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PubMed1990

Humoral modulation of lymphokine-activated killer (LAK)-cell induction in humans: IgG-related and non-IgG inhibitors in sera from cancer patients.

Soluble inhibitors of lymphokine-activated killer (LAK) cell induction were characterized and purified from serous fluids from healthy donors or from patients with advanced cancer. Inhibitory activity in sera from cancer patients was partially absorbed with protein A agarose or anti-human IgG agarose. Following absorption, residual inhibition varied with individual sera, suggesting the presence of IgG-related and non-IgG inhibitory factors, and the proportions varied in the patient population. IgG, purified by affinity chromatography from ascitic fluids, from plasma of cancer patients, and from plasma of healthy donors, significantly inhibited IL-2 induction of LAK cells in a dose-dependent manner. Irrespective of the sources, inhibitory activity resided in the high-molecular-weight IgG fraction composed of IgG aggregates and immune complexes, but not monomeric IgG. Commercially prepared human IgG in aggregated form, but not in monomeric form, inhibited LAK cell induction in a dose-dependent manner. In contrast, neither bovine IgG nor human albumin affected LAK cell induction, even at higher concentrations. Aggregated human IgG inhibited LAK cell induction in unfractionated peripheral blood mononuclear cells (PBMC) but not in monocyte-depleted peripheral blood lymphocytes (PBL). Despite extensive (greater than 99%) depletion of IgG by protein-G affinity chromatography, the serous fluid from cancer patients displayed significant inhibitory activity. Fractionation of the IgG-depleted inhibitory materials by Sephacryl S-300, high-pressure ion-exchange column (HPIEC) or gel-permeation chromatography (HPGPC) demonstrated a 65-kDa inhibitor, distinct from IgG. Affigel-blue affinity chromatography of the 65-kDa fraction depleted albumin but did not remove the inhibitory activity, suggesting that the 65-kDa inhibitor is not serum albumin nor an albumin-bound component. These results suggest that serous fluids from patients with advanced-stage cancer contain 2 distinct regulators for LAK cell induction: (I) aggregated IgG and (2) a 65-kDa inhibitor, distinct from albumin.

Antibodies, Anti-Idiotypic↗
PubMed1993

Interleukin-3 inhibits cycloheximide induction of C-jun mRNA in human monocytes: possible role for a serine/threonine phosphatase.

Cycloheximide is a strong inducer of the c-jun protooncogene mRNA at concentrations (< or = 50 ng/ml) that do not inhibit protein synthesis in human monocytes. This induction is transient lasting 30-60 min in contrast to the sustained induction obtained with concentrations that inhibit protein synthesis. The pluripotent colony stimulating factor interleukin-3 (IL-3) (10 ng/ml) is also a modest inducer of the c-jun gene in these cells; however, in combination with cycloheximide, IL-3 dramatically reduces the c-jun induction below levels induced by cycloheximide alone. This is a true inhibition and is not due to a change in temporal kinetics of induction because the suppression in the presence of IL-3 is observed at both 30 and 60 min after simultaneous addition of both IL-3 and cycloheximide. Preincubation of monocytes with 12.5 nM okadaic acid (a potent inhibitor of protein phosphatases 1 and 2A) and cycloheximide prior to addition of IL-3 restored the level of c-jun induction to that mediated by cycloheximide alone. This concentration of okadaic acid inhibited almost 70% of the phosphorylase phosphatase activity in monocyte lysates. These observations suggest that activation of protein serine/threonine phosphatase(s) underlies the ability of IL-3 to inhibit cycloheximide induction of c-jun in monocytes.

Cycloheximide↗
PubMed1994

Age related induction of platelet-derived growth factor A-chain mRNA in normal human fibroblasts.

We have previously found that stimulation of normal neonatal fibroblasts with PDGF or EGF leads to a transient induction of PDGF A-chain mRNA and the synthesis of PDGF-AA proteins. This finding may imply the existence of an autocrine feedback mechanism to amplify the mitogenic signal under certain conditions. We have now studied the PDGF-BB mediated PDGF A-chain induction in a set of fibroblasts from young and old donors to clarify if the levels of induction are correlated to the donor age and the replicative capacity of the cells. The PDGF A-chain induction was found to be reduced in cells from old donors compared with cells from embryonic and neonatal donors. The different cell strains were also characterized further with respect to PDGF receptor expression and PDGF binding properties. PDGF beta-receptors were found to be enhanced in old donor cell strains, whereas the PDGF alpha-receptors showed more variability in expression between the strains. The PDGF A-chain mRNA induction was also decreased or absent in late passage human fibroblasts (senescent cells) when compared with early passage cells. These data suggest that the PDGF A-chain mRNA induction is regulated by an age related mechanism in human fibroblasts.

