RHAMM CRISPR/Cas9 KO Plasmid (m): sc-420881
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RHAMM CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 RHAMM 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: RHAMM Antibody (H-8): sc-515221
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RHAMM CRISPR/Cas9 KO Plasmid (m) | sc-420881 | 20 µg | $397.00 |
Overview
Hmmr encodes RHAMM (receptor for hyaluronan-mediated motility), a microtubule- and hyaluronan-interacting protein that coordinates cytoskeletal organization, centrosome function, and mitotic spindle assembly. RHAMM contributes to cell migration and proliferation by integrating extracellular matrix cues with intracellular microtubule dynamics and signaling pathways linked to motility and cell-cycle progression. In mouse systems, altered RHAMM activity has been associated with dysregulated mitosis, genomic instability, and aberrant tissue remodeling processes relevant to cancer biology and inflammatory microenvironments. These features make Hmmr a useful target for dissecting how hyaluronan signaling interfaces with spindle regulation and motility programs.
RHAMM CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Hmmr gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Hmmr 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 Hmmr 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 RHAMM protein expression.
This CRISPR knockout system enables efficient generation of Hmmr-deficient cell models for investigation of RHAMM signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Hmmr exon(s) critical for RHAMM 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 Hmmr genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by RHAMM CRISPR/Cas9 KO Plasmid (m) and RHAMM CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Hmmr locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by RHAMM HDR Plasmid (m) and RHAMM HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Hmmr homology arms to support homology-directed repair at defined Hmmr 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.