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Biomedical subjects

C L Wang

Publications and source records attributed to C L Wang.

At least 91 records · Page 5Linked to original sources
PubMed1997

Glutathione synthetase: similarities of the proteins from Schizosaccharomyces pombe and Arabidopsis thaliana.

Glutathione synthetase predicted from the reported gene sequence from Schizosaccharomyces pombe is substantially smaller than the equivalent protein predicted from the cDNAs sequenced from Arabidopsis thaliana, Saccharomyces cerevisiae and other eukaryotes. Sequence alignments of the proteins encoded by the cDNA clones for glutathione synthetase from Arabidopsis and S. pombe show that the Arabidopsis protein contains 200 extra amino acids at the N-terminus. In order to test if this sequence is essential in the function of the protein, the full-length Arabidopsis protein and as two N-terminal deletions (Delta67-71 and Delta67-200) were expressed in S. pombe mutant MN101, which lacks endogenous glutathione synthetase activity. Although the wild-type plant cDNA could complement the yeast mutation, neither deletion mutant was able to restore glutathione-dependent cadmium resistance. When the three proteins were expressed as fusion proteins in Escherichia coli, they accumulated to the same level, but only the plasmid containing the full-length cDNA, pFLAG222, produced detectable enzyme activity in vitro. These results suggested that the N-terminus of the Arabidopsis glutathione synthetase is essential for its function and opened up the possibility that there was a sequencing error in the reported S. pombe sequence. Therefore the gsh2 sequence from wild-type S. pombe and the mutant strain MN101 were determined. The wild-type S. pombe gsh2 encodes a protein that is about the same length as that found in Arabidopsis, and the MN101 mutation involves a frameshift mutation early in the glutathione synthetase reading frame.

Amino Acid Sequence↗
PubMed1997

Formation and persistence of DNA adducts of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) in CDF1 mice fed a high omega-3 fatty acid diet.

The potent bacterial mutagen 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) is carcinogenic in the CDF1 mouse, affecting the liver, lungs and forestomach. IQ forms DNA adducts in both target- and non-target organs of the CDF1 mouse. The chemopreventive effects of menhaden oil (MO), a fish oil high in omega-3 fatty acids, are well known. Because DNA adduct formation is considered to be a critical event in the initiation of carcinogenesis, we have assessed the effects of dietary MO on IQ-DNA adduct formation. For the duration of the study, young adult, male CDF1 mice were maintained on either powdered chow diet, AIN-76A diet, or AIN-76A diet modified to contain 19% MO (19% MO diet). After 2 weeks on these diets, all animals received 0.01% (w/w) IQ in the diet for the next 3 weeks. Groups of 4 animals were killed 1, 2, 4, 6, 8 or 12 days thereafter for analysis of IQ-DNA adducts by 32P-postlabeling. IQ-DNA adduct patterns were qualitatively similar in the liver, lungs, stomach, small intestine, cecum, colon, kidneys, heart and spleen. Adduct levels in the liver, lungs, stomach and colon decreased significantly during the 12-day study period, but only to a relatively small extent and only with certain of the diets. On day 1, the 19% MO diet significantly decreased (35.8-90.0%) adduct levels in the stomach, cecum, colon and kidneys, when compared to chow diet or AIN-76A diet. On day 12, adduct levels in the liver, stomach, heart and spleen were decreased (36.5-64.7%) as a result of MO feeding. With the exception of the liver, heart and spleen on day 12, there were no significant differences in organ adduct levels between the chow diet and the AIN-76A diet. It is concluded that feeding 0.01% (w/w) IQ in the diet for 3 weeks results in a relatively slow rate of adduct removal and that this rate is largely independent of the type of diet. Dietary MO inhibits IQ-DNA adduct formation only in certain target- and non-target organs of the CDF1 mouse, a finding similar to our previous results in the F344 rat. MO may affect the initiation phase of IQ tumorigenesis by inhibiting IQ-DNA adduct formation in certain target organs.

Adenosine Triphosphate↗
PubMed1997

Identification of a putative flexible loop in Arabidopsis glutathione synthetase.

