44094 Search Results


dsm 44094  (ATCC)
91
ATCC dsm 44094
Dsm 44094, supplied by ATCC, 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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plasmid ptf277  (Addgene inc)
93
Addgene inc plasmid ptf277
Plasmid Ptf277, supplied by Addgene inc, 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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gaactccatcagcaataca  (Santa Cruz Biotechnology)
85
Santa Cruz Biotechnology gaactccatcagcaataca
Gaactccatcagcaataca, supplied by Santa Cruz Biotechnology, 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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set7 9 shrna lentivirus  (Santa Cruz Biotechnology)
85
Santa Cruz Biotechnology set7 9 shrna lentivirus
MLL1 knockdown attenuated TGFβ1-induced increases in H3K4me3 on the promoters of TGFBIp and ECM-associated genes. a Wild-type and GCD2-homozygous corneal fibroblasts were infected with MLL1 or control shRNA lentivirus. After puromycin selection, infected cells were stimulated with TGF-β1 (5 ng/ml) for 8 h, and H3K4me3 levels at the indicated gene promoters were analyzed. ChIP assays were performed with H3K4me3 antibody. Immunoprecipitated DNA and input DNA were subjected to qPCR with primers specific for the indicated gene promoters to measure enrichment levels. qPCR data were analyzed using the 2 -ΔΔCt method, and data are presented as mean fold change of the input ± standard error (SE) of enrichment. (mean ± SE; ** P < 0.01 vs. control, n = 3). b Wild-type and GCD2-homozygous corneal fibroblasts were double infected with MLL1 and <t>SET7/9</t> or control shRNA lentivirus. After puromycin selection, infected cells were stimulated with TGFβ1 (5 ng/ml) for 8 h, and mRNA levels of TGFBIp were analyzed by RT-qPCR. Gene expression was normalized to that of GAPDH (internal control), and results are expressed as fold stimulation over control shRNA-infected wild-type control (mean ± standard error (SE); ** P < 0.01 vs. control, n = 3) ( c ) A model showing that in corneal fibroblasts reaching the quiescent state, transcriptional repression of TGFBIp and ECM-associated genes occurs through heterochromatin formation under no stimulation. Lysine 27 from histone H3 (H3K27) near Smad binding elements (SBEs) within promoters was tri-methylated. During TGFβ1 stimulation, MLL1 and SET7/9 were activated, and their recruitment to SBEs was increased and recruitment of Smad to SBEs was increased. H3K4me1/3 became more methylated, and H3K27me3 was de-methylated on the gene promoters, creating a favorable environment for Smad3 binding
Set7 9 Shrna Lentivirus, supplied by Santa Cruz Biotechnology, 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
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oh 44094 216 951 7100 ohio valley specialty chemical  (Ohio Valley Specialty)
86
Ohio Valley Specialty oh 44094 216 951 7100 ohio valley specialty chemical
MLL1 knockdown attenuated TGFβ1-induced increases in H3K4me3 on the promoters of TGFBIp and ECM-associated genes. a Wild-type and GCD2-homozygous corneal fibroblasts were infected with MLL1 or control shRNA lentivirus. After puromycin selection, infected cells were stimulated with TGF-β1 (5 ng/ml) for 8 h, and H3K4me3 levels at the indicated gene promoters were analyzed. ChIP assays were performed with H3K4me3 antibody. Immunoprecipitated DNA and input DNA were subjected to qPCR with primers specific for the indicated gene promoters to measure enrichment levels. qPCR data were analyzed using the 2 -ΔΔCt method, and data are presented as mean fold change of the input ± standard error (SE) of enrichment. (mean ± SE; ** P < 0.01 vs. control, n = 3). b Wild-type and GCD2-homozygous corneal fibroblasts were double infected with MLL1 and <t>SET7/9</t> or control shRNA lentivirus. After puromycin selection, infected cells were stimulated with TGFβ1 (5 ng/ml) for 8 h, and mRNA levels of TGFBIp were analyzed by RT-qPCR. Gene expression was normalized to that of GAPDH (internal control), and results are expressed as fold stimulation over control shRNA-infected wild-type control (mean ± standard error (SE); ** P < 0.01 vs. control, n = 3) ( c ) A model showing that in corneal fibroblasts reaching the quiescent state, transcriptional repression of TGFBIp and ECM-associated genes occurs through heterochromatin formation under no stimulation. Lysine 27 from histone H3 (H3K27) near Smad binding elements (SBEs) within promoters was tri-methylated. During TGFβ1 stimulation, MLL1 and SET7/9 were activated, and their recruitment to SBEs was increased and recruitment of Smad to SBEs was increased. H3K4me1/3 became more methylated, and H3K27me3 was de-methylated on the gene promoters, creating a favorable environment for Smad3 binding
Oh 44094 216 951 7100 Ohio Valley Specialty Chemical, supplied by Ohio Valley Specialty, 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
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Image Search Results


