Biomedical subjects

S Fujii

Publications and source records attributed to S Fujii.

At least 379 records · Page 21Linked to original sources

PubMed1996

[Phase II study of paclitaxel (BMS-181339) in patients with ovarian cancer by 3-hour intravenous infusion].

A phase II study of Paclitaxel in patients with ovarian cancer by 3-hour intravenous infusion was undertaken by a cooperative study group of 30 institutes. Of 66 cases enrolled, 57 cases were evaluable for efficacy, and 63 cases were evaluable for safety. In spite of the fact that all cases for efficacy evaluation were previously treated with chemotherapy including platinum-based drugs, 2 cases of complete response (CR) and 15 cases of partial response (PR) were observed, with a response rate of 29.8% (The 95% confidence interval of response rate was 18.4-43.4%). Paclitaxel also showed 28.2% (11/39) response rate in patients refractory to treatment by platinum-based drugs. Histologically, the response rates were 28.9% (11/38) in serous adenocarcinoma, 40.0% (2/5) in clear cell adenocarcinoma and 25.0% (1/4) in mucinous adenocarcinoma. As the major laboratory abnormalities, leukopenia, neutropenia and decrease in hemoglobin were observed with incidence rates of 98.4% (62/63), 95.2% (59/62) and 85.7% (54/63), respectively. However, these abnormalities were clinically manageable by either withdrawal of medication, administration of antibiotics, G-CSF or metachysis etc. In addition, thrombocytopenia, elevation in GOT and GPT were seen with moderate incidence. Peripheral neuropathy was a major adverse symptom with an incidence of 79.4% (50/63), followed by alopecia, myalgia, arthralgia and fever. However, the majority of these adverse reactions were less than grade 3. From these findings, we confirmed that 3-hour intravenous infusion of Paclitaxel was a clinically useful chemotherapeutic agent in patients with ovarian cancer.

Adult↗

PubMed1996

Roles of dopamine receptors in long-term depression: enhancement via D1 receptors and inhibition via D2 receptors.

The effects of both the activation and the blockade of D1 or D2 dopamine receptors on long-term depression (LTD) of synaptic transmission, and the involvement of NMDA and GABA receptors in LTD, were investigated in CA1 neurons of rat hippocampal slices. Low-frequency stimulation (LFS, 450 pulses at 1 Hz) produced LTD of the slope of field EPSPs (-14.3%, mean, n = 10). The induction of LTD was blocked by the NMDA receptor antagonist, AP5 (1.4%, n = 7), by the D1 receptor antagonist, SCH-23390 (3.5%, n = 8), or by the D2 receptor agonist, LY-171555 (4.4%, n = 8). Either the activation of D1 receptors by SKF-38393 or the blockade of D2 receptors by sulpiride produced significantly larger LTD than the control LTD (-31.1%, n = 11; -30.6%, n = 9, respectively). Although LTD was blocked by picrotoxin, a GABAA receptor/Cl- channel antagonist (4.9%, n = 8), LTD was produced by LFS in the medium containing both SKF-38393 and picrotoxin (-27.3%, n = 7). These results indicate that: (1) the induction of LTD by LFS in hippocampal CA1 neurons is under the influence of both NMDA and GABA receptors; (2) both D1 and D2 receptors are involved in the modulation of LTD in that the activation of D1 receptors enhances LTD, while that of D2 receptors inhibits LTD, and (3) while the induction of LTD is blocked by picrotoxin, this effect is superseded by SKF-38393.

2-Amino-5-phosphonovalerate↗

PubMed1996

The long-term suppressive effect of prior activation of synaptic inputs by low-frequency stimulation on induction of long-term potentiation in CA1 neurons of guinea pig hippocampal slices.

