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Atlas Antibodies
mef2b ![]() Mef2b, supplied by Atlas Antibodies, 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/product/anti+mef2b/Anti-MEF2B/10__1158_slash_2643___3230__bcd___24___0126-430-6-7 Average 93 stars, based on 1 article reviews
mef2b - by Bioz Stars,
2026-11
93/100 stars
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Rabbit anti-Human MEF2B Polyclonal Antibody
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Transcriptional activator which binds specifically to the MEF2 element, 5-YTA[AT](4)TAR-3, found in numerous muscle-specific genes. Activates transcription via this element. May be involved in muscle-specific and/or growth factor-related transcription.Shipped at 4°C. Store at 4°C short
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Rabbit Anti Human MEF2B Polyclonal Affinity Purified (PBS with 0.02% sodium azide, 50% glycerol, pH7.3) (Western Blot) from Innovative Research is a polyclonal antibody in a liquid format, buffered in PBS with 0.02% sodium azide,
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This gene represents numerous read-through transcripts that span GeneID:729991 and 100271849. Many read-through transcripts are predicted to be nonsense-mediated decay (NMD) candidates, and are thought to be non-coding. Some transcripts are predicted to be capable
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This gene represents numerous read-through transcripts that span geneID:729991 and 100271849. Many read-through transcripts are predicted to be nonsense-mediated decay (NMD) candidates, and are thought to be non-coding. Some transcripts are predicted to be capable
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Boster Bio Anti-MEF2B Antibody Picoband® catalog # A05743-1. Tested in ELISA, IHC, WB applications. This antibody reacts with Human, Mouse, Rat. The brand Picoband indicates this is a premium antibody that guarantees superior quality, high
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Boster Bio Anti-MEF-2B Antibody catalog # A05743. Tested in ELISA, IHC, WB applications. This antibody reacts with Human, Mouse.
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Rabbit polyclonal to MEF-2B. Conjugation note: Unconjugated Application note: WB, IHC-p, ELISA Reactivity note: Human, Mouse
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Image Search Results
Journal: Blood Cancer Discovery
Article Title: Selective Enhancer Dependencies in MYC-Intact and MYC-Rearranged Germinal Center B-cell Diffuse Large B-cell Lymphoma
doi: 10.1158/2643-3230.bcd-24-0126
Figure Lengend Snippet: Figure 3. Activation of MYC by ternary complex–bound modules of the BCL6 super-enhancer. A, Schematic diagram of the normal BCL6 locus and parsimonious models for structural rearrangements involving the MYC and BCL6 locus in three DLBCL cell lines based on optical mapping and 4C-seq data. Red lines indicate intra- or inter-chromosomal fusions. See Supplementary Fig. S3A–S3C for details. B, CRISPRi sgRNA depletion or enrichment (log2 fold change) for BCL6 distal super-enhancer regions in the MYC::BCL6-LCR+ cell lines SU-DHL-4 and WSU-DLCL2. Also shown is ChIP-seq signal for H3K27ac and ternary complex TFs MEF2B and OCT2 in SU-DHL-4 (scale: fragments per million mapped fragments). BCL6 locus super-enhancer regions SE1 and SE3 are shown as previously defined (15); region SE1 is equivalent to BCL6-LCR. C, Plot of NFR-level sgRNA depletion or enrichment (MAGeCK RRA log2 fold change, y-axis) for targeted intervals in BCL6 distal super-enhancers in six GCB-DLBCL cell lines. Circles are sized proportionally to −log2(FDR), with neg|FDR used for log2FC <0 and pos|FDR used for log2FC >0. Filled circles represent neg|FDR <0.01. The three MYC::BCL6-LCR+ cell lines are indicated in the legend with a red box. D, Change in viable cellularity for dox-inducible KRAB-dCas9–expressing MYC::BCL6-LCR+ DLBCL cell lines expressing the two indicated sgRNA lentivectors. Cells were transduced with both vectors, sorted for dual tagBFP- and tagRFP-expressing cells, and then grown with or without dox for 7 days. The Y-axis shows the ratio of CellTiter-Glo signal for dox treated/untreated cells (two-tailed Student t test of n = 3 biological replicates per condition for dual-enhancer–targeting sgRNA-transduced vs. dual-control sgRNA-transduced; error bars are 95% CI). E, Differential expression of MYC and BCL6 (qRT-PCR) for populations of MYC::BCL6-LCR+ DLBCL cell lines expressing dox-inducible KRAB-dCas9 and two sgRNA vectors as in (D) (two-tailed Student t test of n = 3 technical replicates per condition for dual-enhancer–targeting sgRNA-transduced vs. dual-control sgRNA-transduced, color-coded by measured transcript per legend; error bars are 95% CI). F, Differential expression of MYC and BCL6 (qRT-PCR) in MYC::BCL6-LCR+ DLBCL cell lines express- ing dox-inducible KRAB-dCas9 after transduction with indicated sgRNAs targeting MEF2B, POU2F2, or POU2AF1 (error bars are the SD of n = 5 technical replicates per sgRNA; bars are color-coded by measured transcript per legend). ***, P < 0.001. FC, fold change; neg ctrl, negative control; pos, positive.