Aged↗
PubMed1996

Novel actions of aspirin and sodium salicylate: discordant effects on nitric oxide synthesis and induction of nitric oxide synthase mRNA in a murine macrophage cell line.

Aspirin and sodium salicylate each inhibit to a similar extent the production of nitric oxide (NO) in the RAW 264.7 murine macrophage cell line following stimulation by either lipopolysaccharide (LPS) or interferon-gamma (IFN-gamma). The similar potencies of aspirin and sodium salicylate indicate that acetylation of cellular macromolecules is not essential for the observed effects. The failure of added prostaglandin E2 to overcome the effects of aspirin or sodium salicylate indicates that these effects are not simply the result of inhibition of prostaglandin synthesis. The inhibition of NO production occurs irrespective of the effect of these agents on induction of nitric oxide synthase (iNOS) mRNA by LPS or IFN-gamma. Aspirin and sodium salicylate inhibit iNOS mRNA induction in LPS-stimulated cells but enhance iNOS mRNA induction in IFN-gamma-stimulated cells. In contrast, these agents consistently inhibit induction of argininosuccinate synthetase mRNA in both LPS- and IFN-gamma-stimulated cells. Concentrations of aspirin in the 3-10 mM range inhibit induced NO production and expression of iNOS protein without inhibiting induction of iNOS mRNA. Discordances between effects on NO synthesis and induction of iNOS mRNA indicate that aspirin and sodium salicylate have multiple sites of action in their effects on pathways that are involved in the production of NO by stimulated RAW 264.7 cells.

Animals↗
PubMed2006

Role of phosphorylation of ERK in induction and maintenance of LTP of the C-fiber evoked field potentials in spinal dorsal horn.

Previous works have shown that activation of extracellular signal-regulated kinase (ERK)/cAMP response element binding protein (CREB) pathway is essential for long-term potentiation (LTP) in hippocampus. In the present study, the role of the ERK/CREB pathway in LTP of C-fiber evoked field potentials in spinal dorsal horn, which is relevant to pathologic pain, was investigated in adult rats. Western blotting analysis showed that the protein level of phosphorylated ERK (p-ERK) in ipsilateral spinal dorsal horn was transiently increased after LTP induction, starting at 15 min and returning to control at 60 min after tetanic stimulation and that the protein level of p-CREB increased at 30 min, persisting for at least 3 hr after LTP induction. Double immunofluorescence staining showed that p-ERK and p-CREB were only located in neurons but not in glial cells in the spinal dorsal horn after LTP induction. More importantly, we found that spinal application of PD 98059 (100 microM), a selective MEK inhibitor, at 30 min before tetanic stimulation blocked LTP induction and prevented the increase in p-ERK and p-CREB in spinal dorsal horn. When applied 15 min after LTP induction, PD98059 reversed established LTP. The drug, however, did not affect the spinal LTP, when applied at 30 min after LTP. Our results suggested that activation of ERK/CREB pathway in spinal dorsal neurons is necessary for induction and maintenance of long-term potentiation of the C-fiber evoked field potentials.

Animals↗
PubMed1989

Induction of c-fos and TIS genes in cultured rat astrocytes by neurotransmitters.

The interaction of neurotransmitters with their specific receptors initiates a cascade of intracellular biochemical events which lead to induction of specific genes. Included in this cascade is the rapid and transient induction of a family of primary early response genes we term TIS genes (Lim et al.: Oncogene 1: 263-270, 1987). Expression of six TIS gene, including c-fos, was examined in secondary cultures of rat neocortical astrocytes exposed to muscarinic and adrenergic agonists and antagonists to study the early genomic responses which accompany neurotransmitter-induced alteration of glial morphology and physiology. Carbachol induced accumulation of mRNA for c-fos and the other TIS genes. Carbachol-mediated induction of TIS mRNA expression was sensitive to atropine blockade and was potentiated by lithium. Norepinephrine (NE), isoproterenol, or phenylephrine also induced TIS mRNA accumulation. In order to determine which second-messenger pathways mediate NE induction of TIS gene expression, the influences of the beta(B) antagonist propranolol (PR), the alpha I(AI) antagonist prazosin (PZ), and the alpha 2(A2) antagonist yohimbine (YB) were examined. The induction of TIS1 mRNA by NE was partially blocked by PR or PZ alone, and completely abolished by both antagonists in combination. YB had no effect on TIS1 mRNA expression. These results suggest that NE induces TIS1 mRNA through both B- and A 1-adrenergic, but not A2, pathways. The lack of effect of inhibitors of phospholipase A2 and cyclooxygenase suggests that the A1 component is mediated through a protein kinase C pathway. The induction of transient gene expression by neurotransmitters may mediate the secondary genomic responses and phenotypic changes occurring in astrocytes in response to alterations in neuronal neurotransmitter release.

