SLC16A12 Knockout Huh-7 Cell Line
Cat.No.:
EDC08242
Species:
Human
Cell Name:
Huh-7
Gene:
SLC16A12
Gene ID:
387700
Size:
1×10⁶cells
SLC16A12 Knockout HuH-7 Cell Line is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performotion Cas9 Protein and Hassle-Free Cell Selection.
| Cat.No. | EDC08242 |
|---|---|
| Product Name | SLC16A12 Knockout HuH-7 Cell Line |
| Species | Human |
| Cell Line | Huh-7 |
| Cellosaurus ID | CVCL_0336 |
| Gene ID | |
| Cell Line Synonyms | HuH-7, HUH-7, HuH7, Huh7, HUH7, HUH7.0, JTC-39, Japanese Tissue Culture-39 |
| Gene | SLC16A12 |
| Summary |
This gene encodes a transmembrane transporter that likely plays a role in monocarboxylic acid transport. A mutation in this gene has been associated with juvenile cataracts with microcornea and renal glucosuria. [provided by RefSeq, Mar 2010]
|
| Digestion Time | 2 min |
| Morphology | Adherent |
| Passage Ratio | 1:4 |
| Complete Culture Medium | DMEM+10% FBS |
| Freezing Medium | 70% complete culture medium+20% FBS+10% DMSO |
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.
| Loci | STR Info (Sample Cell) Sample Cell Line: Huh-7 | STR Info (Cell bank) Cell Line: Huh-7 | ||
| Allele1 | Allele2 | Allele1 | Allele2 | |
| Amelogenin | X | X | ||
| CSF1P0 | 11 | 11 | ||
| D2S1338 | 19 | 19 | ||
| D3S1358 | 15 | 15 | ||
| D5S818 | 12 | 12 | ||
| D7S820 | 11 | 11 | ||
| D8S1179 | 14 | 14 | 15 | |
| D13S317 | 10 | 11 | 10 | 11 |
| D16S539 | 10 | 10 | ||
| D18S51 | 15 | 15 | ||
| D19S433 | 13 | 14 | 13 | 14 |
| D21S11 | 30 | 30 | ||
| FGA | 22 | 23 | 22 | 23 |
| Penta D | 12 | 12 | ||
| Penta E | 11 | 11 | ||
| TH01 | 7 | 7 | ||
| TPOX | 8 | 11 | 8 | 11 |
| vWA | 16 | 18 | 16 | 18 |
| D6S1043 | 13 | 15 | 13 | 15 |
| D12S391 | 20 | 21 | 20 | 21 |
| D2S441 | 12 | 14 | 12 | 14 |
* STR authentication data of this cell line matches with that of cell lines sourced from ATCC, DSMZ, JCRB, and RIKEN databases.
Conclusion: The STR identification of this cell is correct.
Conclusion: The STR identification of this cell is correct.
FAQ
Which is better for studying SLC16A12 function, SLC16A12 Knockout Huh-7 Cell Line or SLC16A12 overexpression Huh-7 Cell Line?
The choice depends on whether you are studying SLC16A12 (MCT12)'s role as a creatine transporter or modeling autosomal dominant juvenile cataracts. The Knockout line is the standard tool for asking whether MCT12 is required for creatine transport — MCT12 has been identified as a creatine transporter distinct from the better-known CRT1/SLC6A8. Overexpression is useful for testing transport activity or for studying disease-associated mutations.
For creatine biology research, the EDITGENE MCT12 Knockout in Huh-7 enables study of MCT12-mediated creatine handling. SLC16A12 mutations cause autosomal dominant juvenile cataracts, glucosuria, and elevated guanidinoacetate — disease variant rescue enables genotype-function correlation. SLC6A8 (CRT1) expression analysis aids interpretation given functional overlap in creatine transport.
What are the application scenarios for this model?
Primary applications:
• Creatine uptake assays: ³H-creatine uptake measurement to quantify MCT12 transport activity.
• Disease modeling: rescue with autosomal dominant juvenile cataract-associated SLC16A12 mutations for genotype-function studies.
• Substrate scope characterization: testing related substrates given MCT12's emerging substrate profile.
• Paralog studies: SLC6A8 (CRT1) expression analysis given the two transporters' overlap in creatine handling.
EDITGENE recommends this model for researchers investigating creatine transport biology and SLC16A12-related cataract disease mechanisms.
Is this SLC16A12 Knockout Huh-7 Cell Line compatible with overexpression rescue experiments?
Yes. MCT12 rescue experiments require attention to creatine transport biology:
• Construct design: use a codon-modified SLC16A12 sequence with a small C-terminal tag (FLAG, HA). The 12-transmembrane SLC16 architecture must be preserved.
• Disease mutation rescue: cataract-associated SLC16A12 mutations enable genotype-function correlation studies.
• Transport-deficient rescue: substrate-binding pocket mutations enable structure-function studies.
• Functional readout: rescue should restore creatine uptake activity measured by ³H-creatine uptake.
Huh-7 transduces efficiently with lentivirus and supports stable rescue line generation.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.