AKT Genetic Alteration Cell Panel (ATCC® TCP-1029)

Components ATCC CRL-2321 HCC1143
ATCC CRL-7245 Hs 343.T
ATCC CRL-1469 PANC-1
ATCC HTB-161 NIH:OVCAR-3
ATCC CRL-1622 KLE
ATCC HTB-183 NCI-H661
ATCC HTB-20 BT-474
ATCC HTB-128 MDA-MB-415
Applications This panel is useful for AKT pathway research, as well as for developing pan-AKT inhibitors or isoform-specific AKT inhibitors as anti-cancer therapeutics.
Biosafety Level 1
Comments AKT is a serine–threonine protein kinase that is expressed as three isoforms (AKT1, -2 and -3). AKT activation is initiated by translocation to the plasma membrane, which is mediated by a receptor tyrosine kinase-PI3K pathway. Activated AKT phosphorylates many key proteins, such as glycogen synthase kinase 3 and FOXOs, and regulates cell survival, proliferation and other cellar processes. Amplification of AKT1 and AKT2 has been discovered in a variety of common tumor types.  AKT1 is linked to tumor cell survival and growth, whereas AKT2 is linked to tumor invasiveness.

The AKT genetic alteration cell panel (ATCC TCP-1029) is composed of eight human tumor cell lines from common cancer types that carry ATK gene copy number changes. The AKT1 and AKT2 gene alteration status of each cell line has been sequenced and validated by ATCC. This panel is useful for AKT pathway research, as well as for developing pan-AKT inhibitors or isoform-specific AKT inhibitors for anti-cancer therapeutics.
Product Format frozen
Storage Conditions LN vapor (less than -130°C) only
Basic Documentation
Other Documentation
FAQs
  1. Tumor Cell Panels


    Date Updated: 3/27/2014

  2. Nucleic acids and cell pellets for ATCC Cell Panels


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  3. Molecular Signature Panels

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  4. Validated genetic information for tumor cell panels
    It depends on the types of panels. There are mainly two kinds ...
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  5. Tumor cell panels by tissue type vs. molecular signature


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  6. Tumor cell panels by tissue type


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  7. Control cell line for tumor cell panels


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  8. Gene mutation information for molecular signature panels


    Date Updated: 3/27/2014