Glutathione synthetase catalyses the ATP-dependent ligation of gamma-glutamylcystene with glycine to form glutathione. Amino acid sequence comparisons between the Arabidopsis and the Escherichia coli proteins suggested that a region, identified as a small flexible loop that covers the active site of the E. coli protein, might be conserved in the eukaryotic protein. Three site-directed mutations in the Arabidopsis protein were generated to test this hypothesis. Two mutations within the conserved region (Lys367/ Pro368-->Asn/Ser and Gly374-->Val) inactivated the enzyme in an in vivo assay based on cadmium resistance in S. pombe, and in an in vitro assay of the activity of the enzyme expressed in E. coli. A third mutation outside of this conserved region (Leu363-->Glu) had a smaller effect in both assays. These results are consistent with the idea that this glycine-rich loop in the Arabidopsis and E. coli proteins might serve the same function in covering the active site of the enzyme.

Amino Acid Sequence↗
PubMed1997

Fibronectinase activity in cultured human trophoblasts is mediated by urokinase-type plasminogen activator.

OBJECTIVE: Human trophoblast proteolytic activity is believed to have implications for early implantation events and maintenance of chorionic structural integrity later in gestation. Abnormal release of chorion-derived extracellular matrix proteins such as fibronectin may identify patients at risk for preterm labor and delivery. The aim of this study was to characterize the enzyme(s) potentially responsible for trophoblast-mediated proteolysis of fibronectin. STUDY DESIGN: Human term cytotrophoblasts were analyzed for their capacity to cleave fibronectin into discrete proteolytic fragments. Selective protease inhibitors were used to characterize trophoblast-derived enzymes with fibronectinase activity. Analysis and quantitation of fibronectin fragment release was determined by Western immunoblots and enzyme-linked immunosorbent assays. RESULTS: Fibronectinase activity in trophoblast cultures was found to be both cell mediated and secreted, with the release of discrete fibronectin fragments into the media. Cell-mediated proteolytic activity could be partially inhibited by serum, whereas conditioned media containing fibronectinase activity was completely inhibited by serum, a serine protease inhibitor, and a selective inhibitor of urokinase-type plasminogen activator. Digestion of fibronectin with pure urokinase produced a similar pattern of fibronectin fragments compared with fibronectinase-generated fragments. Immunodepletion of urokinase from trophoblast media abolished fibronectinase activity. CONCLUSIONS: Trophoblast-derived urokinase-type plasminogen activator has significant proteolytic activity in vitro with the capability of cleaving fibronectin into discrete fragments. In early pregnancy this activity could be part of the enzymatic cascade leading to uterine extracellular matrix remodeling and implantation. Later in pregnancy trophoblast derived urokinase could promote normal or inflammation-induced changes in the chorionic extracellular matrix.

Antibodies↗
PubMed1997

Phosphatidylserine liposomes can be tethered by caldesmon to actin filaments.

Rotary shadowing electron microscopy revealed that attachment of caldesmon to phosphatidylserine (PS) liposomes was mainly through its C-terminal end. To determine the PS-binding sites of caldesmon, we have made use of synthetic peptides covering the two C-terminal calmodulin binding sites and a recombinant fragment corresponding to the N-terminal end of the C-terminal domain that contains an amphipathic helix. Interactions of these peptides with the PS liposomes were studied by nondenaturing gel electrophoresis and fluorescence spectroscopy. The results showed that both calmodulin-binding sites of caldesmon were able to interact with PS. The affinity (Kd) of PS for these sites was in the range of 1.8-14.3 x 10(-5) M, compared to 0.69 x 10(-5) M for the whole caldesmon molecule. Fragments located outside of calmodulin-binding sites bound PS weakly (3.85 x 10(-4) M) and thus may contain a second class of lipid-binding sites. Binding of PS induced conformational changes in regions other than the C-terminal PS-binding sites, as evidenced by the changes in the susceptibility to proteolytic cleavages. Most significantly, the presence of caldesmon greatly increased binding of PS to F-actin, suggesting that caldesmon may tether PS liposomes to actin filaments. These results raise the possibility that caldesmon-lipid interactions could play a functionally important role in the assembly of contractile filaments near the membranes.

Actins↗
PubMed1997

Hydrosalpinx fluid enhances human trophoblast viability and function in vitro: implications for embryonic implantation in assisted reproduction.