MLL1 knockdown attenuated TGFβ1-induced increases in H3K4me3 on the promoters of TGFBIp and ECM-associated genes. a Wild-type and GCD2-homozygous corneal fibroblasts were infected with MLL1 or control shRNA lentivirus. After puromycin selection, infected cells were stimulated with TGF-β1 (5 ng/ml) for 8 h, and H3K4me3 levels at the indicated gene promoters were analyzed. ChIP assays were performed with H3K4me3 antibody. Immunoprecipitated DNA and input DNA were subjected to qPCR with primers specific for the indicated gene promoters to measure enrichment levels. qPCR data were analyzed using the 2 -ΔΔCt method, and data are presented as mean fold change of the input ± standard error (SE) of enrichment. (mean ± SE; ** P < 0.01 vs. control, n = 3). b Wild-type and GCD2-homozygous corneal fibroblasts were double infected with MLL1 and SET7/9 or control shRNA lentivirus. After puromycin selection, infected cells were stimulated with TGFβ1 (5 ng/ml) for 8 h, and mRNA levels of TGFBIp were analyzed by RT-qPCR. Gene expression was normalized to that of GAPDH (internal control), and results are expressed as fold stimulation over control shRNA-infected wild-type control (mean ± standard error (SE); ** P < 0.01 vs. control, n = 3) ( c ) A model showing that in corneal fibroblasts reaching the quiescent state, transcriptional repression of TGFBIp and ECM-associated genes occurs through heterochromatin formation under no stimulation. Lysine 27 from histone H3 (H3K27) near Smad binding elements (SBEs) within promoters was tri-methylated. During TGFβ1 stimulation, MLL1 and SET7/9 were activated, and their recruitment to SBEs was increased and recruitment of Smad to SBEs was increased. H3K4me1/3 became more methylated, and H3K27me3 was de-methylated on the gene promoters, creating a favorable environment for Smad3 binding

Journal: BMC Medical Genomics

Article Title: Histone methylation levels correlate with TGFBIp and extracellular matrix gene expression in normal and granular corneal dystrophy type 2 corneal fibroblasts

doi: 10.1186/s12920-015-0151-8

Figure Lengend Snippet: MLL1 knockdown attenuated TGFβ1-induced increases in H3K4me3 on the promoters of TGFBIp and ECM-associated genes. a Wild-type and GCD2-homozygous corneal fibroblasts were infected with MLL1 or control shRNA lentivirus. After puromycin selection, infected cells were stimulated with TGF-β1 (5 ng/ml) for 8 h, and H3K4me3 levels at the indicated gene promoters were analyzed. ChIP assays were performed with H3K4me3 antibody. Immunoprecipitated DNA and input DNA were subjected to qPCR with primers specific for the indicated gene promoters to measure enrichment levels. qPCR data were analyzed using the 2 -ΔΔCt method, and data are presented as mean fold change of the input ± standard error (SE) of enrichment. (mean ± SE; ** P < 0.01 vs. control, n = 3). b Wild-type and GCD2-homozygous corneal fibroblasts were double infected with MLL1 and SET7/9 or control shRNA lentivirus. After puromycin selection, infected cells were stimulated with TGFβ1 (5 ng/ml) for 8 h, and mRNA levels of TGFBIp were analyzed by RT-qPCR. Gene expression was normalized to that of GAPDH (internal control), and results are expressed as fold stimulation over control shRNA-infected wild-type control (mean ± standard error (SE); ** P < 0.01 vs. control, n = 3) ( c ) A model showing that in corneal fibroblasts reaching the quiescent state, transcriptional repression of TGFBIp and ECM-associated genes occurs through heterochromatin formation under no stimulation. Lysine 27 from histone H3 (H3K27) near Smad binding elements (SBEs) within promoters was tri-methylated. During TGFβ1 stimulation, MLL1 and SET7/9 were activated, and their recruitment to SBEs was increased and recruitment of Smad to SBEs was increased. H3K4me1/3 became more methylated, and H3K27me3 was de-methylated on the gene promoters, creating a favorable environment for Smad3 binding

Article Snippet: MLL1 shRNA lentivirus (sc-38039-v), SET7/9 shRNA lentivirus (sc-44094-v), and control shRNA lentivirus (sc-108080) was purchased from Santa Cruz Biotechnology Inc. (Heidelberg, Germany).

Techniques: Infection, shRNA, Selection, Immunoprecipitation, Quantitative RT-PCR, Expressing, Binding Assay, Methylation