LMX1B CRISPR/Cas9 KO Plasmid (h): sc-402945
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LMX1B 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 LMX1B 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: LMX1B Antibody (1D12): sc-293262
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LMX1B CRISPR/Cas9 KO Plasmid (h) | sc-402945 | 20 µg | $397.00 |
Overview
LMX1B encodes a LIM homeobox transcription factor that regulates cell fate specification and tissue patterning during development, with prominent roles in dorsal limb identity, podocyte differentiation, and neuronal subtype programs. It controls gene expression by coordinating LIM-domain interactions with transcriptional co-regulators and homeodomain-mediated DNA binding, influencing morphogenesis, extracellular matrix organization, and cytoskeletal architecture. In kidney biology, LMX1B supports glomerular filtration barrier integrity by modulating podocyte gene networks, linking it to pathways governing slit diaphragm structure and actin dynamics. Genetic perturbation of LMX1B is associated with nail–patella syndrome and related renal and skeletal phenotypes, making it a relevant target for studying transcriptional regulation in development and organogenesis.
LMX1B CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the LMX1B gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the LMX1B 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 LMX1B 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 LMX1B protein expression.
This CRISPR knockout system enables efficient generation of LMX1B-deficient cell models for investigation of LMX1B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting LMX1B exon(s) critical for LMX1B 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 LMX1B genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by LMX1B CRISPR/Cas9 KO Plasmid (h) and LMX1B CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the LMX1B locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by LMX1B HDR Plasmid (h) and LMX1B HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by LMX1B homology arms to support homology-directed repair at defined LMX1B 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.