OBJECTIVE: To assess the effects of hydrosalpinx fluid on human cytotrophoblast viability and function in vitro. DESIGN: Human cytotrophoblasts obtained from third-trimester placentas were cultured in vitro with hydrosalpinx fluid, and cell viability and protein production were assayed. SETTING: A university hospital. PATIENT(S): Ten hydrosalpinx fluid samples obtained from seven women with clearly diagnosed hydrosalpinges. INTERVENTION(S): Recovery of hydrosalpinx fluid by transvaginal aspiration or at the time of surgery. MAIN OUTCOME MEASURE(S): Cell viability was assessed by the XTT assay. Secretion of trophoblast oncofetal fibronectin (tropho-uteronectin) and beta-hCG by cultured trophoblasts was determined by Western blot and ELISA of the culture media. RESULT(S): With increasing concentrations of hydrosalpinx fluid from 0% to 20%, there was a significant increase in trophoblast cell viability (1.63-fold increase in 20% hydrosalpinx fluid). Likewise, both Western blot and ELISA assays demonstrated a significant increase in tropho-uteronectin production by trophoblasts with increasing hydrosalpinx fluid concentrations (3.76-fold increase in 20% hydrosalpinx fluid). beta-Human chorionic gonadotropin production also increased significantly in the presence of hydrosalpinx fluid (3.31-fold increase in 20% hydrosalpinx fluid). CONCLUSION(S): These findings suggest that hydrosalpinx fluid improves human trophoblast viability in vitro and enhances the production of tropho-uteronectin and beta-hCG by these cells.

Adult↗
PubMed1997

Vascular endothelial growth factor, placenta growth factor and their receptors in isolated human trophoblast.

The expression of the angiogenic growth factors, vascular endothelial cell growth factor (VEGF) and placenta growth factor (PIGF) was demonstrated in isolated human term cytotrophoblast and in vitro differentiated syncytiotrophoblast. RNase protection assays demonstrated VEGF expression in both cytotrophoblast and syncytiotrophoblast while prominent PIGF expression was detected in both types of trophoblast by Northern blot analyses. VEGF expression increased approximately eightfold in trophoblast cultured under hypoxic conditions (1 per cent O2) yet PIGF expression decreased 73 +/- 5.5 per cent in the same trophoblast. These results suggest distinct regulatory mechanisms govern expression of VEGF and PIGF in trophoblast. Characterization of the VEGF/PIGF receptors, KDR and flt-1, revealed the presence of flt-1 mRNA in isolated cytotrophoblast and in vitro differentiated syncytiotrophoblast. KDR was not detected in the isolated trophoblast. Exogenous rhVEGF induced c-Jun N-terminal kinase (JNK) activity in the normal trophoblast indicating that the flt-1 receptors on trophoblast are functional. Trophoblast-derived VEGF/PIGF could act in a paracrine fashion to promote uterine angiogenesis and vascular permeability within the placental bed. In addition, presence of function flt-1 on normal trophoblast suggests that VEGF/PIGF functions in an autocrine manner to perform an as yet undefined role in trophoblast invasion, differentiation, and/or metabolic activity during placentation.

Blotting, Northern↗
PubMed1997

Early protein restriction and obesity independently induce hypertension in 1-year-old rats.

1. Recent studies have revealed a link between fetal and early post-natal, growth retardation and the development of features of the insulin resistance syndrome in later life. Obesity is also a strong risk factor for this syndrome. The aim of this study was to assess whether maternal and early protein restriction, which causes growth retardation, and obesity are risk factors that are independent for the development of certain features of the insulin resistance syndrome, especially hypertension. 2. Pregnant Sprague-Dawley rats were given either 20% or 8% protein isocaloric diets throughout pregnancy and lactation. Female offspring were weaned onto the same diets as their mothers and they remained on these diets until 70 days of age. Half the rats were then given standard laboratory chow, whilst the remainder were fed a highly palatable cafeteria-style diet. Rats were maintained on these diets for the remainder of the study. 3. Rats given the 8% protein diet remained physically lighter than comparable animals fed the 20% protein diet throughout the study. In contrast, cafeteria-fed rats showed excessive weight gain. At 1 year of age the rats had their systolic blood pressures and fasting lipids measured, as well as undergoing an intraperitoneal glucose-tolerance test. 4. Cafeteria-fed rats had worse glucose tolerances than controls and hypertriacylglycerolaemia. The early 8% protein rats had significantly increased blood pressures, as did the cafeteria-fed rats. These increases were additive, suggesting that early protein restriction, and later obesity, are indeed independent risk factors for the development of hypertension.