Article Snippet: The following primary antibodies were used:
Techniques: Activation Assay, ChIP-sequencing, Expressing, Transduction, Two Tailed Test, Control, Quantitative Proteomics, Quantitative RT-PCR, Negative Control
Journal: Blood Cancer Discovery
Article Title: Selective Enhancer Dependencies in MYC-Intact and MYC-Rearranged Germinal Center B-cell Diffuse Large B-cell Lymphoma
doi: 10.1158/2643-3230.bcd-24-0126
Figure Lengend Snippet: Figure 5. The GME-1 MYC enhancer shows selective transactivation in MYC-intact cell lines and is directly regulated by the OCT2 ternary com- plex. A, Detail of the GME-1 enhancer with ATAC-seq, H3K27 ChIP-seq, and ChIP-seq for OCT2, OCA-B, MEF2B, and p300 in the indicated cell lines. OCT2 BioChIP in BJAB cells is from Hodson and colleagues (39) and represents binding of a transgenically expressed biotinylated OCT2 protein, whereas all other ChIP-seq datasets profile endogenous proteins. Inset at bottom shows further detail of the Phastcons conserved element track for sub-region 195B (see Supplementary Fig. S5E for further detail), with the positions of the conserved OCT2 motif and the genomic duplica- tion identified in the SU-DHL-5 cell line indicated. B, Differential expression of MYC and BCL6 (qRT-PCR) in GME-1–dependent DLBCL cell lines expressing dox-inducible KRAB-dCas9 after transduction with indicated sgRNAs targeting MEF2B, POU2F2, and POU2AF1 (error bars are the SD of five technical replicates per sgRNA; bars are color-coded by measured transcript per legend). C, Transcriptional reporter assays conducted in MYC-intact and MYC::BCL6-LCR+ DLBCL cell lines with conserved subregions of essential MYC and BCL6 NFRs cloned into the STARR-seq_Ori lu- ciferase vector. See Supplementary Fig. S5E–S5H for details of the indicated regions. The signal ratio and statistical comparison for MYC enhancer 195B vs. each BCL6 enhancer is indicated for each cell line (two-tailed Student t test of biological replicates (n = 3); error bars are 95% confidence interval). D, Transcriptional reporter assays in MYC-intact cell lines for constructs bearing the reference NFR 195B enhancer region or the same region with deletion of the OCT2 motif (“195B_MYC_OCT2Del”) indicated in (A) [two-tailed Student t test of biological replicates (n = 3); error bars are 95% CI]. E, Transcriptional reporter assays conducted in HT cells expressing inducible KRAB-dCas9 and transduced with the indicated sgRNAs. Following puromycin selection, cells were electroporated with the indicated constructs and induced with dox for 48 hours prior to Dual-Glo lucifer- ase assay [two-tailed Student t test of biological replicates (n = 3); error bars are 95% CI]. F, Transcriptional reporter assays in MYC-intact cell lines for constructs bearing the reference NFR 195B enhancer region or a clone of the same region from the SU-DHL-5 cell line bearing a partial tandem duplication (“195B_MYC_Dup”) as indicated in (A) [two-tailed Student t test of biological replicates (n = 3); error bars are 95% CI]. **, P < 0.01; ***, P < 0.001; ns, not significant; P ≥ 0.05. FC, fold change; neg ctrl, negative control.
Article Snippet: The following primary antibodies were used:
Techniques: ChIP-sequencing, Binding Assay, Quantitative Proteomics, Quantitative RT-PCR, Expressing, Transduction, Clone Assay, Plasmid Preparation, Comparison, Two Tailed Test, Construct, Selection, Negative Control