c12 (B15ECiii2) (ATCC® CRL-2710)

Organism: Mus musculus, mouse  /  Cell Type: epithelial  /  Disease: hepatoma

Permits and Restrictions

View Permits

Organism Mus musculus, mouse
Cell Type epithelial
Product Format frozen
Morphology epithelial
Culture Properties adherent
Biosafety Level 1
Disease hepatoma
Strain C57L/J
Applications
The c12 (B15ECiii2) cell line expresses reduced levels of aryl hydrocarbon receptor (AHR) mRNA and protein, due to an unknown factor required for AHR expression.
This cell line is a useful tool to study the molecular mechanism of these processes.
AHR binds a number of xenobiotic compounds and mediates pathogenesis (including carcinogenesis) by these compounds.
The c12 (B15ECiii2) cell line was derived from Hepa-1c1c7 (ATCC CRL-2026).
Storage Conditions liquid nitrogen vapor phase
Derivation
The c12 (B15ECiii2) cell line was derived from Hepa-1c1c7 (ATCC CRL-2026). Hepa-1c1c7 has high aryl hydrocarbon hydroxylase (AHH) activity. The cells were exposed to ethyl methane sulfonate (EMS) and mutant colonies were selected for benzo[a]pyrene resistance. The c12 (B15ECiii2) cell line expresses reduced levels of aryl hydrocarbon receptor (AHR) mRNA and protein, due to an unknown factor required for AHR expression. AHR binds a number of xenobiotic compounds and mediates pathogenesis (including carcinogenesis) by these compounds. This cell line is a useful tool to study the molecular mechanism of these processes.
Receptor Expression
aryl hydrocarbon (Ah)
Comments
The c12 (B15ECiii2) cell line was derived from Hepa-1c1c7 (ATCC CRL-2026). Hepa-1c1c7 has high aryl hydrocarbon hydroxylase (AHH) activity. The cells were exposed to ethyl methane sulfonate (EMS) and mutant colonies were selected for benzo[a]pyrene resistance. The c12 (B15ECiii2) cell line expresses reduced levels of aryl hydrocarbon receptor (AHR) mRNA and protein, due to an unknown factor required for AHR expression. AHR binds a number of xenobiotic compounds and mediates pathogenesis (including carcinogenesis) by these compounds. This cell line is a useful tool to study the molecular mechanism of these processes.
Complete Growth Medium Alpha minimum essential medium without ribonucleosides and deoxyribonucleosides with 2 mM L-glutamine, 90%; heat-inactivated fetal bovine serum, 10%
Subculturing
Protocol:
  1. Remove and discard culture medium.
  2. Briefly rinse the cell layer with 0.25% (w/v) Trypsin- 0.53 mM EDTA solution to remove all traces of serum that contains trypsin inhibitor.
  3. Add 2.0 to 3.0 ml of Trypsin-EDTA solution to flask and observe cells under an inverted microscope until cell layer is dispersed (usually within 5 to 15 minutes).
    Note: To avoid clumping do not agitate the cells by hitting or shaking the flask while waiting for the cells to detach. Cells that are difficult to detach may be placed at 37°C to facilitate dispersal.
  4. Add 6.0 to 8.0 ml of complete growth medium and aspirate cells by gently pipetting.
  5. Add appropriate aliquots of the cell suspension to new culture vessels.
  6. Incubate cultures at 37°C.
Subcultivation Ratio: A subcultivation ratio of 1:5 to 1:6 is recommended
Medium Renewal: Every 2 to 3 days
Cryopreservation
Freeze medium: Complete growth medium supplemented with 5% (v/v) DMSO
Storage temperature: liquid nitrogen vapor phase
Culture Conditions
Atmosphere: air, 95%; carbon dioxide (CO2), 5%
Temperature: 37.0°C
Name of Depositor O Hankinson
References

Hankinson O. Single-step selection of clones of a mouse hepatoma line deficient in aryl hydrocarbon hydroxylase. Proc. Natl. Acad. Sci. USA 76: 373-376, 1979. PubMed: 106390

Hankinson O. Dominant and recessive aryl hydrocarbon hydroxylase-deficient mutants of mouse hepatoma line, Hepa-1, and assignment of recessive mutants to three complementation groups. Somatic Cell Genet. 9: 497-514, 1983. PubMed: 6623311

Zhang J, et al. Basis for the loss of aryl hydrocarbon receptor gene expression in clones of a mouse hepatoma cell line. Mol. Pharmacol. 50: 1454-1462, 1996. PubMed: 8967965

The c12 (B15ECiii2) cell line was derived from Hepa-1c1c7 (ATCC CRL-2026). Hepa-1c1c7 has high aryl hydrocarbon hydroylase (AHH) activity. The cells were exposed to ethyl methane sulfonate (EMS) and mutant colonies were selected for benzo[a]pyrene resistance. The c12 (B15ECiii2) cell line expresses reduced levels of aryl hydrocarbon receptor (AHR) mRNA and protein, due to an unknown factor required for AHR expression. AHR binds a number of xenobiotic compounds and mediates pathogenesis (including carcinogenesis) by these compounds. This cell line is a useful tool to study the molecular mechanism of these processes.

Hepa-1c1c7 cells were treated with ethylmethanesulfonate (EMS)

Notice: Necessary PermitsPermits

These permits may be required for shipping this product:

  • Customers located in the state of Hawaii will need to contact the Hawaii Department of Agriculture to determine if an Import Permit is required. A copy of the permit or documentation that a permit is not required must be sent to ATCC in advance of shipment.
Basic Documentation
References

Hankinson O. Single-step selection of clones of a mouse hepatoma line deficient in aryl hydrocarbon hydroxylase. Proc. Natl. Acad. Sci. USA 76: 373-376, 1979. PubMed: 106390

Hankinson O. Dominant and recessive aryl hydrocarbon hydroxylase-deficient mutants of mouse hepatoma line, Hepa-1, and assignment of recessive mutants to three complementation groups. Somatic Cell Genet. 9: 497-514, 1983. PubMed: 6623311

Zhang J, et al. Basis for the loss of aryl hydrocarbon receptor gene expression in clones of a mouse hepatoma cell line. Mol. Pharmacol. 50: 1454-1462, 1996. PubMed: 8967965

The c12 (B15ECiii2) cell line was derived from Hepa-1c1c7 (ATCC CRL-2026). Hepa-1c1c7 has high aryl hydrocarbon hydroylase (AHH) activity. The cells were exposed to ethyl methane sulfonate (EMS) and mutant colonies were selected for benzo[a]pyrene resistance. The c12 (B15ECiii2) cell line expresses reduced levels of aryl hydrocarbon receptor (AHR) mRNA and protein, due to an unknown factor required for AHR expression. AHR binds a number of xenobiotic compounds and mediates pathogenesis (including carcinogenesis) by these compounds. This cell line is a useful tool to study the molecular mechanism of these processes.

Hepa-1c1c7 cells were treated with ethylmethanesulfonate (EMS)