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Key Documents

SRP5159

Sigma-Aldrich

14-3-3 σ , GST tagged human

recombinant, expressed in E. coli, ≥70% (SDS-PAGE), buffered aqueous glycerol solution

Sinónimos:

SFN, YWHAS, stratifin

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About This Item

Número de CAS:
UNSPSC Code:
12352202
NACRES:
NA.32

biological source

human

recombinant

expressed in E. coli

assay

≥70% (SDS-PAGE)

form

buffered aqueous glycerol solution

mol wt

~51 kDa

NCBI accession no.

application(s)

cell analysis

shipped in

dry ice

storage temp.

−70°C

Gene Information

human ... SFN(2810)

General description

14-3-3σ or stratifin is a protein that is strongly induced by gamma irradiation and other DNA-damaging agents. The induction of 14-3-3σ is mediated by a p53 responsive element. Exogenous introduction of 14-3-3σ into cycling cells results in a G2 cell cycle arrest. Knockout of 14-3-3σ in cells showed that the cells are unable to maintain cell cycle arrest after DNA damage. The 14-3-3σ -/- cells die as they enter mitosis. This process is associated with a failure of the 14-3-3σ -deficient cells to sequester the proteins that initiate mitosis and prevent them from entering the nucleus. Thus, 14-3-3σ plays an important role in maintaining the G2 checkpoint in cells and preventing mitotic death.

Physical form

Supplied in 50mM Tris-HCl, pH 7.5, 150mM NaCl, 10mM glutathione, 0.1mM EDTA, 0.25mM DTT, 0.1mM PMSF, 25% glycerol.

Preparation Note

after opening, aliquot into smaller quantities and store at -70 °C. Avoid repeating handling and multiple freeze/thaw cycles

Storage Class

10 - Combustible liquids

wgk_germany

WGK 1


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T A Chan et al.
Nature, 401(6753), 616-620 (1999-10-19)
14-3-3Sigma is a member of a family of proteins that regulate cellular activity by binding and sequestering phosphorylated proteins. It has been suggested that 14-3-3sigma promotes pre-mitotic cell-cycle arrest following DNA damage, and that its expression can be controlled by
H Hermeking et al.
Molecular cell, 1(1), 3-11 (1998-07-11)
Exposure of colorectal cancer (CRC) cells to ionizing radiation results in a cell-cycle arrest in G1 and G2. The G1 arrest is due to p53-mediated induction of the cyclin-dependent kinase inhibitor p21WAF1/CIP1/SDI1, but the basis for the G2 arrest is

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