Animals↗
PubMed1995

Tumor necrosis factor-alpha induces substance P in sympathetic ganglia through sequential induction of interleukin-1 and leukemia inhibitory factor.

The present study establishes that tumor necrosis factor-alpha (TNF-alpha) induction of sympathetic substance P (SP) requires sequential induction of both interleukin (IL-1) and leukemia inhibitory factor (LIF). TNF-alpha dose-dependently induces SP, an induction that is secondary to an increase in the SP precursor, preprotachykinin (PPT), mRNA. Since TNF-alpha conditioned medium (CM) mimics the effect of TNF-alpha by raising SP, actions that are not antagonized by a neutralizing TNF-alpha antibody, TNF-alpha induction of SP is mediated by a soluble intermediate or intermediates. The blockade of TNF-alpha action by a specific IL-1 receptor antagonist and the induction of IL-1 mRNA by TNF-alpha suggest that IL-1 is one of the intermediates. Moreover, because immunoprecipitation with LIF antibodies decreases SP-inducing activity of TNF-alpha CM, and because LIF mRNA is also induced by TNF-alpha, LIF is a second intermediate. Furthermore, TNF-alpha-induced LIF mRNA is blocked by the IL-1 receptor antagonist, whereas IL-1-induced LIF mRNA is not affected by TNF-alpha antibodies, suggesting that TNF-alpha first induces IL-1, and IL-1 subsequently induces LIF. These data suggest that TNF-alpha induces SP in sympathetic ganglia through the sequential inductions of IL-1 and LIF.

Animals↗
PubMed2005

Sputum induction in children with difficult asthma: safety, feasibility, and inflammatory cell pattern.

Difficult childhood asthma is defined by persistent symptoms despite maximal conventional therapy. We aimed to establish a safe method of sputum induction for these children and to study cytology and the relationship to exhaled nitric oxide (eNO). Sputum induction was performed in 38/40 children (aged 6-16 years) with difficult asthma, using 3.5% saline for four 5-min periods after bronchodilator pretreatment. Two children were excluded from sputum induction because postbronchodilator forced expired volume in 1 sec (FEV(1)) was <65% predicted. Seven of 38 children had symptoms (dyspnea and wheezing) during induction; of these, 3 experienced a fall in FEV(1) of >20% from postbronchodilator FEV(1), readily reversed with salbutamol. Sputum induction was successful in 28/38 children, with a higher success rate in children >/= 12 years than in younger children (87% vs. 50%, P = 0.02). Only 9/28 had abnormal sputum cytology; of these, 6 had predominant sputum eosinophilia (>2.5% eosinophils, </=54% neutrophils), while 3 had sputum neutrophilia (</=2.5% eosinophils, >54% neutrophils). Of 23 children with elevated eNO values, only 6 had sputum eosinophilia. In conclusion, sputum induction can be used to assess airway inflammation in children with difficult asthma, but abnormal sputum cytology is only present in a minority. Raised nitric oxide is only poorly predictive of sputum eosinophilia in these children.

Adolescent↗
PubMed2006

Sputum induction in children with asthma: a tertiary-center experience.

Our aims were 1) to report on our experience with sputum induction (SI), and 2) to determine predictive factors associated with successful SI in asthmatic children. Children with asthma attending the chest clinic of a university teaching hospital between October 2003-December 2004 were recruited. They completed a visual analogue scale for symptom severity, and underwent physical examination, skin-prick test, exhaled nitric oxide (eNO) measurement, spirometry, and SI. Adequate sputum contained <50% squamous epithelial cells. Predictors for successful induction were evaluated using multivariate logistic regression analysis. One hundred and thirty subjects were recruited. The median age was 11.25 years (range 7.0-17.5), and the majority were boys (75%). All except two had normal percent predicted forced expired volume in 1 sec (>80%). The median eNO was 48.95 ppb. Sputum induction was successful in 93 subjects (74.5%). Sore throat and chest discomfort occurred in 20 (15%) and 8 (6%) subjects, respectively, and the procedure was prematurely terminated in three cases. Levels of eNO were found to be a predictor for successful induction (area under the ROC (receiver operator characteristics curves) curve, 0.634). Sputum induction was well-tolerated by all subjects, and was successful in 74.5% of cases. Exhaled nitric oxide may be a useful marker for successful induction.

