TMEM135 Double Nickase Plasmid (h): sc-407333-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TMEM135 Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- TMEM135 Double Nickase Plasmid (h) and TMEM135 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TMEM135. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TMEM135 Double Nickase Plasmid (h) | sc-407333-NIC | 20 µg | $410.00 | |||
TMEM135 Double Nickase Plasmid (h2) | sc-407333-NIC-2 | 20 µg | $410.00 |
TMEM135 encodes a conserved multi-pass membrane protein implicated in mitochondrial and peroxisomal homeostasis, with reported roles in organelle dynamics, lipid handling, and cellular bioenergetics. TMEM135 has been linked to transcriptional programs that regulate fatty acid metabolism and oxidative stress responses, positioning it at the interface of metabolic adaptation and organelle quality control. Perturbation of TMEM135 expression has been associated with altered mitochondrial morphology and peroxisome-related processes, which are commonly disrupted in metabolic and neurodegenerative disease contexts. As a result, TMEM135 is studied in pathways involving lipid oxidation, reactive oxygen species management, and organelle cross-talk that influences cell survival and metabolic state.
TMEM135 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TMEM135 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TMEM135. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt TMEM135 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of TMEM135-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.