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Biomedical subjects

C Li

Publications and source records attributed to C Li.

At least 649 records · Page 36Linked to original sources
PubMed1998

The effects of fetal adrenalectomy at 110 days gestational age on AVP and CRH mRNA expression in the hypothalamic paraventricular nucleus of the ovine fetus.

AVP and CRH produced in the parvocellular neurons of the paraventricular nucleus (PVN) have both been implicated in the regulation of anterior pituitary ACTH synthesis and secretion. In sheep, fetal ACTH secretion increases around 120 days gestational age (dGA). Little is known about adrenal regulation of AVP and CRH immediately prior to this critical period. We investigated the effects of adrenalectomy and subsequent cortisol (F) administration on PVN AVP and CRH mRNA in the fetal sheep PVN at 109-125 dGA. At 109-113 dGA, fetal sheep adrenals were removed (ADX)(n = 8); or sham surgery performed (CONT)(n = 4). From day 6 post ADX, maternal plasma cortisol and fetal plasma ACTH and cortisol levels were determined daily by radioimmunoassays. From day 7 post ADX, cortisol (4 micrograms/min) was continuously infused intravenously to four ADX fetuses (ADX + F). Fetal hypothalami were collected at 123-125 dGA, and studied by in-situ hybridization and quantitative autoradiography for AVP and CRH mRNA. Plasma cortisol levels remained low in CONT and ADX fetuses (< 4.9 ng/ml), while during cortisol infusion to ADX + F fetuses, plasma F increased to 16.4 +/- 2.2 and 22.3 +/- 3.2 ng/ml (mean +/- S.E.M.) on day 10 and 13, respectively. Plasma ACTH levels increased significantly in ADX compared with CONT fetuses. This ACTH increase was completely suppressed in ADX + F fetuses. AVP mRNA abundance in the whole PVN was the same in all three groups, however, a separate analysis of AVP mRNA abundance in parvocellular and magnocellular regions of the PVN revealed that AVP mRNA in the parvocellular PVN showed a significant increase in ADX and suppression in ADX + F fetuses when compared to CONT. AVP mRNA in the magnocellular PVN remained unchanged. PVN CRH mRNA expression was augmented in ADX and suppressed in ADX + F when compared to CONT fetuses. We conclude that in fetal sheep at 109-125 dGA: AVP and CRH mRNA abundance in the parvocellular region of the PVN are increased by adrenalectomy and that cortisol inhibits this increase.

Adrenal Glands↗
PubMed1998

Protein N-arginine methylation in adenosine dialdehyde-treated lymphoblastoid cells.

Protein arginine methyltransferase was recently identified to be associated with some proteins in signal transduction pathways. N-Arginine methylation in RNA binding proteins with arginine- and glycine-rich RGG motifs is known to be the major protein methylation in cells. Considering that arginine methylation might be involved in certain human disorders, we used human lymphoblastoid cells that can be easily prepared from lymphocytes as a model system to study the methylation. Lymphoblastoid cells grown in the presence of 20 microM indirect methyltransferase inhibitor adenosine dialdehyde (AdOx) for 72 h appeared to accumulate high levels of hypomethylated proteins for the endogenous protein methyltransferase or recombinant glutathion S-transferase-fused yeast arginine methyltransferase (RMT1). Analysis of methyl-accepting polypeptides in AdOx-treated lymphoblastoid cells by SDS-PAGE and fluorography showed that many polypeptides between 29,000 and 90,000 Da were methylated by the endogenous methyltransferase. A few polypeptides could be methylated to a higher extent upon the addition of yeast GST-RMT1 fusion protein. A peptide (GGRGRGGGF) could compete for the majority of the methyl-accepting protein substrates in the AdOx-treated lymphoblastoid cell extracts, whether or not exogenous yeast RMT1 was included in the reaction. When the arginine residues in the peptide were replaced by lysine, no competition was observed. The results indicated that the protein methyl acceptors in lymphoblastoid cells share similar RGG motifs and that arginine residues should be the site of methylation.

