PCR for ISG54 and p21 WAF1/Cip1 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (C) HeLa cells were treated with IFN-α for 6 h in the absence or presence of increasing concentrations of romidepsin, RGFP966, or RGFP233, as indicated. RNA was quantified by real-time RT-PCR for IRF9 expression, normalized to GAPDH, and represented as fold induction over untreated cells. (D and E) HEK293 cells were transfected with siRNA against HDAC1, HDAC2, or E2F4 separately (D) or with a combination of HDAC1 and HDAC2 targeting oligonucleotides (E), and cells were stimulated with IFN-α for 6 h (α) in the presence (αΤ) or absence of TSA, as indicated. Whole-cell extracts were analyzed for expression of the indicated proteins by Western blotting (left). ISG54 expression was quantified by real-time RT-PCR and represented in arbitrary units (right). MW, molecular weight. A.U., arbitrary units. (F) HEK293T cells were transfected with pcDNA3 (Ctl), HDAC1, or HDAC2 expression constructs, and ISG54 expression was quantified after stimulation with IFN-α for 10 h. Representative data from two experiments are shown. (G) Sin3A F/– and Sin3A F/– Sin3B F/– immortalized mouse embryonic fibroblasts expressing Cre-ERT2 were treated for 3 d with 4OH-tamoxifen (4OH-T) or left untreated. Nuclear extracts were analyzed for expression of Sin3B by Western blotting (middle). Expression of Sin3A, represented as percent expression relative to levels before tamoxifen treatment (left) and expression of IRF9 mRNA before and after tamoxifen (right), were quantified by real-time RT-PCR and normalized to GAPDH mRNA expression. Weak expression of Sin3B protein in Sin3A F/– Sin3B F/– fibroblasts before 4OH-T treatment is likely due to some leakiness of Cre recombinase expression. Quantitative data are representative examples of three (A and F) or two (B, C, E, and G) independent experiments, each performed in duplicate, and error bars represent +SD. *, P < 0.05; **, P < 0.005; ***, P < 0.001.

Article Snippet: Antibodies used were anti-IRF9 , anti-STAT1, anti-STAT2, anti-phospho-STAT1 and anti-phospho-STAT2 (Invitrogen), anti–α-tubulin (T9026; Sigma), anti-HDAC1 (clone 2E10, 05-614; Millipore Sigma), anti-HDAC2 (clone 3F3, 05-814; Millipore Sigma), anti-E2F4 (A-20, sc-1082; Santa Cruz Biotechnology), anti-Sin3B (AK-12; Santa Cruz Biotechnology), anti–NELF-E (H140; Santa Cruz Biotechnology), anti-Brd4 (A-301-985A100; Bethyl Laboratories), anti-actin (Clone C4, MAB1501; Millipore Sigma).

Techniques: Expressing, Quantitative RT-PCR, Transfection, Western Blot, Molecular Weight, Construct