FEM1B CRISPR/Cas9 KO Plasmid (m): sc-420316
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FEM1B 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 FEM1B 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 | |
FEM1B CRISPR/Cas9 KO Plasmid (m) | sc-420316 | 20 µg | $397.00 |
Overview
Fem1b encodes FEM1B, a conserved ankyrin repeat–containing protein implicated in ubiquitin-dependent proteostasis and cellular stress responses. FEM1B has been linked to substrate recognition in E3 ubiquitin ligase pathways and contributes to regulation of apoptosis and cell-cycle–associated processes, with downstream effects on mitochondrial homeostasis and metabolic signaling. In mouse systems, Fem1b function has been studied in contexts including energy balance, endocrine regulation, and tissue maintenance, making it relevant for mechanistic work on metabolic dysfunction and stress-adaptive phenotypes. Altered FEM1B activity has also been associated with changes in protein quality control networks that can influence susceptibility to degenerative and metabolic disease models.
FEM1B CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Fem1b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Fem1b 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 Fem1b 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 FEM1B protein expression.
This CRISPR knockout system enables efficient generation of Fem1b-deficient cell models for investigation of FEM1B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Fem1b exon(s) critical for FEM1B 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 Fem1b genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FEM1B CRISPR/Cas9 KO Plasmid (m) and FEM1B CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Fem1b locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FEM1B HDR Plasmid (m) and FEM1B HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Fem1b homology arms to support homology-directed repair at defined Fem1b 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.