Adenosine↗
PubMed1998

Assessment of the efficacy of in vivo CFTR protein replacement therapy in CF mice.

Cystic Fibrosis (CF) is caused by mutations in the CF gene that lead, for the most part, to mislocalization of the protein product, the cystic fibrosis transmembrane conductance regulatory (CFTR). CFTR is a chloride channel normally situated in the apical membrane of epithelial cells where it contributes to transepithelial ion transport. In this study we demonstrated the feasibility of in vivo transfer of purified CFTR protein via phospholipid liposomes into the apical membrane of nasal epithelia of CFTR knockout mice. Membrane incorporation of immunogold-labeled CFTR could be visualized by electron microscopy and correction of CF-related defects in ion transport measured by nasal potential difference (PD) measurements in about one-third of the animals treated. Although these initial results are promising, effectiveness of this therapeutic approach appears to be limited by the inefficient incorporation of CFTR into the apical epithelial cell membrane.

Amiloride↗
PubMed1998

Differentiation and antiproliferation effects of retinoic acid receptor beta in hepatoma cells.

Evidence indicates that the retinoic acid receptor beta (RARbeta) gene might be a tumor suppressor gene. Previously, we have shown that the expression of the RARbeta gene was either inhibited or downregulated in tumorigenic hepatoma cell lines such as McA-RH8994. McA-RH8994 cells expressed RARalpha and gamma and three types of retinoid X receptor (RXRalpha, beta and gamma), but not RARbeta mRNA. To further analyze the molecular mechanisms which might account for RARbeta gene inactivation, the rat RARbeta gene promoter was cloned from McA-RH8994 cells and no mutation was detected. By transient transfection, McA-RH8994 cells contained the necessary factors to activate the RARbeta gene. To study the possible roles of RARbeta in hepatoma cells, the expression of the RARbeta gene was restored in McA-RH8994 cells by stable transfection. A RARbeta positive cell line named McA-RH8994beta was characterized. The results demonstrated that expression of the RARbeta gene resulted in increased sensitivity of the hepatoma cells to the antiproliferative effect of retinoic acid (RA). Furthermore, expression of RARbeta resulted in a spontaneous differentiation of the hepatoma cells. These data indicate that RARbeta plays important roles in differentiation and antiproliferation.

Animals↗
PubMed1998

A role for B cells in the development of T cell helper function in a malaria infection in mice.

B cell knockout mice are unable to clear a primary erythrocytic infection of Plasmodium chabaudi chabaudi. However, the early acute infection is controlled to some extent, giving rise to a chronic relapsing parasitemia that can be reduced either by drug treatment or by adoptive transfer of B cells. Similar to mice rendered B-cell deficient by lifelong treatment with anti-mu antibodies, B cell knockout mice (muMT) retain a predominant CD4+ Th1-like response to malarial antigens throughout a primary infection. This contrasts with the response seen in control C57BL/6 mice in which the CD4+ T-cell response has switched to that characteristic of Th2 cells at the later stages of infection, manifesting efficient help for specific antibodies in vitro and interleukin 4 production. Both chloroquine and adoptive transfer of immune B cells reduced parasite load. However, the adoptive transfer of B cells resulted in a Th2 response in recipient muMT mice, as indicated by a relative increase in the precursor frequency of helper cells for antibody production. These data support the idea that B cells play a role in the regulation of CD4+ T subset responses.

Animals↗
PubMed1998

Identification of two distinct deleted regions on chromosome 13 in prostate cancer.

