SLC27A5 Knockout HEK293 Cell Line
Cat.No.:
EDJ-KQ7238
Species:
Human
Cell Name:
HEK293
Gene:
SLC27A5
Gene ID:
10998
Size:
1×10⁶cells
SLC27A5 Knockout Cell Line (HEK293) is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performance Cas9 Protein and Hassle-Free Cell Selection.
| Cat.No. | EDJ-KQ7238 |
|---|---|
| Product Name | SLC27A5 Knockout Cell Line (HEK293) |
| Cell Line | HEK293 |
| Cellosaurus ID | CVCL_0045 |
| Cell Line Synonyms | Hek293, HEK-293, HEK/293, (HEK)293, HEK 293, HEK,293, 293, 293 HEK, 293 Ad5, Graham 293, Graham-293, Human Embryonic Kidney 293 |
| Gene | |
| NCBI Gene ID | |
| Gene Synonyms | ACSB|ACSVL6|BACS|BAL|FACVL3|FATP-5|FATP5|VLACSR|VLCS-H2|VLCSH2 |
| Summary |
The protein encoded by this gene is an isozyme of very long-chain acyl-CoA synthetase (VLCS). It is capable of activating very long-chain fatty-acids containing 24- and 26-carbons. It is expressed in liver and associated with endoplasmic reticulum but not with peroxisomes. Its primary role is in fatty acid elongation or complex lipid synthesis rather than in degradation. This gene has a mouse ortholog. [provided by RefSeq, Jul 2008]
|
| Associated Diseases | Non-tumor |
| Morphology | Adherent |
| Passage Ratio | 1/5，2days |
| Complete Culture Medium | DMEM + 10% FBS |
| Freezing Medium | 95% Complete culture medium+ 5% DMSO |
| QC | Indels validated by Sanger sequencing; sterility confirmed via microbial testing. |
* 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: HEK293 | STR Info (Cell bank) Cell Line: HEK293 | ||
| Allele1 | Allele2 | Allele1 | Allele2 | |
| Amelogenin | X | X | ||
| CSF1P0 | 12 | 11 | 12 | |
| D2S1338 | 19 | 19 | ||
| D3S1358 | 15 | 17 | 15 | 17 |
| D5S818 | 8 | 8 | 9 | |
| D7S820 | 11 | 12 | 11 | 12 |
| D8S1179 | 12 | 14 | 12 | 14 |
| D13S317 | 12 | 14 | 12 | 14 |
| D16S539 | 9 | 13 | 9 | 13 |
| D18S51 | 17 | 18 | 17 | 18 |
| D19S433 | 15 | 18 | 15 | 18 |
| D21S11 | 28 | 30.2 | 28 | 30.2 |
| FGA | 23 | 23 | ||
| Penta D | 9 | 10 | 9 | 10 |
| Penta E | 7 | 15 | 7 | 15 |
| TH01 | 7 | 9.3 | 7 | 9.3 |
| TPOX | 11 | 11 | ||
| vWA | 16 | 19 | 16 | 19 |
| D6S1043 | 11 | 11 | ||
| D12S391 | 19 | 21 | 11 | 15 |
| D2S441 | 11 | 15 | 11 | 15 |
* 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.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.
Research Publications
Tetraspanin TM4SF5 in hepatocytes negatively modulates SLC27A transporters during acute fatty acid supply.
IF=3
Archives of biochemistry and biophysics
Transmembrane 4 L six family member 5 (TM4SF5) is involved in nonalcoholic steatosis and further aggravation of liver disease. However, its mechanism for regulating FA accumulation is unknown. We investigated how TM4SF5 in hepatocytes affected FA accumulation during acute FA supply. TM4SF5-expressing hepatocytes and mouse livers accumulated less FAs, compared with those of TM4SF5 deficiency or inactivation. Binding of TM4SF5 to SLC27A2 increased gradually upon acute FA treatment, whereas TM4SF5 constitutively bound SLC27A5. Suppression of either SLC27A2 or SLC27A5 in hepatocytes expressing TM4SF5 differentially modulated initial and maximal FA uptake levels for a fast turnover of fatty acid. Altogether, TM4SF5 negatively modulates FA accumulation into hepatocytes via association with the transporters for an energy homeostasis, when FA are supplied acutely.
This KO model may be useful for:
- Investigating the regulatory role of SLC27A5 in hepatic fatty acid uptake and transport.
- Studying the functional interaction between SLC27A transporters and tetraspanin TM4SF5 in lipid metabolism.
- Elucidating signaling pathways involved in acute fatty acid supply responses in hepatocytes.
- Screening for compounds that modulate SLC27A5-dependent lipid transport or metabolic stress.
- Validating mechanisms of hepatocyte metabolic adaptation under lipid overload conditions.
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