We have investigated the effects of prior activation of afferent inputs by a train of low-frequency stimulation (LFS) on the induction of long-term potentiation (LTP) induced by high-frequency stimulation (tetanus, 100 Hz, 100 pulses) in CA1 neurons of guinea pig hippocampal slices. The parameters of the LFS were altered systematically: the frequency (1 or 5 Hz); the number of pulses (80, 200 or 1000); and the time lag from the LFS to the tetanus (20, 60 or 100 min). Conditioning effects of the LFS on the induction of LTP were evaluated in terms of the slope of the field excitatory postsynaptic potential (S-EPSP) and the amplitude of the population spike (A-PS). LTP could reliably be induced by 100 Hz tetanic stimulation delivered to a naive slice. In contrast, the attempt to induce LTP 60 min after LFS of 200 or 1000 pulses at 1 Hz resulted only in short-term potentiation while the LFS itself produced no significant change in the responses. The suppressive effect on LTP was significantly reduced for 1 Hz LFS with a smaller number of pulses (80 pulses), or a shorter (20 min) or longer (100 min) time lag from the LFS to the tetanus, or with LFS at a higher frequency (5 Hz). When the LFS of 1000 pulses at 1 Hz was delivered in the presence of the N-methyl-D-aspartate (NMDA) receptor antagonist AP5 (D,L-4-amino-5-phosphonovalerate, 50 microM), which was washed out after the end of the LFS, the tetanus given 60 min after application of the LFS produced stable LTP, indicating the involvement of NMDA receptor/channels in the mechanisms of this particular form of synaptic plasticity-long-term suppression of LTP.

2-Amino-5-phosphonovalerate↗

PubMed1996

Retinal control on the axial length mediated by transforming growth factor-beta in chick eye.

PURPOSE: To clarify retinal control on scleral growth in form-deprivation myopia (FDM) in the chick, the authors studied change in transforming growth factor-beta (TGF-beta) in the form-deprived eye and the effect of this growth factor on scleral cell proliferation and axial length. METHODS: Change in TGF-beta in FDM in the chick was measured by reverse transcriptase polymerase chain reaction (RT-PCR), immunoblot, and immunohistochemistry. The effect of TGF-beta on [3H]thymidine uptake of scleral chondrocytes was determined by organ culture. Urokinase plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) were administered to determine the effect of TGF-beta activation on the axial length in normal and FDM eyes. RESULTS: The content of TGF-beta messenger RNA (mRNA) and the active form of TGF-beta protein were reduced in FDM eyes compared with the control specimen. Reduced immunoreactivity of TGF-beta in FDM eyes was found in the photoreceptor layer. The TGF-beta inhibited [3H]thymidine uptake into scleral chondrocytes. In the nondeprived eyes, the vitreous chamber depth and axial length were reduced after uPA treatment, whereas PAI-1 increased them. In the form-deprived eyes, uPA inhibited vitreous depth and axial length elongation, but PAI-1 had no effect. CONCLUSIONS: The authors' results suggest that TGF-beta mediates retinal control of ocular growth. Axial elongation in FDM probably is correlated with the reduction of TGF-beta in the retina, retinal pigment epithelium, and choroid. The uPA and PAI-1 treatment controls the activation of TGF-beta and affects axial length.

Animals↗

PubMed1996

Thoracoscopic lung resection for lung metastasis of colorectal cancer.

We performed thoracoscopic lung resection seven times in four patients with lung metastases from colorectal cancer. This procedure allowed a short operation time, minimal blood loss, and a short hospital stay. Thoracoscopic lung resection was chosen for resection of lung metastases from colorectal cancer because it allowed simultaneous bilateral lung resection and early postoperative adjuvant chemotherapy.

Adult↗

PubMed1995

A novel mutation substituting tryptophan with arginine in the carboxyl-terminal, non-collagenous domain of collagen X in a case of Schmid metaphyseal chondrodysplasia.

A novel nucleotide change in the collagen X gene was identified in a Japanese family with Schmid metaphyseal chondrodysplasia (SMCD). The T to C change at nucleotide 1951 resulted in replacement of tryptophan by arginine at residue 651 (W651R). This missense mutation is considered to be responsible for SMCD because 1, the same mutation was not be identified in the collagen X gene from normal individuals; 2, the mutation segregated with the SMCD phenotype in the index family; 3, the substituted amino acid is highly conserved in type X collagens, and 4, the mutation causes a marked change in the hydrophobicity profile of the surrounding region in the NC1 domain. This novel mutation (W651) seems to have the same impact on bone development as W651X mutation.

Amino Acid Sequence↗

PubMed1995

Contribution of hydrophobic residues to the stability of human lysozyme: calorimetric studies and X-ray structural analysis of the five isoleucine to valine mutants.