Aberrations of 13q occur frequently in prostate cancer and this chromosome contains two known tumor suppressor genes, BRCA2 and Rb1. This study analysed 13q LOH, DNA ploidy, BRCA2 mutation and pRb expression in prostate cancers. In total, 13q deletions were found in 18 of 36 tumors but did not correlate with histological grade, stage or DNA ploidy. Two smallest regions of overlapping deletions were defined: one flanked by D13S218 and D13S153; the other flanked by D13S31 and D13S137. BRCA2 was less frequently deleted whereas Rb1 did have a high frequency of deletion. None of the two genes was located in any of these two regions. Furthermore, BRCA2 mutation was not found in the five tumors where deletions had involved the BRCA2 locus. Neither did the Rb1 deletion correlate with absent pRb expression. In addition, tetraploidy was found in 14 out of 25 tumors analysed and correlated with aberrant pRb expression. Our results indicate that 13q deletion is an early non-random event. Tumor suppressor genes other than BRCA2 or Rb1 may be the target of 13q deletions. Aberrant pRb expression may not reflect the two-hit Rb1 inactivation but may be involved in the tetraploidization of prostate cancer cells.

Aged↗
PubMed1998

Myelin associated glycoprotein modulates glia-axon contact in vivo.

Myelin-associated glycoprotein (MAG) was postulated to play an important role in myelination. However, we showed previously that MAG null mutants exhibited no gross abnormality in myelination. Ultrastructural studies revealed subtle alterations in periaxonal organisation, indicating a restricted structural role for MAG in the formation and maintenance of periaxonal structures (Li et al., 1994). Here we show that myelination in MAG deficient mice is not as finely controlled as it is in wild type mice. The abnormalities manifest themselves as a decrease in the proportion of myelinated axons and a reciprocal increase in the proportion of unmyelinated axons in mutants' optic nerves. In addition, dysregulated myelination is occasionally observed in the form of multiply myelinated fibres, grouping of myelinated axons and myelin debris by a large myelin sheath, redundant myelin loops and, very rarely, massive myelin surrounding relatively small axons. Thus, in the absence of MAG, some glial cells seem unable to determine when, where and how much myelin should be laid down. These data support the notion of MAG being a glial recognition/adhesion molecule. A model is proposed regarding the roles MAG could play in the formation and maintenance of myelin structure.

Animals↗
PubMed1998

Population-based study of fertility in women with HIV-1 infection in Uganda.

BACKGROUND: To assess the effects of HIV-1 and other sexually transmitted infections on pregnancy, we undertook cross-sectional and prospective studies of a rural population in Rakai district, Uganda. METHODS: 4813 sexually active women aged 15-49 years were surveyed to find out the prevalence of pregnancy by interview and selective urinary human chorionic gonadotropin tests. The incidence of recognised conception and frequency of pregnancy loss were assessed by follow-up. Samples were taken to test for HIV-1 infection, syphilis, and other sexually transmitted diseases. FINDINGS: At time of survey 757 (21.4%) of 3544 women without HIV-1 infection or syphilis were pregnant, compared with 46 (14.6%) of 316 HIV-1-negative women with active syphilis, 117 (14.2%) of 823 HIV-1-positive women with no concurrent syphilis, and 11 (8.5%) of 130 women with both syphilis and HIV-1 infection. The multivariate adjusted odds ratio of pregnancy in HIV-1-infected women was 0.45 (95% CI 0.35-0.57); the odds of pregnancy were low both in HIV-1-infected women without symptoms (0.49 [0.39-0.62]) and in women with symptoms of HIV-1-associated disease (0.23 [0.11-0.48]). In women with concurrent HIV-1 infection and syphilis the odds ratio was 0.28 (0.14-0.55). The incidence rate of recognised pregnancy during the prospective follow-up study was lower in HIV-1-positive than in HIV-1-negative women (23.5 vs 30.1 per 100 woman-years; adjusted risk ratio 0.73 [0.57-0.93]). Rates of pregnancy loss were higher among HIV-1-infected than uninfected women (18.5 vs 12.2%; odds ratio 1.50 [1.01-2.27]). The prevalence of HIV-1 infection was significantly lower in pregnant than in non-pregnant women (13.9 vs 21.3%). INTERPRETATION: Pregnancy prevalence is greatly reduced in HIV-1-infected women, owing to lower rates of conception and increased rates of pregnancy loss. HIV-1 surveillance confined to pregnant women underestimates the magnitude of the HIV-1 epidemic in the general population.

