284572

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Showing 1-14 of 14 results for "284572" within Papers

Effect of inhibitors of poly(ADP-ribose)polymerase on the radiation response of HeLa S3 cells.

P Burgman et al.

Radiation research, 119(2), 380-386 (1989-08-01)

The purpose of this study was to investigate possible involvement of poly(ADP-ribosyl)ation reactions in X-ray-induced cell killing, repair of potentially lethal damage (PLD), and formation and repair of radiation-induced DNA damage. As tools we used the inhibitors of poly(ADP-ribose)polymerase, 3-aminobenzamide

Exosite interactions determine the affinity of factor X for the extrinsic Xase complex.

R J Baugh et al.

The Journal of biological chemistry, 275(37), 28826-28833 (2000-07-13)

The initiation of coagulation results from the activation of factor X by an enzyme complex (Xase) composed of the trypsin-like serine proteinase, factor VIIa, bound to tissue factor (TF) on phospholipid membranes. We have investigated the basis for the protein

The development of a semi-preparatory scale supercritical-fluid chromatograph for high-throughput purification of 'combi-chem' libraries.

T A Berger et al.

Journal of biochemical and biophysical methods, 43(1-3), 87-111 (2000-06-28)

A unique separator was developed which allowed automatic separation and peak collection using semi-preparative supercritical fluid chromatography (SFC). A peak detector switched the effluent between waste and special collection cassettes. Up to 50 mg of various solutes were injected onto

Kinetics of heparin action.

J D Shore et al.

Annals of the New York Academy of Sciences, 556, 75-80 (1989-01-01)

Mechanism and pathways underlying the self-sensitized photodegradation of methotrexate under simulated solar irradiation.

Ming-Hao Hsu et al.

Journal of hazardous materials, 373, 468-475 (2019-04-03)

Methotrexate, a chemotherapeutic agent, was found to undergo self-sensitized photodegradation in aqueous environments. As the initial concentration increased, methotrexate was able to enhance its own direct photolysis reaction not only in DI but also in natural waters. The methotrexate degradation

Effect of inhibitors of poly(ADP-ribose) polymerase on the heat response of HeLa S3 cells.

P Burgman et al.

Radiation research, 116(3), 406-415 (1988-12-01)

The purpose of this study was to investigate a possible involvement of poly(ADP-ribosyl)ation reactions in hyperthermic cell killing and hyperthermic DNA strand-break induction and repair in HeLa S3 cells. The inhibitors of poly(ADP-ribose) polymerase, 3-aminobenzamide (3AB) and 4-aminobenzamide (4AB), were

The role of bicarbonate anions in methotrexate degradation via UV/TiO

Webber Wei-Po Lai et al.

Water research, 112, 157-166 (2017-02-06)

Bicarbonate anion (HCO

Inhibitors of poly(ADP-ribose) synthesis enhance X-ray killing of log-phase Chinese hamster cells.

E Ben-Hur et al.

Radiation research, 97(3), 546-555 (1984-03-01)

Postirradiation incubation of V79 Chinese hamster cells with inhibitors of poly(ADP-ribose) synthesis was found to potentiate the killing of cells by X rays. Potentiation increased with incubation time and with concentration of the inhibitor. Preirradiation incubation had only a small

Cell death protection by 3-aminobenzamide and other poly(ADP-ribose)polymerase inhibitors: different effects on human natural killer and lymphokine activated killer cell activities.

D Monti et al.

Biochemical and biophysical research communications, 199(2), 525-530 (1994-03-15)

The death of target cells by cytotoxic effector cells is a relevant biological phenomenon, where cells are activated and a very quick apoptotic program occurs. In order to test the hypothesis that the nuclear enzyme poly(ADP-ribose)polymerase (PADPRP) plays a role

Polyamide curvature and DNA sequence selective recognition: use of 4-aminobenzamide to adjust curvature.

Jamie Lajiness et al.

Medicinal chemistry (Shariqah (United Arab Emirates)), 5(3), 216-226 (2009-05-16)

Imidazole and pyrrole-containing polyamides belong to an important class of compounds that can be designed to target specific DNA sequences, and they are potentially useful in applications of controlling gene expression. The extent of polyamide curvature is an important consideration

Interferon-gamma inhibits insulin release and induces cell death in the pancreatic beta-cell line INS-1 independently of nitric oxide production.

R Laffranchi et al.

Experimental cell research, 237(1), 217-222 (1998-01-07)

Interferon-gamma is among the cytokines which have been implicated as effector molecules of beta-cell destruction in autoimmune diabetes. Its mechanism of action is, however, largely unknown. In the present study rat pancreatic beta-cells, INS-1, were incubated with rat interferon-gamma (rIRN-gamma)

Inhibition of nitric oxide induced cytotoxicity in pancreatic b-cells.

S A Brennan et al.

Biochemical Society transactions, 24(1), 73S-73S (1996-02-01)

Ca(2+)-calmodulin antagonist chlorpromazine and poly(ADP-ribose) polymerase modulators 4-aminobenzamide and nicotinamide influence hepatic expression of BCL-XL and P53 and protect against acetaminophen-induced programmed and unprogrammed cell death in mice.

S D Ray et al.

Free radical biology & medicine, 31(3), 277-291 (2001-07-20)

Acetaminophen (AAP), the analgesic hepatotoxicant, is a powerful inducer of oxidative stress, DNA fragmentation, and apoptosis. The anti-apoptotic oncogene bcl-XL, and the pro-apoptotic oncogene p53 are two key regulators of cell cycle progression and/or apoptosis subsequent to DNA damage in

Differential effects of IH636 grape seed proanthocyanidin extract and a DNA repair modulator 4-aminobenzamide on liver microsomal cytochrome 4502E1-dependent aniline hydroxylation.

S D Ray et al.

Molecular and cellular biochemistry, 218(1-2), 27-33 (2001-05-02)

Previous studies from our laboratories have linked the protective abilities of IH636 grape seed proanthocyanidin extract (GSPE) with inactivation of anti-apoptotic gene bcl-XL, and modification of several other critical molecular targets such as DNA-damage/DNA-repair, lipid peroxidation and intracellular Ca2+ homeostasis.

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