In order to understand the contribution of hydrophobic residues to the conformational stability of human lysozyme, five Ile mutants (Ile --> Val) in the interior of the protein were constructed. The thermodynamic parameters characterizing the denaturation of these mutant proteins were determined by scanning calorimetry, and the three-dimensional structure of each mutant protein was solved at high resolution by X-ray crystallography. The thermodynamic analyses at 64.9 degrees C and at pH 2.7 revealed the following. (1) The stabilities of all the mutant proteins were decreased as compared with that of the wild-type protein. (2) The changes in the calorimetric enthalpies were larger than those in the Gibbs energies, and were compensated by entropy changes. (3) The destabilization mechanism of the mutant proteins differs, depending on the location of the mutation sites. X-ray analyses showed that the overall structures of all the mutant human lysozymes examined were identical to that of the wild-type protein, and only small structural rearrangements were observed locally around some of the mutation sites. The most striking change among the mutant proteins was found in the mutant protein, 159V, which contains a new water molecule in the cavity created by the mutation. The thermodynamic stabilities of the mutant proteins are discussed in light of the high-resolution X-ray structures of the wild-type and five mutant human lysozymes examined.

Calorimetry, Differential Scanning↗

PubMed1995

Efficacy of TNF-alpha gene-transduced tumor cells in treatment of established in vivo tumor.

The therapeutic effect of TNF gene-transduced mouse fibrosarcoma cells (Meth-A: C5) on pre-inoculated parental cells (Meth-A: M0) was studied. Subcutaneous (s.c.) transplantation of M0 cells into one flank of syngeneic BALB/c mice was followed by s.c. injection of irradiated MO or C5 into the opposite flank 1 week later. The initial M0 tumor (T-MO) completely regressed in C5-vaccinated mice, whereas in M0-vaccinated mice continuous growth of T-M0 was observed. When a similar experiment was carried out in SCID mice, no regression of T-MO was observed, suggesting that the tumor regression in BALB/c mice was not due to direct anti-tumor activity of TNF secreted from C5, but to systemic immunity. Regression of the rechallenged M0 tumor was observed in mice which had shown T-MO regression by C5 vaccination, but rechallenged Colon 26 cells (syngeneic to BALB/c mice) continued to grow, indicating a specific immunity to Meth-A cells). The systemic immunity evoked in C5-vaccinated mice was directly demonstrated by enhanced killer activities of LAK and CTL with a proliferation of T-cell population in their splenocytes. Abrogation of the therapeutic effect of C5 vaccination with anti-Thy 1 and anti-Lyt 2 also demonstrates the involvement of cellular immunity in tumor regression.

Animals↗

PubMed1995

Inactivation of glutathione peroxidase by nitric oxide. Implication for cytotoxicity.

S-nitro-N-acetyl-DL-penicillamine (SNAP), a nitric oxide (NO) donor, inactivated bovine glutathione peroxidase (GPx) in a dose- and time-dependent manner. The IC50 of SNAP for GPx was 2 microM at 1 h of incubation and was 20% of the IC50 for another thiol enzyme, glyceraldehyde-3-phosphate dehydrogenase, in which a specific cysteine residue is known to be nitrosylated. Incubation of the inactivated GPx with 5 mM dithiothreitol within 1 h restored about 50% of activity of the start of the SNAP incubation. A longer exposure to NO donors, however, irreversibly inactivated the enzyme. The similarity of the inactivation with SNAP and reactivation with dithiothreitol of GPx to that of glyceraldehyde-3-phosphate dehydrogenase, suggested that NO released from SNAP modified a cysteine-like essential residue on GPx. When U937 cells were incubated with 100 microM SNAP for 1 h, a significant decrease in GPx activity was observed although the change was less dramatic than that with the purified enzyme, and intracellular peroxide levels increased as judged by flow cytometric analysis using a peroxide-sensitive dye. Other major antioxidative enzymes, copper/zinc superoxide dismutase, manganese superoxide dismutase, and catalase, were not affected by SNAP, which suggested that the increased accumulation of peroxides in SNAP-treated cells was due to inhibition of GPx activity by NO. Moreover, stimulation with lipopolysaccharide significantly decreased intracellular GPx activity in RAW 264.7 cells, and this effect was blocked by NO synthase inhibitor N omega-methyl-L-arginine. This indicated that GPx was also inactivated by endogenous NO. This mechanism may at least in part explain the cytotoxic effects of NO on cells and NO-induced apoptotic cell death.