Adolescent↗
PubMed1998

Electron microscopic studies of antlerogenic cells from five developmental stages during pedicle and early antler formation in red deer (Cervus elaphus).

Previous studies using light microscopy have revealed that histogenesis of deer pedicle and antler has four ossification stages. The first of these stages is the development of the permanent pedicle. Initial development of the pedicle is from the cellular layer cells of the antlerogenic periosteum and these cells have been termed initial antlerogenic cells (IACs). Apart from the IACs, it has also been shown that the cellular layer cells of the apical periosteum/perichondrium, the peripheral periosteum of pedicles or antlers, and the marginal periosteum surrounding the pedicles are also capable of either partially or fully generating a pedicle or an antler. Therefore, these cells can all be considered antlerogenic cells and called apical antlerogenic cells (AACs), peripheral antlerogenic cells (PACs), and marginal antlerogenic cells (MACs), respectively. The aim of this study was to examine the ultrastructure of these antlerogenic cells, and to determine whether there were ultrastructural correlates with the changes of these antlerogenic cells and ossification stages. The ultrastructure of each type of antlerogenic cells was systematically examined using transmission electron microscopy, at each stage of pedicle and first antler growth. At the first ossification stage, the IACs were spindle-shaped and inactive. The most obvious feature was the presence of abundant intracellular glycogen. The MACs were similar to the IACs. During the early second stage, most of the AACs changed in appearance from preosteoblasts to prechondroblasts. Much less heterochromatin was found in the AACs than in the IACs. The most striking attribute of the AACs was the existence of intracellular collagen fibers. The MACs showed abnormal dilation of the rough endoplasmic reticulum (RER). During the late second stage, the majority of the AACs were prechondroblasts. AAC nucleoli were clearly discernible and the cisternae of the RER were arranged in parallel. The MACs contained a greater proportion of abnormally-dilated RER. During the third stage, the AACs were all prechondroblasts. The Golgi apparatus in these cells was well developed. Many free ribosomes in rosettes were scattered in the cytoplasm. Most cytoplasm of the majority of the MACs was occupied by abnormally-dilated RER (the lumen of the RER was extremely dilated and appeared electron-lucent). During the fourth stage, the AACs were similar to their counterparts from the third stage, but the boundaries of some AACs were ill-defined. Some MACs were found to be undergoing apoptosis. The PACs were becoming less and less active from distal to proximal along the shaft of the antler. It is a novel finding that antlerogenic cells change in appearance and subcellular content from preosteoblasts to prechondroblasts prior to the transition from intramembranous to endochondral ossification during pedicle formation. Therefore, the differentiation process from antlerogenic cells to chondroblasts is a matter of maturation from prechondroblasts to chondroblasts. The fact that the antlerogenic cells are rich in glycogen makes them more like embryonic cells. The local membrane deficiency of some AACs at the fourth stage and the presence of mature collagen fibrils within the AACs may reflect the unusually high demand for collagen fibrils during the period of rapid antler growth.

Animals↗
PubMed1998

Effects of streptozotocin-induced hyperglycemia on brain damage following transient ischemia.

Hyperglycemia is known to aggravate ischemic brain damage. The present experiments were undertaken to explore whether hyperglycemia caused by streptozotocin-induced diabetes exacerbates brain damage following transient brain ischemia as it does in animals acutely infused with glucose. Experimental diabetes was induced by injection of streptozotocin in rats which were subjected to 10 min of forebrain ischemia either 1 week (1-wk) or 4 weeks (4-wk) after the induction of diabetes. Normoglycemic rats exposed to the same duration of ischemia and sham-operated diabetic rats served as controls. The animals underwent evaluation of clinical outcome and histopathological analysis of brain damage. Postischemic seizures developed in 35.3 and 42.1% of 1-wk and 4-wk diabetic hyperglycemic animals, respectively. The incidence of seizure was not different between the two groups. None of the diabetic animals with plasma glucose concentrations below 12 mM exhibited seizure activity. The extent and distribution of brain damage were similar between 1-and 4-wk diabetic animals. In the CA1 and in the subicular regions of hippocampus, both diabetic hyperglycemic and normoglycemic animals showed 70-80% cell death. Diabetic hyperglycemic animals had more severe neuronal necrosis in the parietal cortex than normoglycemic animals. In diabetic hyperglycemic animals, neuronal damage involved additional brain structures, e.g., cingulate cortex, thalamus nuclei, substantia nigra, pars reticulata, and the hippocampal CA3 sector, i.e., structures in which neurons were not affected in normoglycemic ischemic subjects at this duration of ischemia. These findings demonstrate that diabetic hyperglycemic animals frequently develop postischemic seizures and that streptozotocin-induced hyperglycemia results exacerbated postischemic brain damage of the same density and distribution as in acutely glucose-infused animals.