Adolescent↗
PubMed1993

Cytochrome P450 2B enzyme (CYP2B) induction defect following phenobarbital treatment in the fa/fa Zucker rat: molecular characterization.

The present study describes the mechanism of the dampened induction of the CYP2B1 and CYP2B2 genes following phenobarbital treatment in the phenotypically obese fa/fa Zucker rat. The fa/fa Zucker rat demonstrated a threefold lower level of CYP2B1/2B2 enzyme induction, as indicated by reduced testosterone oxidation at the 16 beta position and resorufin formation from pentoxy- and benzyloxyresorufin, protein concentration (Western blot analysis), and steady-state mRNA levels (Northern and slot blot analyses) following in vivo treatment with phenobarbital than the Fa/? littermate controls. A primary hepatocyte cell culture system was used to determine if the dampened induction of the CYP2B1/2B2 enzyme is dependent on hormonal influences. Phenobarbital-treated (0.75 mM) hepatocytes from fa/fa Zucker rats showed approximately a three-fold lower induction response based on measurements of CYP2B1/2B2 (R-17 cDNA probe) and CYP2B1 (oligo probe) mRNAs. In order to evaluate whether this dampened response was at the level of transcriptional activation or initiation, as opposed to altered message stability, we measured the rate of transcription of CYP2B1/2B2 genes in nuclei from cultured hepatocytes during run-off experiments. Compared to Fa/? controls, the fa/fa Zucker rat had a greater than threefold lower nuclear transcription rate of CYP2B1/2B2 mRNA. These results suggest that the defective induction of the CYP2B1 and CYP2B2 genes exists at the transcriptional level in the mutant obese fa/fa Zucker rat. These data provide strong evidence that at least two genes are involved. Multiple gene involvement would suggest that the defect is not due to a mutation of the CYP2B gene cis-acting sequence. Instead, the lack of binding of a trans-acting factor, the presence of a repressor, or a defect in transcriptional activation is more likely the molecular mechanism(s) for this enzyme induction defect.

Animals↗
PubMed2000

Induction of the heme oxygenase-1 gene by metalloporphyrins.

Induction of expression of heme oxygenase-1 (HO-1) has been studied in primary cultures of chick embryo liver cells and in the LMH line of avian hepatoma cells. Cells were transiently transfected with selected constructs containing portions of the 5'-untranslated (promoter) region of the HO-1 gene linked to luciferase as reporter gene. LMH cells that had been stably transfected with selected wild type or mutant constructs were also studied. Metalloporphyrins, especially Fe protoporphyrin (heme) and Co protoporphyrin strongly induced luciferase expression in both types of transfected cells. Low concentrations of Zn mesoporphyrin, an inhibitor of HO activity, exerted a synergistic effect on heme-, but not Co protoporphyrin-dependent induction. The antioxidant and &bond;SH donor N-acetyl cysteine had little effect on the metalloporphyrin-dependent inductions of HO-1, in contrast to its marked inhibitory effect on the sodium arsenite-dependent induction of the HO-1 gene. Deletional analysis showed that the key element(s) required for the metalloporphyrin-dependent induction of HO-1 is located between -3.6 and -5.6 kb upstream of the transcription starting point. Data from electrophoretic mobility shift and site-directed mutagenesis experiments excluded a role for consensus AP-1 binding elements at -1576, -3647, or -4578 in the inductions produced by heme or Co protoporphyrin.

Animals↗
PubMed1998

Radiation induction of p53 in cells from Nijmegen breakage syndrome is defective but not similar to ataxia-telangiectasia.

p53-mediated signal transduction after exposure to ionizing radiation was examined in cells from patients with Nijmegen breakage syndrome (NBS), an autosomal recessive disease characterized by microcephaly, immunodeficiency, predisposition to malignancy, and a high sensitivity to ionizing radiation. NBS cells accumulated p53 protein in a dose-dependent fashion, with a peak level 2 hrs after irradiation with 5 Gy. However, the maximal level of p53 protein in NBS cells was constantly lower than in normal cells. Moreover, this attenuation of p53 induction was confirmed by decreased levels of p21WAF1 protein, which is transcriptionally regulated by p53 protein. This defective induction of p53 protein in NBS is similar to that in ataxia-telangiectasia (AT), although the induced levels of p53 protein in NBS appeared to be the intermediate between normal cells and AT cells. This moderate p53 induction in NBS cells is consistent with the relatively mild radiation sensitivity and the abnormal cell cycle regulation post-irradiation, as present in NBS. Furthermore, all NBS cell lines used here exhibited time courses of p53 induction similar to normal cells, which is in contrast with p53 induction in AT cells, where the maximum induction shows a delay of approximately 2 hrs compared with normal cells. These evidences suggest a different function of each gene product in an upstream p53 response to radiation-induced DNA damage.

