K562 cells

Theodorakis, N.G., Zand, D.J., Kotzbauer, P.T., Williams, G.T., Morimoto, R.I. (1989). Hemin induced transcriptional activation of the hsp70 gene during erythroid maturation in K562 cells is due to a heat shock factor mediated stress response. Mol. Cell. Biol. 9,3166-3173. 

The human DNA in this SRM comes from a female (K562) cell line and a male (TAW) source. The cells and DNA are provided as ... 

Wang HY, Cai B, Cui CB, Zhang DY, Yang BF. Vitexicarpin, a flavonoid from Vitex trifolia L, induces apoptosis in K562 cells via mitochondria-controlled apoptotic pathway. Yao Xue Xue Bao 2005 40 27-31. 

Li J, Xu LZ, Yao JJ, Guo WJ, Xia P, Chen Y (2001a) Reversal effects of droloxifene on multidrug resistance in adriamycin-resistant K562 cell line. Acta Pharmacol Sin 22(11) 1023—1027... 

Xiao H, Yang LS, Zou HF, Yang L, Le XC (2007) Analysis of oxidized multi-walled carbon nanotubes in single K562 cells by capillary electrophoresis with laser-induced fluorescence. Anal Bioanal Chem 387 119-126. 

Fig. 7. Chemical structure of azumamide A-E and activity against the crude enzyme extract from K562 cells. ...

Figures. Comet assay is shown for human K562 cells exposed to an extract produced from particulate matter released from sample PM 5 filters, to an extract derived from an unloaded filter, or to hydrogen peroxide (100 pM) as a control. Cells with little or no DNA damage are labeled 1 and 2, and those with extensive damage are labeled 3 and 4.

In 1994, the tyrphostin AG957 (9) was identified as an inhibitor of Bcr-Abl that blocked the proliferation of K562 cells [64] (Scheme 4). Solubility and... 

Antisense oligonucleotides directed against PKC II led to loss of proliferative capacity in K562 cells (Murray et al., 1993). Dowmnodulation of PKC by antisense had no effect on the proliferation and saturation density in K562 cells (Murray et al., 1997). However, Spitaler et al. (1999) found that down-modulation of PKC with antisense oligonucleotides in HeLa cells led to the induction of apoptosis. 

In K562 cells TPA activated the MDRl promoter and led to increased MDRl mRNA levels. This activation was mediated by the zinc finger transcription factor EGRl. This activation by TPA was inhibited by the Wilms Tumor suppressor WTl (McCoy et al., 1995 McCoy et al., 1999). Controversial response to TPA may depend on the presence or absence of EGRl or WTl in the cell lines investigated. 

Ask A, Persson L, Rehnholm A, Frostesjo L, Holm I, Heby O (1993) Development of resistance to hydroxyurea during treatment of human myelogenous leukemia K562 cells with alpha-difluoromethylornithine as a result of coamplification of genes for ornithine decarboxylase and ribonucleotide reductase R2 subunit. Cancer Res 53 5262-5268... 

Berkovic D, Berkovic K, Fleer EA, Eibl H, Unger C (1994) Inhibition of calcium-dependent protein kinase C by hexadecylphosphocholine and l-O-octadecyl-2-O-methyI-rac-glycero-3-phosphocholine do not correlate with inhibition of proliferation of HL60 and K562 cell lines. Eur J Cancer 30A 509-515... 

Murray NR, Baumgardner GP, Burns DJ, Fields AP (1993) Protein kinase C isotypes in human erythroleukemia (K562) cell proliferation and differentiation. Evidence that beta II protein kinase C is required for proliferation. J Biol Chem 268 15847-15853... 

Sakurada K, Zheng B, Kuo JF (1992) Comparative effects of protein phosphatase inhibitors (okadaic acid and calyculin A) on human leukemia HL60, HL60/ADR and K562 cells. Biochem Biophys Res Commun 187 488-492... 

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