HK2 Knockout HeLa Cell Line
Cat.No.:
EDJ-KQ21128
Species:
Human
Cell Name:
HeLa
Gene:
HK2
Gene ID:
3099
Size:
1×10⁶cells
HK2 Knockout Cell Line (Hela) 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-KQ21128 |
|---|---|
| Product Name | HK2 Knockout Hela Cell Line |
| Cell Line | Hela |
| Cellosaurus ID | CVCL_0030 |
| Cell Line Synonyms | HELA, Hela, He La, He-La, HeLa-CCL2, Henrietta Lacks cells, Helacyton gartleri |
| Gene | HK2 |
| NCBI Gene ID | |
| Gene Synonyms | HKII|HXK2 |
| Summary |
Hexokinases phosphorylate glucose to produce glucose-6-phosphate, the first step in most glucose metabolism pathways. This gene encodes hexokinase 2, the predominant form found in skeletal muscle. It localizes to the outer membrane of mitochondria. Expression of this gene is insulin-responsive, and studies in rat suggest that it is involved in the increased rate of glycolysis seen in rapidly growing cancer cells. [provided by RefSeq, Apr 2009]
|
| Associated Diseases | Cervical Carcinoma |
| Morphology | Adherent |
| Passage Ratio | 1/5, 2days |
| Complete Culture Medium | MEM + 10% FBS |
| Freezing Medium | 70%Complete culture medium+ 20% FBS+ 10% 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: HeLa | STR Info (Cell bank) Cell Line: HeLa | ||
| Allele1 | Allele2 | Allele1 | Allele2 | |
| Amelogenin | X | X | ||
| CSF1PO | 9 | 10 | 9 | 10 |
| D1S1656 | 12 | 15 | 12 | 15 |
| D2S1338 | 17 | 17 | ||
| D3S1358 | 15 | 18 | 15 | 18 |
| D5S818 | 11 | 12 | 11 | 12 |
| D6S1043 | 18 | 18 | ||
| D7S820 | 8 | 12 | 8 | 12 |
| D8S1179 | 12 | 13 | 12 | 13 |
| D12S391 | 20 | 25 | 20 | 25 |
| D13S317 | 12 | 14 | 12 | 14 |
| D16S539 | 9 | 10 | 9 | 10 |
| D18S51 | 16 | 16 | ||
| D19S433 | 13 | 14 | 13 | 14 |
| D21S11 | 27 | 28 | 27 | 28 |
| FGA | 18 | 21 | 18 | 21 |
| Penta D | 8 | 15 | 8 | 15 |
| Penta E | 7 | 17 | 7 | 17 |
| TPOX | 8 | 12 | 8 | 12 |
| VWA | 16 | 18 | 16 | 18 |
* 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.
Related Publications
CDK6 increases glycolysis and suppresses autophagy by mTORC1-HK2 pathway activation in cervical cancer cells.
IF=3.4
Cell cycle (Georgetown, Tex.)
Cervical carcinoma is a leading malignant tumor among women worldwide, characterized by the dysregulation of cell cycle. Cyclin-dependent kinase 6 (CDK6) plays important roles in the cell cycle progression, cell differentiation, and tumorigenesis. However, the role of CDK6 in cervical cancer remains controversial. Here, we found that loss of CDK6 in cervical adenocarcinoma HeLa cell line inhibited cell proliferation but induced apoptosis as well as autophagy, accompanied by attenuated expression of mammalian target of rapamycin complex 1 (mTORC1) and hexokinase 2 (HK2), reduced glycolysis, and production of protein, nucleotide, and lipid. Similarly, we showed that CDK6 knockout inhibited the survival of CDK6-high CaSki but not CDK6-low SiHa cervical cancer cells by regulation of glycolysis and autophagy process. Collectively, our studies indicate that CDK6 is a critical regulator of human cervical cancer cells, especially with high CDK6 level, through its ability to regulate cellular apoptosis and metabolism. Thus, inhibition of CDK6 kinase activity could be a powerful therapeutic avenue used to treat cervical cancers.
This KO model may be useful for:
- Investigating the role of HK2 in glycolysis regulation and metabolic reprogramming in cervical cancer
- Studying the mTORC1-HK2 signaling axis in autophagy suppression
- Evaluating CDK6-mediated metabolic pathways and their downstream effects
- Functional validation of HK2 as a target for cancer metabolism-based therapies
- Exploring cross-talk between cell cycle regulators (e.g., CDK6) and metabolic enzymes in tumor progression