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Kinase Resistance

BVdU is degraded by thymidine phosphorylase more rapidly than the natural substrate, thymidine. This rapid enzymic degradation may present a problem in its clinical use. Moreover, herpes vimses develop resistance to BVdU, apparendy because of mutant vimses that have lower thymidine kinase activity. G. D. Seade has dropped further development of BVdU because of increased animal tumor incidence induced by prolonged dosing (1). [Pg.305]

FIAC- (also FMAU-, FAU-, and FAC-)resistant variants of HSV-1 and -2 are unable - " to phosphorylate these nucleosides because of decreased activity of the thymidine kinase (TK) and, therefore, are 6,000-fold less pathogenic " (for the HSV-1 variant) than the parent virus. This decreased TK activity (production) seems to be one of the characteristic features of resistant viruses. [Pg.248]

Fig. 9.4 Organization of glycopeptide-resistance genes in transposon Tnl546. IR, invested repeats HPK, histidine protein kinase TcR, low level teicoplanin resistance. Fig. 9.4 Organization of glycopeptide-resistance genes in transposon Tnl546. IR, invested repeats HPK, histidine protein kinase TcR, low level teicoplanin resistance.
A putative regulatory cofactor has been identified for the renal brush border Na /H exchanger (resistant-type) [50]. Morell et al. [50] identified a 42-kDa protein that was distinct from the transporter itself and appeared to be involved in regulation by cAMP-dependent protein kinase (PKA). Evidence supporting this conclusion was ... [Pg.260]

Brognard, J., Clark, A.S., Ni, Y., and Dennis. P.A. 2001. Akt/protein kinase b is constitutively active in nonsmall cell lung cancer cells and promotes cellular survival and resistance to chemotherapy and radiation. [Pg.479]

Our working hypothesis is that subunit stoichiometry or changes in the structure of individual receptor subunits give rise to the different conductance subtypes and that phosphorylation by the different kinase enzymes has major effects on the P-open values of the receptor. Should the hypothesis hold, then alterations in the phosphorylation state of the receptor by the different kinase enzymes may (as stated earlier) be important in the development of anthelmintic resistance. [Pg.467]

BCR-ABL tyrosine kinase Cancer Point mutation causes resistance to STI-571 compound 21... [Pg.146]

As described in several monographs [4], bryostatin 1 exhibits significant in vitro and in vivo antineoplastic activity against a range of tumor cell lines including murine leukemia, B-cell lymphoma, reticulum cell sarcoma, ovarian carcinoma, and melanoma. It is also effective in the modulation of apoptotic function [5], the reversal of multidrug resistance [6], and stimulation of the immune system [7]. These unique features displayed by bryostatin 1 are attributed to its high affinity for protein kinase C (PKC) isozymes and its ability to selectively modulate their functions [8]. PKCs are a type of intracellular serine and threonine kinase that... [Pg.104]

Itani SI, Ruderman NB, Schmieder F and Boden G. 2002. Lipid-induced insulin resistance in human muscle is associated with changes in diacylglycerol, protein kinase C, and IkappaB-alpha. Diabetes 51(7) 2005-2011. [Pg.172]

It has been suggested that tamoxifen, one of the most effective therapeutic and chemopreventive agent for breast cancer, modulates protein kinase C through oxidative stress in breast cancer cells [194], Unfortunately, most breast cancers initially responsive to tamoxifen treatment later become resistant. Schiff et al. [195] suggested that the conversion of breast tumors to a tamoxifen-resistant phenotype is associated with oxidative stress and depends on significantly enhanced SOD activity in tumors. [Pg.929]

Interleukin 1 (IL-1) is produced mainly by activated monocytes-macropha-ges, and its principal action is to stimulate thymocytes. A pleiotropic cytokine, IL-1 induces the expression of a large diversity of cytokines such as IL-6, leukaemia inhibitory factor (LIF), and other proinflammatory molecules (Di-marello 1994). IL-1 and TNF-a carry out as part of their function increasing the expression of NF-/cB and JNK (c-Jun N-terminal kinase). The importance of IL-1 in OCS is demonstrated because the IL-1-receptor-deficient mouse is resistant to ovariectomy (OVX)-induced bone loss (Lorenzo et al. 1998). The importance in pathological bone loss is also illustrated by the fact that treatment with IL-1 receptor antagonist slows down bone erosion for patients affected with rheumatoid arthritis (Kwan et al. 2004). IL-1 increases osteoclast differentiation rather than mature osteoclast activity, and infusion of IL-1 into mice induces hypercalcemia and bone resorption. Finally, IL-1 and TNF-a... [Pg.175]


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See also in sourсe #XX -- [ Pg.122 ]




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Insulin resistance kinase

Kinase Mutations and Resistance in Cancer

Kinase imatinib resistance

Mutations/drug resistance kinase activation

Resistance Mutations Kinase

Resistance mechanisms not involving kinase domain mutations

Resistance mutations to imatinib and successor compounds (Kit kinase)

Resistance sugar kinases

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