Animals↗

PubMed1995

Electron paramagnetic resonance studies of ferric cytochrome c' from photosynthetic bacteria.

Electronic ground nature of ferric cytochromes c' isolated from five photosynthetic bacteria. Chromatium vinosum ATCC 17899, Rhodobacter capsulatus ATCC 11166, Rhodopseudomonas palustris ATCC 17001, Rhodospirillum molischianum ATCC 14031, and Rhodospirillum rubrum ATCC 11170 has been investigated by electron paramagnetic resonance (EPR) spectroscopy. EPR spectra indicate that the electronic ground state of five ferric cytochromes c' is a quantum mechanical admixed-spin state of a high spin (S = 5/2) and an intermediate spin (S = 3/2) at pH 7.2 and is high-spin state at pH 11.0. At physiological pH, however, the content of an intermediate spin state differs with the bacterial source of the protein: approximately 50%, Chromatium vinosum; approximately 40%, Rhodobacter capsulatus and Rhodopseudomonas palustris; approximately 10%, Rhodospirillum molischianum and Rhodospirillum rubrum. Computer simulation of the spectra supports this diversity of the contribution of an intermediate spin state. Model studies of the ferric porphyrin complexes suggest that the correlation between content of an intermediate spin state and heme iron displacement from the mean heme plane. Therefore, the variation of the content of an intermediate spin state observed in the present study reflects the subtle difference in the degree of heme iron displacement among the proteins.

Chromatium↗

PubMed1995

Attenuation of the synthesis of plasminogen activator inhibitor type 1 by niacin. A potential link between lipid lowering and fibrinolysis.

BACKGROUND: Plasminogen activator inhibitor type 1 (PAI-1), the primary physiological inhibitor of endogenous plasminogen activators, has been implicated as a potentiating factor in atherogenesis as well as in coronary thrombosis. We and others have observed attenuation of PAI-1 expression by gemfibrozil both in vivo and in vitro. METHODS AND RESULTS: To determine whether other lipid-lowering agents with different mechanisms of action exert similar effects, we exposed Hep G2 cells, a highly differentiated human hepatoma cell line, to selected concentrations of niacin. Accumulation of PAI-1 protein, assayed with an ELISA, decreased in conditioned media by 72% in 48 hours in a specific, concentration-dependent fashion. Metabolic labeling experiments demonstrated a decrease in the rate of PAI-1 synthesis. Northern blot analysis demonstrated a preceding, parallel, and specific decrease in the concentration of PAI-1 mRNA. Niacin attenuated the increased PAI-1 synthesis induced by mediators released from thrombi as well. Thus, with 4.25 ng/mL transforming growth factor-beta 1, PAI-1 accumulation increased 4.5-fold in conditioned media in 48 hours. However, niacin attenuated the increase by 65%. Again, both the rate of PAI-1 synthesis and PAI-1 mRNA were reduced. The increased plasma PAI-1 activity and PAI-1 mRNA in liver induced by dexamethasone (0.8 mg IP) in vivo in rats were attenuated by 3 weeks of pretreatment with niacin. CONCLUSIONS: These results suggest that niacin, by decreasing PAI-1 expression, may potentiate fibrinolysis, thereby decreasing the stimulation of atherogenesis by clot-associated mitogens associated with microthrombi. Furthermore, the results imply that a pathogenetic link may exist between intracellular lipid metabolism and regulation of expression of fibrinolytic system components.

Animals↗

PubMed1995

Chemical modification and inactivation of phospholipases A2 by a manoalide analogue.