Analysis of Variance↗
PubMed1997

Cadmium removal by a new strain of Pseudomonas aeruginosa in aerobic culture.

A fluorescent pseudomonad (strain CW-96-1) isolated from a deep-sea vent sample grew at 30 degrees C under aerobic conditions in an artificial seawater medium and tolerated cadmium concentrations up to 5 mM. After 140 h, strain CW-96-1 removed > 99% of the cadmium from solution. Energy dispersive microanalysis revealed that the cadmium was removed by precipitation on the cell wall; sulfide production was confirmed by growth on Kligler's agar. Based on 16S ribosomal DNA sequencing and fatty acid analysis, the microorganism is closely related to Pseudomonas aeruginosa.

Aerobiosis↗
PubMed1997

Stretch-dependent activation and desensitization of mitogen-activated protein kinase in carotid arteries.

Arterial smooth muscle stretch is an important physiological modulator of vascular function. To identify intracellular processes altered during muscle stretch, we found previously that extracellular signal-regulated kinase-mitogen-activated protein kinase (MAPK) activity increased in response to the application of mechanical loads. In the present study, stretch-dependent activation of MAPK in porcine carotid arteries was investigated as was the phosphorylation of the thin filament-binding protein caldesmon, which is known to be a substrate for the kinase in fully differentiated smooth muscle. MAPK activity was 67 pmol.min-1.mg protein-1 in unloaded muscle strips immediately after attachment to force transducers and 139 pmol.min-1.mg protein-1 within 30 s of muscle stretch. When muscle strips were continually stretched, MAPK activity remained elevated for approximately 2 h and then decreased over 16 h to 16 pmol.min-1.mg protein-1. When muscle strips were stretched and then unloaded, MAPK activity decreased within 1 h to the level present in the muscle before the stretch. These effects of muscle stretch on MAPK activity were additive to the effects of KCl or phorbol ester stimulation and were partially inhibited by reducing extracellular Ca2+. Eliminating extracellular Ca2+ had no effect on phorbol 12,13-dibutyrate (PDBu)-dependent contractions or MAPK activity; however, KCl-dependent contractions and MAPK activity were completely abolished by this procedure. An antibody specific for detecting caldesmon phosphorylated by MAPK, vs. protein kinase C (PKC), was developed and used to assess relative caldesmon phosphorylation in unstimulated and PDBu-stimulated muscle strips. In all cases investigated, the level of MAPK activity correlated with phosphocaldesmon immunoreactivity. Because arterial MAPK activity is regulated by PKC- and stretch-dependent mechanisms, these data are consistent with a role for MAPK and the subsequent phosphorylation of caldesmon as mediators in the stretch activation of vascular smooth muscle.

Animals↗
PubMed1997

Poor fetal nutrition causes long-term changes in expression of insulin signaling components in adipocytes.

Insulin action on adipocytes was studied in the offspring of mothers who had been fed either a control (20% protein) or a low (8%)-protein diet during pregnancy and lactation. Adipocytes isolated from low-protein offspring had significantly higher basal and insulin-stimulated glucose uptakes than controls. This may be related to a threefold increase in insulin receptors in low-protein adipocytes. Consistent with these observed changes in glucose transport, adipocytes from low-protein animals had significantly higher basal and insulin-stimulated insulin receptor substrate (IRS)-1-associated phosphatidylinositol 3-kinase (PI 3-kinase) activities. There was also more p85-associated PI 3-kinase activity in these adipocytes. There was no difference in expression in the p85 regulatory subunit or the p110-alpha catalytic subunit of PI 3-kinase. In contrast, there was a sixfold reduction in the p110-beta catalytic subunit of PI 3-kinase in adipocytes from low-protein animals. These results suggest that poor fetal nutrition during pregnancy and lactation can have long-term effects on glucose transport and on the expression of key components of the insulin signaling pathway in adipocytes.

Adipocytes↗
PubMed1997

Systemic lupus erythematosus in Malaysia: a study of 539 patients and comparison of prevalence and disease expression in different racial and gender groups.