Ataxia Telangiectasia↗
PubMed1998

The spontaneous induction of glutamine synthetase in pig hepatocytes cocultured with RL-ET-14 cells is completely inhibited by trijodothyronine and okadaic acid.

Cocultivation of primary pig hepatocytes with RL-ET-14 cells, an endothelial-like cell line resulted in spontaneous induction of glutamine synthetase (GS)-activity in the hepatocytes by more than 10-fold within 120 h to 144 h. Hepatocyte-specific induction was confirmed by immunocytochemistry. Addition of trijodothyronine (T3) to the culture medium inhibited the induction in a concentration dependent manner. No comparable influence of T3 was seen with pure cultures of either cell type suggesting that only the spontaneous induction was affected. Other hormones such as glucagon, insulin, growth hormone, epinephrine and testosterone did not interfere with the induction. Addition of several protein kinase-inhibitors such as staurosporine and genistein were without influence. However, a strong inhibition was found after addition of okadaic acid in nanomolar concentrations indicating an involvement of protein-phosphatase 2A in the induction process.

Animals↗
PubMed1994

Differential expression of activation markers during tolerance induction by superantigens in T-cell receptor (beta-chain) transgenic mice.

To investigate the process of tolerance induction we have developed an in vivo model using TCR beta-chain transgenic mice tolerized with the superantigen staphylococcal enterotoxin B. We have previously demonstrated that tolerized peripheral T cells were anergic when stimulated in vitro with immunogenic peptides, superantigens, mitogens, and immobilized anti-TCR mAb. However, the development of anergy is preceded by an induction phase which produces expansion followed by contraction of the peripheral T cell population presumably due to proliferation and programmed cell death, respectively. The current experiments focus on the induction phase of tolerance. A kinetic functional analysis showed that the inhibition of proliferation was apparent 2-3 days post-tolerization. Interestingly, the inhibition of proliferation correlated with the loss of IL-2R alpha expression, which occurred 2 days post-tolerization following an initial increase in IL-2R alpha expression. In addition, the expression of multiple activation markers including CD44, Ly-6A/E, and very early activation marker H1.2F3 is induced, whereas the expression of CD45RB is decreased during tolerance induction. Elevated expression of Ly-6A/E persists up to 28 days post-tolerization; however, altered expression of the other markers does not persist and near baseline levels of the other markers are noted 7 to 28 days post-tolerization. These results show that tolerance induction is an active process which has functional and phenotypic similarities to antigen-specific immunity. However, tolerance induction in our system differs from immunity in terms of the early loss of IL-2R alpha expression, the persistent increased expression of Ly-6A/E, and the lack of development of CD45RBlo memory-type T cells.

Animals↗
PubMed1996

Extracellular cAMP depletion triggers stalk gene expression in Dictyostelium: disparities in developmental timing and dose dependency indicate that prespore induction and stalk repression by cAMP are mediated by separate signaling pathways.

During Dictyostelium development, amoebae differentiate into spores and stalk cells. Earlier studies showed that extracellular cAMP is essential for induction of prespore differentiation and that cAMP represses stalk gene expression in vitro. We show that the repressive pathway is operative in vivo, because activation of the stalk-specific promoter region of the ecmB gene is strongly enhanced by overexpression of a phosphodiesterase that depletes extracellular cAMP. To test whether a single cAMP transduction pathway controls the choice between prespore or stalk cell differentiation, we compared the timing and dose dependency of the effects of cAMP on both responses. Cells acquire competence for cAMP repression of ecmB promoter activity 4 hr later than for prespore gene induction. Half-maximal prespore induction requires 30 microM stable cAMP analog Sp-cAMPs, while ecmB induction is half-maximally repressed by 200 nM Sp-cAMPs, which is equivalent to about 3 to 13 nM cAMP. At concentrations exceeding 10 microM, Sp-cAMPs stimulates ecmB expression from the intact promoter, but not from the stalk-specific subregion. These data suggest that distinct signaling pathways operating at different developmental stages control induction of prespore genes on one hand and repression of stalk genes on the other. Both stalk gene repression and prespore gene induction by Sp-cAMPs are antagonized by millimolar adenosine concentrations. However, an adenosine analog that is resistant to extracellular metabolism is active at 10 microM. Since adenosine inhibits cAMP binding to cAMP receptors, it may facilitate stalk gene expression by reducing the perceived cAMP concentration.

