
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BICD1 CRISPR Activation Plasmid (h) | sc-410704-ACT | 20 µg | $397.00 | |||
BICD1 CRISPR Activation Plasmid (h2) | sc-410704-ACT-2 | 20 µg | $397.00 |
BICD1 (bicaudal D homolog 1) is a coiled-coil adaptor protein that links cytoplasmic dynein–dynactin motors to cargo, coordinating minus-end–directed microtubule transport. It contributes to vesicle and organelle positioning, Golgi organization, and centrosome-associated trafficking, supporting processes such as cell polarity and mitotic progression. Through its role in intracellular trafficking networks, BICD1 can influence signaling dynamics by controlling receptor and endosome movement and spatial organization. Dysregulation of dynein adaptor function is broadly relevant to cellular stress responses and phenotypes observed in neurodevelopmental and neurodegenerative research contexts.
BICD1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BICD1 expression without altering the underlying DNA sequence.
BICD1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BICD1 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 BICD1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BICD1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BICD1 locus and enabling the study of BICD1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BICD1 pathway restoration in tumor cells with silenced or reduced BICD1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.