MYBPHL CRISPR/Cas9 KO Plasmid (h): sc-406488
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MYBPHL CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the MYBPHL genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MYBPHL CRISPR/Cas9 KO Plasmid (h) | sc-406488 | 20 µg | $397.00 |
Overview
MYBPHL (myosin-binding protein H-like) encodes a putative sarcomeric accessory protein expressed predominantly in striated muscle, where it is thought to associate with myosin-containing thick filaments and contribute to myofibrillar organization. By influencing actomyosin contractile architecture, MYBPHL is linked to processes such as sarcomere assembly, cytoskeletal stability, and mechanotransduction signaling in cardiomyocytes and skeletal muscle cells. Altered expression patterns of myosin-binding protein family members have been reported in cardiac remodeling contexts, supporting the use of MYBPHL as a mechanistic node for studying stress-responsive contractile pathways. Functional interrogation of MYBPHL can inform how myofibril-associated proteins modulate muscle cell differentiation and contractility-related gene networks.
MYBPHL CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MYBPHL gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MYBPHL together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the MYBPHL open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish MYBPHL protein expression.
This CRISPR knockout system enables efficient generation of MYBPHL-deficient cell models for investigation of MYBPHL signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting MYBPHL exon(s) critical for MYBPHL function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple MYBPHL genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by MYBPHL CRISPR/Cas9 KO Plasmid (h) and MYBPHL CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MYBPHL locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by MYBPHL HDR Plasmid (h) and MYBPHL HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MYBPHL homology arms to support homology-directed repair at defined MYBPHL target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.