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Protein Kinase CKII

Another example where C-terminal sequencing aided in the characterization of a recombinant protein was for Protein Kinase CKII. SDS-PAGE of two different preparations of the protein revealed CKII bands with slightly different electrophoretic mobilities one band with the expected mobility, and one suggesting a lower molecular weight protein. The two CKII proteins were found to have identical N-terminal sequences, and both reacted with antibodies to CKII beta. However, different crystal forms were obtained from each preparation. A truncation at the C-terminus of the protein seemed a possible explanation. [Pg.233]

Figure 2. C-terminal sequencing analysis of a heterogenous, truncated sample of the p-subunit of Protein Kinase CKII. Figure 2. C-terminal sequencing analysis of a heterogenous, truncated sample of the p-subunit of Protein Kinase CKII.
G. Bouche, V. Baldin, P. Belenguer, H. Prats, and F. Amalric, Activation of rDNA transcription by FGF-2 key role of protein kinase CKII, Cell Mol Biol Res 40, 547-554 (1994). [Pg.160]

HeLa cell lysates Inhibiting oncogenic disease through the inhibition of protein kinase CKII activity which protein kinase CKII is involved in cell proliferation and oncogenesis [102]... [Pg.246]

The lithium cation (Li" ) has been shown to inhibit GSK-3P with a potency around 2 mM IC50 (3.3 mM K ) and, although weak, this concentration is achievable clinically, thus offering the potential as a useful therapeutic. Other than GSK-3, Ii+ has been shown to also inhibit polyphosphate 1-phosphatase, inositol monophosphatase, casein kinase-II (CKII), MAP kinase-activated protein kinase-2 (MAPKAP-K2) and p38-regulated/activated kinase (PRAK) as well as activating, in cells, PI3-kinase/PKB and c-jun N-terminal kinase (JNK) [63-66]. Naturally this polypharmacology complicates the interpretation between target and function of Li+. [Pg.147]

The flavonoid crysin and benzothiophenes have been shown to inhibit casein kinase II (CKII), a cellular protein that may regulate HIV-1 transcription by phosphorylating (other) cellular proteins involved in the HIV-1 transcription transactivation process. This mechanism of action is independent of the nuclear factor kB-driven transcription pathway. Thus, flavonoids interfere with HIV-1 transcription and hence prevent HIV expression in latently infected cells. Their specificity and usefulness as HIV transcription inhibitors remain to be assessed. [Pg.393]


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