Adenosine↗
PubMed2001

Mechanism of Tet repressor induction by tetracyclines: length compensates for sequence in the alpha8-alpha9 loop.

Natural Tet repressor (TetR) variants are alpha-helical proteins bearing a large loop between helices 8 and 9, which is variable in sequence and length. We have deleted this loop consisting of 14 amino acid residues in TetR(D) and rebuilt it stepwise with up to 42 alanine residues. All except the mutant with the longest alanine loop show wild-type repression, but none is inducible with tetracycline. This demonstrates the importance of the alpha8-alpha9 loop and its amino acid sequence for induction. The induction efficiencies increase with loop length, when the more tightly binding inducer anhydrotetracycline is used. The largest increase of inducibility was observed for TetR mutants with loop lengths between eight and 17 alanine residues. Since loop residues Asp/Glu157 and Arg158 are conserved in the natural TetR sequence variants, we constructed a mutant in which all other residues of the loop were replaced by alanine. This mutant exhibits increased anhydrotetracycline induction compared to the corresponding alanine variant. Thus, these residues are important for induction. Binding constants for the anhydrotetracycline-TetR interaction are below the detection level of 10(5) M(-1) for the mutant with a loop of two alanine residues and increase sharply until a loop size of ten residues is reached. TetR variants with longer loops have similar anhydrotetracycline-binding constants, ranging between 2.6 x 10(9) M(-1) and 8.0 x 10(9) M(-1), about 500-fold lower than wild-type TetR. The increase of the affinity occurs at shorter loop lengths than that of inducibility. We conclude that the induction defect of the polyalanine variants arises from two increments: (i) the loop must have a minimal length-to allow efficient inducer binding; (ii) the loop must structurally participate in the conformational change associated with induction.

Amino Acid Sequence↗
PubMed1999

Collective Induction: Twelve Postulates.

Collective induction is the cooperative search for descriptive, predictive, and explanatory generalizations, rules, and principles. This article presents 12 postulates on collective induction and supportive evidence for the postulates. Postulates 1-6 set collective induction within the general social combination approach to cooperative group decision making. Postulates 7 and 8 formalize the social combination processes of group hypothesis formation in collective induction. Postulates 9-12 summarize research on collective versus individual induction, the relative importance of multiple hypotheses and multiple evidence, influence in simultaneous collective and individual induction, and the relative effectiveness of positive and negative hypothesis tests. We then consider the history and fundamental emphasis of the social combination approach to small group performance. Copyright 1999 Academic Press.

Journal Article↗
PubMed1989

Beta globin gene transcripts originating in the promoter region during early hexamethylene bisacetamide and dimethylsulfoxide induction of Friend erythroleukemia cells.

The beta-globin transcripts which are induced by dimethylsulfoxide (DMSO) and hexamethylene bisacetamide (HMBA) have been characterized in order to assess potential differences in their mechanisms of induction. Transcripts which initiate in the 5' flanking promoter region are likely indicators of promoter accessibility and were therefore characterized during the time course of induction with each inducer in Friend Erythroleukemia cells. S1 analysis with probes labeled at - 12 or +82 relative to the (+1) cap site showed no major differences between 5' ends of the upstream initiated transcripts in cells induced by DMSO or HMBA. We detected several upstream bands with each inducer corresponding to beta-globin transcripts with 5' ends between - 190 and -55 relative to the cap site and found that cells induced with DMSO and HMBA show a similar transcription response as measured by initiation in the 5' flanking region of the beta-globin gene. Interestingly, the upstream initiated transcripts reach their peak concentration levels much earlier in the time course of induction than do the mRNA transcripts with 5' ends at the major (+1) cap site. Northern blot analysis detected the upstream initiated transcripts as early as 16 hours after induction with DMSO, primarily in unprocessed large transcripts. We find that the promoter region containing transcripts constitute a higher percent of total beta-globin transcripts at the start of the induction and may therefore have an early function in the multistep induction process.

Acetamides↗