Chemical modification and inactivation of bovine pancreatic, porcine pancreatic, Naja naja atra and Pseudechis australis phospholipases A2 (PLA2s), belonging to Group I, and of Trimeresurus flavoviridis, Vipera russelli russelli and Agkistrodon halys blomhoffii PLA2s, belonging to Group II, were investigated by the use of a manoalide (MLD)-analogue, 1-(2,5-dihydro-hydroxy-5-oxo-3-furanyl)-8,12-dimethyl-4-formyl-3,7, 11-tridecatrienol. At appropriate time intervals, residual PLA2 activities towards monodispersed, anionic mixed micellar and non-ionic mixed micellar substrates were measured. We tested the protective effect of micellar n-dodecylphosphocholine (n-C12PC) on enzyme inactivation. Inactivation of pancreatic PLA2s (Group I) was only observed towards anionic mixed micellar substrates. This inactivation was completely prevented by the presence of micellar n-C12PC. From a fragmentation study of modified bovine pancreatic PLA2 using lysyl endopeptidase, we speculated that Lys-56 of this enzyme was modified by MLD-analogue and that this modification was responsible for enzyme inactivation. Inactivation of non-pancreatic PLA2s was observed towards all types of substrate, except that no significant inactivation of N. naja atra PLA2 (Group I) towards monodispersed substrate was noted. Micellar n-C12PC protected N. naja atra PLA2 (Group I) completely from inactivation by MLD-analogue, but had lesser protective effects on P. australis PLA2 (Group I), T. flavoviridis and V. russelli russelli PLA2s (Group II). However, no significant protection of A. halys blomhoffii PLA2s (Group II) activity was observed. These results indicate that the inactivation of pancreatic and N. naja atra PLA2s originates from the modification of Lys residues at the interfacial recognition site, and that inactivation of P. australis, T. flavoviridis and V. russelli PLA2s arises from the modification of Lys residues at the catalytic site, interfacial recognition site and regions outside both sites. The inactivation of A. halys blomhoffii PLA2 was assumed to be due to the modification of Lys residues outside the two sites described above.

Amino Acid Sequence↗

PubMed1995

Activation of dopamine D1 receptors enhances long-term depression of synaptic transmission induced by low frequency stimulation in rat hippocampal CA1 neurons.

The effects of both activation and blockade of dopamine (DA) D1 receptors on long-term depression (LTD) of synaptic transmission were examined in CA1 neurons of rat hippocampal slices. Low frequency stimulation (LFS) consisting of 450 pulses at 1 Hz induced LTD (-14.3%, mean, n = 10) in the slope of the field excitatory postsynaptic potential. SKF-38393 (3-10 microM), an agonist of DA D1 receptors, significantly enhanced LFS-induced LTD (-31.1%, n = 11). SCH-23390 (2 microM), an antagonist of DA D1 receptors, blocked the induction of LTD by LFS (2.5%, n = 6). These results indicate that DA D1 receptors play an important role in the modulation of LFS-induced LTD in rat hippocampal CA1 neurons.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1995

Massive cell death of immature hematopoietic cells and neurons in Bcl-x-deficient mice.

bcl-x is a member of the bcl-2 gene family, which may regulate programmed cell death. Mice were generated that lacked Bcl-x. The Bcl-x-deficient mice died around embryonic day 13. Extensive apoptotic cell death was evident in postmitotic immature neurons of the developing brain, spinal cord, and dorsal root ganglia. Hematopoietic cells in the liver were also apoptotic. Analyses of bcl-x double-knockout chimeric mice showed that the maturation of Bcl-x-deficient lymphocytes was diminished. The life-span of immature lymphocytes, but not mature lymphocytes, was shortened. Thus, Bcl-x functions to support the viability of immature cells during the development of the nervous and hematopoietic systems.

Animals↗

PubMed1995

Extracellular phosphorylation of membrane protein modifies theta burst-induced long-term potentiation in CA1 neurons of guinea-pig hippocampal slices.

The involvement of ecto-protein kinase activity in activity-dependent long-term potentiation (LTP) was studied in CA1 neurons of guinea-pig hippocampal slices. Application of 5 microM K-252b, an ecto-protein kinase inhibitor, blocked LTP induced by a theta-burst stimulation (3 bursts composed of 5 pulses at 100 Hz with inter-burst intervals of 200 ms). On the other hand, under 10 microM RK682, an ecto-phosphatase inhibitor, a robust LTP was induced by a weak theta-burst stimulation (3 bursts composed of 3 pulses) which was just at the threshold for the induction of LTP in the control perfusate. These findings suggest that ATP released from presynaptic terminals during the burst stimulation plays an important role in the induction of LTP through phosphorylation of extracellular domains of synaptic membrane proteins, as the substrate for ecto-protein kinase.

Animals↗

PubMed1995

The mechanism of ATP-induced long-term potentiation involves extracellular phosphorylation of membrane proteins in guinea-pig hippocampal CA1 neurons.