The aims of this study were to examine the clinical and laboratory features of Malaysian patients with systemic lupus erythematosus (SLE) and to identify any difference in disease expression between the different genders and among the three major ethnic groups of Malaysia. Retrospective analysis of all patients with SLE admitted to and followed-up at University Hospital Kuala Lumpur from 1974-90 was undertaken. Ethnic Chinese had the highest prevalence of SLE compared to other ethnic groups. There was a high incidence of renal disease, 74% of patient had significant proteinuria and half of these had associated nephrotic syndrome. Indian patients had significantly less incidence of skin manifestation compared to other racial groups. No difference in disease expression was detected between the ethnic Chinese and Indians and between the male and female patients. The overall 5 y and 10 y survival rates were 82% and 70% respectively. Indian patients had the poorest survival rates. Survival rates are similar among the Chinese and Malay patients. Our findings are in broad agreement with those previously reported.

Adolescent↗
PubMed1997

Ultrasonographic examination of the posterior tibial tendon.

The posterior tibial tendons (PTTs) of 16 patients with PTT dysfunction and 10 age-matched healthy subjects were examined ultrasonographically, using a 10-MHz linear-array transducer. Normal PTTs appeared hyperechoic (more echogenic) and oval, with an average diameter of 7.8 mm x 3.7 mm at the medial malleolar level. Degenerated PTTs appeared hypoechoic (less echogenic) and swollen (9.8 mm x 5.0 mm). Peritendinitis presented as a hypoechoic rim on the longitudinal sonogram (along the long axis of the tendon) and a "target sign" (hyperechoic central structure with a hypoechoic halo) on the transverse sonogram (at the right angle to the long axis of the tendon). Complete rupture of the PTT revealed an empty tibial groove at the level of the medial malleolus on the transverse sonogram and a wavy fibril pattern over the distal end on the longitudinal sonogram. Compared with the operative findings or the results of the magnetic resonance imaging, ultrasonography was sensitive and specific in diagnosing tenosynovitis and complete rupture of the PTT.

Ankle↗
PubMed1997

[Determation of strychnine and brucine in Strychnos by HPLC].

This paper describes the determination of strychnine and brucine in the seeds, root, stem and leaves of Strychnos species by HPLC. The analytical column used was ZY110 YNG-C18. The mobile phase was KH2PO4(0.01 mol.L-1)--MeOH(73:27), pH2.5, regulated by 10% H3PO4. Flow rate was 1.0 ml.min-1. The detection wavelength was 264 nm. The linear ranges of strychmine and brucine were 0.18-7.26 micrograms and 0.11-4.32 micrograms, respectively. The recoveries of strychnine and brucine were 98.27% and 98.04%, respectively. The analytical results showed that the contents of strychnine and brucine in samples showed great difference between different species. The contents of strychnine in the seeds of Strychnos wallichiana and S. ignatii were 5.6% and 3.9%, respectively. These results show that the two Strychnos species may be developed as the resources of strychnine.

Chromatography, High Pressure Liquid↗
PubMed1997

Cutaneous microcirculation of diabetic foot: combined isolated cold stress testing and laser Doppler flowmetry study.

We evaluated the peripheral microvascular response to an isolated cold stress test in patients with diabetes of various severities. We studied four groups: diabetics without neuropathy (group A: six patients), diabetics with peripheral motosensory neuropathy (group B: 12 patients), diabetics with peripheral vascular disease (group C: eight patients), and healthy controls (group D: 16 patients). Digital temperatures of all four groups decreased during the 20-minute cooling period, though more in the controls, then increased during the 20-minute rewarming period with no difference among the groups. The digital temperatures of diabetics with and without neuropathy were higher than those of diabetics with peripheral vascular disease and controls throughout. Higher mean digital skin temperature was also noted in groups A and B throughout. Significant decreases in laser Doppler flowmetry value from the last minute of acclimatization to the last minute of the cooling session were found in groups A, B, and D. A significant increase during rewarming was found only in group A (p = 0.0475). Our study showed that increased digital vascular flow was consistent with arteriovenous shunting and abnormal vascular control in diabetics with and without neuropathy. Diabetic patients with peripheral vascular disease had the lowest value and the least fluctuation in laser Doppler flowmetry, but their digital skin temperature did not differ significantly from that of the normal subjects.

Adult↗
PubMed1996

Anti-IgM-mediated regulation of c-myc and its possible relationship to apoptosis.

