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c4 (B13NBii1)
    c4 (B13NBii1)
  • 平臺編號:bio-68463
  • 國際編號:CRL-2717?
  • 細胞信息: c4 (B13NBii1)
  • 規(guī)格:frozen
  • 用途:ATCC原裝細胞
  • 服務(wù)費用:
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  • 注意事項:僅用于科學(xué)研究或者工業(yè)應(yīng)用等非醫(yī)療目的不可用于人類或動物的臨床診斷或治療,非藥用,非食用(產(chǎn)品信息以出庫為準(zhǔn))

數(shù)量:大量
細胞形態(tài):上皮樣
運輸方式:凍存運輸
器官來源:肝
品系:C57L/J
生長狀態(tài):貼壁生長
ATCC Number:CRL-2717?
相關(guān)疾病:肝癌
細胞類型:上皮細胞
是否是腫瘤細胞:0
物種來源:小鼠
規(guī)格:0.1ml Designations: c4 (B13NBii1)
Depositors: ?O Hankinson
Biosafety Level:1
Shipped: frozen
Medium & Serum: See Propagation Growth Properties:adherent
Organism: Mus musculus deposited as mouse
Morphology:epithelial


Source: Organ: liver
Strain: C57L/J
Disease: hepatoma
Cell Type: epithelial
Permits/Forms:In addition to the MTA mentioned above, other ATCC and/or regulatory permits may be required for the transfer of this ATCC material. Anyone purchasing ATCC material is ultimately responsible for obtaining the permits. Please click here for information regarding the specific requirements for shipment to your location.
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.
Propagation: ATCC complete growth medium: Alpha minimum essential medium without ribonucleosides and deoxyribonucleosides with 2 mM L-glutamine, 90%; heat-inactivated fetal bovine serum, 10%
Atmosphere: air, 95%; carbon dioxide (CO2), 5%
Temperature: 37.0°C
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
Preservation: Freeze medium: Complete growth medium supplemented with 5% (v/v) DMSO
Storage temperature: liquid nitrogen vapor phase
Related Products:parental cell line:ATCC CRL-2026
derivative:ATCC CRL-2712
References: 22593: 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
61152: 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
61153: Hoffman EC, et al. Cloning of a factor required for activity of the Ah (dioxin) receptor. Science 252: 954-958, 1991. PubMed: 1852076
61215: 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
61228: Hankinson OMutants of cultured hepatoma cells deficient in aryl hydrocarbon hydroxylaseIn: Hankinson OMicrosomes, drug oxidations, and chemical carcinogenesis2New YorkAcademic Presspp. 1149-1152, 1980

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