The mechanism of ATP-induced long-term potentiation was studied pharmacologically using guinea-pig hippocampal slices. Application of 1-10 microM ATP for 10 min transiently depressed and then slowly augmented the synaptic transmission in CA1 neurons leading to long-term potentiation (LTP). This ATP-induced LTP was blocked by the addition of K-252b, an ecto-protein kinase inhibitor, but was enhanced by the addition of RK682, an ecto-phosphatase inhibitor, both of which do not permeate the cell membrane. These results suggest that ATP applied to the perfusate provides enough substrate for ecto-protein kinase to induce LTP through phosphorylation of extracellular domains of membrane proteins in CA1 neurons.

Adenosine Triphosphate↗

PubMed1995

Induction of plasminogen activator inhibitor type-1 (PAI-1) by proinsulin and insulin in vivo.

BACKGROUND: Fasting hyperinsulinemia (reflected by elevations in immunoreactive "insulin") is typical of patients with non-insulin-dependent diabetes mellitus (NIDDM) and is often associated with obesity and hypertension. The elevated concentrations detected are indicative not only of insulin but also of its immunologically cross-reactive precursors, including proinsulin. Fasting hyperinsulinemia appears to be associated with decreased fibrinolytic activity in blood, which results from increased activity of plasminogen activator inhibitor type-1 (PAI-1), a potential independent risk factor for coronary artery disease. Patients who were given proinsulin in a previous clinical study by others exhibited an increased incidence of cardiovascular events. Thus, a "proinsulin-PAI-1 axis" may predispose to coronary thrombosis. To define the possible presence of such an axis, this study was designed to determine whether insulin, its precursors, or both increase the concentrations of PAI-1 in rabbits in vivo. METHODS AND RESULTS: Equimolar proinsulin (n = 10), insulin (n = 11), C-peptide (n = 4), or vehicle alone (n = 10) was administered intravenously over 1 hour to euglycemic, conscious rabbits. Plasma PAI-1 activity increased 3.8-fold with proinsulin (P = .002) and 3.6-fold with insulin (P = .002). By contrast, no increase occurred after C-peptide or vehicle was administered. The increased PAI-1 activity was shown to be attributable to PAI-1 protein by reverse fibrin autography. As judged from changes in mRNA in tissues, proinsulin and insulin increased PAI-1 gene expression within 3 hours by 2.1- and 2.1-fold, respectively, in aorta (P = .025 each) and by 1.9- and 2.4-fold in liver (P = .015 and P = .001), with return of values to baseline within 24 hours (n = 4 experiments in each case). CONCLUSIONS: These results extend our previous observations from studies in vitro and suggest that hyperinsulinemia attributable to augmented concentrations of proinsulin and insulin in plasma increase plasma PAI-1 activity and may contribute to acceleration of atherosclerosis and impairment of coronary thrombolysis in patients with NIDDM.

Animals↗

PubMed1995

High-performance liquid chromatographic assay for farnesyl-protein transferase activity with dabsylated peptide.

An HPLC assay for farnesyl-protein transferase activity using a dabsylated peptide is described. The substrates used were a synthetic dabsylated nonapeptide, N-dabsyl-L-serinyl-L-methioninyl-L-glycinyl-L-++ +leucinyl-L-prolinyl-L-cysteinyl- L-valinyl-L-valinyl-L-methionine, corresponding to the C-terminal peptide sequence of human N-Ras p21 without the N-terminal serine, and farnesyl diphosphate. The product was separated from the substrates on a reversed-phase C18 column, using gradient elution with acetonitrile (0.05% trifluoroacetic acid)-water (0.1% trifluoroacetic acid) and was detected at 436 nm. The addition of the farnesyl group to the peptide was confirmed by MS and NMR. Enzymatic reaction was ascertained from the dependences on time, on the protein of the enzyme source and on the substrates. The reaction was specifically inhibited by L-cysteinyl-L-valinyl-L-valinyl-L-methionine, the tetrapeptide corresponding to the "CAAX" motif. The limit of detection was 2 pmol per 100-microliters reaction mixture. The farnesyl-protein transferase activity can quantitatively be measured up to 200 micrograms cytosolic protein in human liver. This method provides a convenient and quantitative assay for crude materials, such as tissue homogenate from clinical samples, without the use of radioactive probes and large amounts of Ras protein.

Alkyl and Aryl Transferases↗