HM3 Cell Line
Invented by Dr Simon Cook at Babraham Institute
- Datasheet
- References (8)
- Inventor Info
Info
| Catalogue Number | 153329 |
| Antigen/Gene or Protein Targets | c-Raf1 |
| Parental Line | HEK 293 |
| Synonyms | RAF proto-oncogene serine/threonine-protein kinase (EC:2.7.11.1), Proto-oncogene c-RAF, cRaf, Raf-1 |
| Host | Human |
| Tissue | Kidney |
| Disease Keywords | Cell signalling pathways; cancer; inflammation |
| Relevance |
HR1 cells are HEK 293 cells stably expressing conditional kinase ∆Raf-1:ER* from the pCMV Neo Myc plasmid. ∆Raf-1:ER* (also known as ∆CRAF:ER*) consists of the isolated kinase domain of c-Raf1 fused in-frame to a modified form of the hormone binding domain of the estrogen receptor (hbER*) that can be de-repressed by 4-hydroxytamoxifen (4-HT) but not β-estradiol. In this case the * refers to a point mutation that ablates estradiol binding but allows 4-HT binding. Activation of ∆Raf-1:ER* leads to the selective activation of the ERK1/2 pathway. This cell line can be used to study the cellular role and factors impacting on the ERK1/2 signalling pathway such as gene expression, cell proliferation, cell cycle arrest and cell death. The cells are G418 resistant. Conditional kinase activation of ∆Raf-1:ER* can be induced with 100nM 4-HT. |
| Production Details | HEK 293 cells were transfected with the pCMV Neo Myc plasmid expressing ∆Raf-1:ER*. Stable transfectants were selected by neomycin resistance using G418 (Geneticin) and ring cloning. |
| Conditional | Yes |
| Conditional Description | Stable transfectant, conditional functionality: c-Raf1 kinase activity and ERK1/2 signalling pathway activated following 4-hydroxytamoxifen (4-HT) treatment of cells. |
| Research Area | Apoptosis and Programmed Cell Death, Cancer, Cell Cycle, Cell Signaling & Signal Transduction, Immunology |
| Growth/Phenotype Keywords | Adherent cell line |
| Recommended Growing Conditions | Phenol red-free Dulbecco’s modified Eagle’s medium (DMEM) high glucose version, 2 mM L-glutamine, 10% fetal bovine serum (FBS), 400 µg/ml G418 (Geneticin). |
| Cellosaurus ID | CVCL_2676 |
References: 8 entries
Gilley et al. 2009. Cell Signal. 21(6):969-77. PMID: 19249353.
ERK1/2, but not ERK5, is necessary and sufficient for phosphorylation and activation of c-Fos.
Europe PMC ID: 19249353
Wiggins et al. 2007. Cell Signal. 19(12):2605-11. PMID: 17884340.
c-Cbl is not required for ERK1/2-dependent degradation of BimEL.
Europe PMC ID: 17884340
Ewings et al. 2007. EMBO J. 26(12):2856-67. PMID: 17525735.
ERK1/2-dependent phosphorylation of BimEL promotes its rapid dissociation from Mcl-1 and Bcl-xL.
Europe PMC ID: 17525735
Boughan et al. 2006. J Biol Chem. 281(17):11637-48. PMID: 16513653.
Nucleotide-binding oligomerization domain-1 and epidermal growth factor receptor: critical regulators of beta-defensins during Helicobacter pylori infection.
Europe PMC ID: 16513653
Add a reference
References: 8 entries
Gilley et al. 2009. Cell Signal. 21(6):969-77. PMID: 19249353.
ERK1/2, but not ERK5, is necessary and sufficient for phosphorylation and activation of c-Fos.
Wiggins et al. 2007. Cell Signal. 19(12):2605-11. PMID: 17884340.
c-Cbl is not required for ERK1/2-dependent degradation of BimEL.
Ewings et al. 2007. EMBO J. 26(12):2856-67. PMID: 17525735.
ERK1/2-dependent phosphorylation of BimEL promotes its rapid dissociation from Mcl-1 and Bcl-xL.
Boughan et al. 2006. J Biol Chem. 281(17):11637-48. PMID: 16513653.
Nucleotide-binding oligomerization domain-1 and epidermal growth factor receptor: critical regulators of beta-defensins during Helicobacter pylori infection.
Add a reference