Anti-IgM treatment of Burkitt's lymphoma cells is followed by either growth arrest or induction of apoptosis. In this study we have explored the role of c-myc in these events. Our results in Ramos cells indicate the following. (a) The decline in c-myc mRNA occurs at about 4 h; inhibition of about 80% being observed. (b) The stability of c-myc message is involved since the half-life of c-myc mRNA is decreased from about 30 min in untreated cells to about 15 min following treatment with anti-IgM. In the presence of cycloheximide, a protein synthesis inhibitor, the half-life is increased to about 50 min and was unaltered by treatment with anti-IgM. (c) By contrast, nuclear run-on experiments indicated no change in transcription rates for c-myc message due to treatment with anti-IgM. (d) A decrease in c-myc causes apoptosis since specific repression of c-myc with antisense oligonucleotides decreases the levels of c-Myc, inhibits growth rate, decreases viability, and induces apoptosis. (e) Anti-CD40 inhibition of apoptosis occurs without alteration in anti-IgM-induced down-regulation of c-myc mRNA, suggesting that it acts distally to c-myc down-regulation. Other cell lines were also investigated. In Epstein-Barr virus (EBV)-positive cell lines (Daudi, Raji, and Namalwa), anti-IgM treatment for 24 h results in growth inhibition without induction of apoptosis. In EBV-negative cell lines (ST486 and CA46, as well as Ramos), a more heterogeneous pattern of responses to anti-IgM are observed. Ramos and ST486 cells both show growth inhibition and apoptosis upon anti-IgM treatment; CA46 cells shown only growth inhibition but not apoptosis. Anti-IgM causes a decline in c-myc mRNA levels in all of these lines, as well as in c-Myc protein level in the two lines investigated, Daudi and Ramos, regardless of apoptosis. Addition of antisense c-myc oligonucleotides to the cells reduced growth in both Daudi and Ramos cells lines, however it resulted in substantial apoptosis only in Ramos cells. These results suggest that anti-IgM destabilizes c-myc mRNA by a process that involves mRNA turnover, rather than transcription rates. However anti-IgM exerts differential effects in EBV-positive and EBV-negative cell lines. EBV-positive cells are uniformly resistant to apoptosis, while EBV-negative cell lines show a tendency to apoptosis but with exceptions. Growth inhibition can be uncoupled from apoptosis in EBV-positive cell lines, but not in those EBV-negative cell lines prone to apoptosis. Furthermore, down-regulation of c-myc message correlates with growth inhibition in these cells, but is an insufficient link to apoptosis. By contrast inhibition of apoptosis by anti-CD40 occurs even though c-myc mRNA is decreased.

Antibodies, Anti-Idiotypic↗
PubMed1996

TNF-alpha inhibits anti-IgM-mediated apoptosis in Ramos cells.

We have examined the effects of tumor necrosis factor-alpha (TNF-alpha) as an inducer or modulator of necrosis and/or apoptosis in B cell lines. TNF-alpha does not induce either necrosis or apoptosis in EBV-positive or -negative cell lines, regardless of the culture conditions of the cells or the presence or absence of cytokines. By contrast anti-IgM induces apoptosis in two EBV-negative cell lines (Ramos and ST486) but not in EBV-positive cell lines. Since TNF receptor and CD40 belong to the TNF receptor superfamily and anti-CD40 is a known inhibitor of apoptosis, we tested for TNF-alpha's effects on the inhibition of apoptosis induced by anti-IgM. Our results indicate that TNF-alpha inhibits apoptosis induced by anti-IgM in Ramos cells but not in ST486. The effects are dose and time dependent; the degree of apoptosis achieved and the selectivity of the effect among cell lines are strikingly similar for both TNF-alpha and anti-CD40. Furthermore when both agents are tested together no additivity in the inhibition is observed. The inhibition of apoptosis is a direct effect of TNF-alpha and not a permissive effect of another cytokine, since it is observed in defined medium. Although anti-IgM induces both TNF-alpha secretion and TNF receptors in Ramos cells, the concentration of secreted TNF-alpha is too low to affect apoptosis. Inhibition does not involve perturbation of the cell cycle distribution of Ramos cells. Furthermore rapid induction of c-fos and the decrease in c-myc observed after anti-IgM treatment are both unaltered by TNF-alpha. Our results suggest that TNF-alpha is an inhibitor of apoptosis in Ramos cells, that its overall pattern of inhibition is similar to that of anti-CD40, and that both agents act at some point distal to the alteration of c-fos and c-myc by anti-IgM.

Apoptosis↗