k562 cells การใช้

• In K562 cells, apoptosis was the primary mechanism, with paraptosis occasionally found.
• KIAA1704 promoter showed significant histone 3 lysine 4 trimethylation peaks in K562 cells ( erythroid cell line ).
• Recent evidence has shown that CTX III may induce apoptosis in K562 cells via the release of cytochrome c.
• The ability to induce these changes in K562 cell cycle and cell cycle regulation provides targets for cancer drugs.
• The problem with K562 cells, and many other cancer cell types, is that there is an overabundance of Aurora kinases.
• Apoptosis is an important mechanism in regulating K562 cells and can be induced by the changes in the metabolic state of the cells.
• Many factors and components play a role in the cell cycle of K562 cells in terms of growth, cell differentiation, and apoptosis.
• Cell differentiation is induced by the deacytylase activity in these  undifferentiated progenitor cells, which alters the phenotype and morphology of the K562 cells.
• Polysaccharides isolated from " C . furcata " were shown to induce cell death ( " apoptosis " ) in human leukemia K562 cells.
• The change in phenotype induces a decrease in the growth rate and leads the K562 cells to the terminal path of becoming mature erythroids, monocytes, and mature macrophages.
• The offset of these cellular components from their balance point causes morphological changes, which result in the K562 cells being arrested in the G2 / M phase of the cell cycle.
• Other methods being focused on in the regulation of K562 cells include therapeutic methods like Polyphylin D, which caused differentiation from the progenitor state to occur, and for apoptosis to begin.
• These changes and the imbalance in the protein levels within the K562 cells cause spindle defects and arrests the cell in the G2-M phase of the cell cycle, ultimately causing the cell to undergo apoptosis.
• It has been supported that this medical plant helps regulate K562 cell growth by inhibiting Aurora kinase activity, up regulating apoptosis proteins such as p53 and Bax, as well as reducing the levels of the Bcl-2 anti-apoptosis protein.
• Knockdown of ASH1L in K562 cells causes up-regulation of the ?-globin gene and down-regulation of myelomoncytic markers GPIIb and GPIIIa, and knockdown of ASH1L in lineage marker-negative hematopoietic progenitor cells skews differentiation from myelomonocytic towards lymphoid or erythroid lineages.
• Its mRNA is also express but at rather low levels in several other human cell lines including : K562 cells ( human myelogenous leukemia cells ); Jurkat cells ( T lymphocye cells ); Hut78 cells ( T cell lymphoma cells ), HEK 293 cells ( primary embryonic kidney cells ), MCF-7 cells ( mammary adenocarcinoma cellss ), and EJ cells ( bladder carcinoma cells ).
• The G protein-coupled receptor, GPR31, cloned from PC3 human prostate cancer cell line is a high affinity ( Kd = 4.8 nM ) receptor for 12 ( " S " )-HETE; GPR31 does not bind 12 ( " R " )-HETE and has relatively little affinity for 5 ( " S " )-HETE or 15 ( " S " )-HETE . GPR31 mRNA is expressed at low levels in several human cell lines including K562 cells ( human myelogenous leukemia cell line ), Jurkat cells, ( T lymphocye cell line ), Hut78 cells ( T cell lymphoma cell line ), HEK 293 cells ( primary embryonic kidney cell line ), MCF7 cells ( mammary adenocarcinoma cell line ), and EJ cells ( bladder carcinoma cell line ).