c4 (B13NBii1) (ATCC® CRL-2717)

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

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 parental cell line c4 (B13NBii1) (ATCC CRL-2717) lacks functional ARNT while its derivative vT{2} (ATCC CRL-2712) possesses a complete transfected ARNT cDNA. Together, they can be used to study ARNT processes and the role of ARNT in vivo.
ARNT is directly involved in the regulation of xenobiotic metabolism (including chemical carcinogenesis), hypoxia and differentiation during embryogeneses.
The c4 (B13NBii1) cell line lacks functional aryl hydrocarbon receptor nuclear translocator protein (ARNT), due to a point mutation (Gly-326 to Asp) in the ARNT gene.
The c4 (B13NBii1) cell line was derived from Hepa-1c1c7 (ATCC CRL-2026).
Storage Conditions liquid nitrogen vapor phase
Derivation
The c4 (B13NBii1) cell line was derived from Hepa-1c1c7 (ATCC CRL-2026). Hepa-1c1c7 has high aryl hydrocarbon hydroxylase (AHH) activity. The cells were exposed to N-methyl-N'-nitro-N- nitrosoguanidine (MNNG) and mutant colonies were selected for benzo[a]pyrene resistance. The c4 (B13NBii1) cell line lacks functional aryl hydrocarbon receptor nuclear translocator protein (ARNT), due to a point mutation (Gly-326 to Asp) in the ARNT gene. ARNT is directly involved in the regulation of xenobiotic metabolism (including chemical carcinogenesis), hypoxia and differentiation during embryogeneses. The parental cell line c4 (B13NBii1) (ATCC CRL-2717) lacks functional ARNT while its derivative vT{2} (ATCC CRL-2712) possesses a complete transfected ARNT cDNA. Together, they can be used to study ARNT processes and the role of ARNT in vivo.
Comments
The c4 (B13NBii1) cell line was derived from Hepa-1c1c7 (ATCC CRL-2026). Hepa-1c1c7 has high aryl hydrocarbon hydroxylase (AHH) activity. The cells were exposed to N-methyl-N'-nitro-N- nitrosoguanidine (MNNG) and mutant colonies were selected for benzo[a]pyrene resistance. The c4 (B13NBii1) cell line lacks functional aryl hydrocarbon receptor nuclear translocator protein (ARNT), due to a point mutation (Gly-326 to Asp) in the ARNT gene. ARNT is directly involved in the regulation of xenobiotic metabolism (including chemical carcinogenesis), hypoxia and differentiation during embryogeneses. The parental cell line c4 (B13NBii1) (ATCC CRL-2717) lacks functional ARNT while its derivative vT{2} (ATCC CRL-2712) possesses a complete transfected ARNT cDNA. Together, they can be used to study ARNT processes and the role of ARNT in vivo.
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 which 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 1:2 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

Legraverend C, et al. Regulatory gene product of the Ah locus. Characterization of receptor mutants among mouse hepatoma clones. J. Biol. Chem. 257: 6402-6407, 1987. PubMed: 6896205

Hoffman EC, et al. Cloning of a factor required for activity of the Ah (dioxin) receptor. Science 252: 954-958, 1991. PubMed: 1852076

Numayama-Tsuruta K, et al. A point mutation responsible for defective function of the aryl-hydrocarbon-receptor nuclear translocator in mutant Hepa-1c1c7 cells. Eur. J. Biochem. 246: 486-495, 1997. PubMed: 9208942

Hankinson OMutants of cultured hepatoma cells deficient in aryl hydrocarbon hydroxylaseIn: Hankinson OMicrosomes, drug oxidations, and chemical carcinogenesis2New YorkAcademic Presspp. 1149-1152, 1980

The c4 (B13NBii1) cell line was derived from Hepa-1c1c7 (ATCC CRL-2026). Hepa-1c1c7 has high aryl hydrocarbon hydroxylase (AHH) activity. The cells were exposed to N-methyl-N'-nitro-N- nitrosoguanidine (MNNG) and mutant colonies were selected for benzo[a]pyrene resistance. The c4 (B13NBii1) cell line lacks functional aryl hydrocarbon receptor nuclear translocator protein (ARNT), due to a point mutation (Gly-326 to Asp) in the ARNT gene. ARNT is directly involved in the regulation of xenobiotic metabolism (including chemical carcinogenesis), hypoxia and differentiation during embryogeneses. The parental cell line c4 (B13NBii1)(CRL-2717) lacks functional ARNT while its derivative vT{2} (CRL-2712) possesses a complete transfected ARNT cDNA. Together, they can be used to study ARNT processes and the role of ARNT in vivo.

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

Legraverend C, et al. Regulatory gene product of the Ah locus. Characterization of receptor mutants among mouse hepatoma clones. J. Biol. Chem. 257: 6402-6407, 1987. PubMed: 6896205

Hoffman EC, et al. Cloning of a factor required for activity of the Ah (dioxin) receptor. Science 252: 954-958, 1991. PubMed: 1852076

Numayama-Tsuruta K, et al. A point mutation responsible for defective function of the aryl-hydrocarbon-receptor nuclear translocator in mutant Hepa-1c1c7 cells. Eur. J. Biochem. 246: 486-495, 1997. PubMed: 9208942

Hankinson OMutants of cultured hepatoma cells deficient in aryl hydrocarbon hydroxylaseIn: Hankinson OMicrosomes, drug oxidations, and chemical carcinogenesis2New YorkAcademic Presspp. 1149-1152, 1980

The c4 (B13NBii1) cell line was derived from Hepa-1c1c7 (ATCC CRL-2026). Hepa-1c1c7 has high aryl hydrocarbon hydroxylase (AHH) activity. The cells were exposed to N-methyl-N'-nitro-N- nitrosoguanidine (MNNG) and mutant colonies were selected for benzo[a]pyrene resistance. The c4 (B13NBii1) cell line lacks functional aryl hydrocarbon receptor nuclear translocator protein (ARNT), due to a point mutation (Gly-326 to Asp) in the ARNT gene. ARNT is directly involved in the regulation of xenobiotic metabolism (including chemical carcinogenesis), hypoxia and differentiation during embryogeneses. The parental cell line c4 (B13NBii1)(CRL-2717) lacks functional ARNT while its derivative vT{2} (CRL-2712) possesses a complete transfected ARNT cDNA. Together, they can be used to study ARNT processes and the role of ARNT in vivo.