Date published: 2026-7-11

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BimEL CRISPR Activation Plasmid (h): sc-400515-ACT

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • BimEL CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
  • BimEL CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
  • The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
  • gRNAs encoded by BimEL CRISPR Activation Plasmid (h) and BimEL CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the BCL2L11 transcriptional start site. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    BimEL CRISPR Activation Plasmid (h)

    sc-400515-ACT
    20 µg
    $397.00

    BimEL CRISPR Activation Plasmid (h2)

    sc-400515-ACT-2
    20 µg
    $397.00

    BCL2L11 encodes Bim, a BH3-only pro-apoptotic member of the BCL-2 family that couples cellular stress cues to mitochondrial outer membrane permeabilization and caspase activation. The Bim_EL isoform is a major phosphorylation-regulated form that integrates signals from MAPK/ERK, JNK, and PI3K/AKT pathways to tune apoptosis, anoikis, and immune cell homeostasis. Through antagonism of anti-apoptotic BCL-2 proteins and activation of BAX/BAK, Bim helps determine cell fate under growth factor withdrawal, ER stress, and cytoskeletal perturbation. Dysregulated BCL2L11 expression or signaling control is implicated in cancer cell survival, therapy resistance mechanisms, and immune-related pathobiology, making it a key node for apoptosis and stress-response research.

    BimEL CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BCL2L11 expression without altering the underlying DNA sequence.

    BimEL CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BCL2L11 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

    Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the BCL2L11 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BimEL expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BCL2L11 locus and enabling the study of BimEL-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BimEL pathway restoration in tumor cells with silenced or reduced BCL2L11 expression.

    For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.