Animals↗
PubMed1998

Inducible nitric oxide production and expression of transforming growth factor-beta1 in serum and CSF after cerebral ischaemic stroke in man.

A residual blood supply to the ischaemic brain is a crucial determinant for tissue survival. Early changes in the vascular network and subsequent angiogenesis may be mediated by short-lived molecules like nitric oxide (NO) or growth factors such as transforming growth factor-beta1 (TGF-beta1). Although TGF-beta1 can inhibit NO production, this interaction has not been studied after ischaemia in humans. Serum samples were taken from patients at 24 h and 6 months and cerebrospinal fluid (CSF) samples at 24 h and 1 week later for possible correlation between the two factors. Tissue expression of TGF-beta1 and of the inducible isoform of NO synthase (NOS2) was assessed by immunohistochemistry. CSF levels of NO2-/NO3- as well as total (active + latent) TGF-beta1 were higher in stroke patients as compared to controls 24 h after the stroke. Both NO2-/NO3- and TGF-beta1 were lower 6 months after the stroke compared to 24 h. Levels of NO2-/NO3- correlated with levels of TGF-beta1 within the time points (P = 0.041, Kendall correlation coefficient). There was a strong staining for NOS2 in brain tissue sections in neurones, reactive astrocytes, infiltrating white blood cells, and endothelial cells of larger microvessels. TGF-beta1 expression was mainly limited to neurones and reactive astrocytes. These findings suggest that the interaction between TGF-beta1 and NOS2 might be important for angiogenesis after cerebral ischaemia and may indicate that TGF-beta1 is upregulated as a negative feedback response to elevated levels of NO.

Adult↗
PubMed1998

Recovering and reamplifying of the differentially expressed cDNA bands isolated from mRNA differential display. A modified method.

Methods for retrieving and reamplifying the differentially expressed cDNA bands have been modified. Direct reamplification of differentially expressed bands after cutting from a polyacrylamide gel (PAG) followed by a simple rinse and crush step has proved to be more convenient and effective than the traditional glycogen-precipitation method. Combination of 30 cycles of differential display (DD) polymerase chain reaction (PCR) and 20 cycles of standard PCR reaction also yielded higher reamplification rates.

DNA, Complementary↗
PubMed1998

The protein expression of Bcl-2, Bax, Fas/Apo-1 in acute myeloid leukemia.

The protein expression of bcl-2, bax, Fas/Apo-1 in 19 cases of acute myeloid leukemia (AML) were investigated by Western blot and ApAAp techniques. High expression of bcl-2 protein was found in most of the AML cases, and some of the cases expressed Fas/Apo-1 and bax. High expression of bcl-2 protein was associated with a bad clinical prognosis and a poor response after intensive chemotherapy. Bax seemed to coexpress with bcl-2 and so appeared to be a bad prognostic factor instead of a good one. The expression of Fas/Apo-1 was inversely correlated with bcl-2 and seemed to be a good prognostic factor which may reflect the relative homeostasis of apoptotic pathway. It is concluded that apoptosis-induced pathways in AML often exhibit disturbance features. Coregulation of bcl-2, Bax and Fas/Apo-1 genes formed the apoptosis-induced pathway, which is the biological factor affecting response to chemotherapy.

Adaptor Proteins, Signal Transducing↗
PubMed1998

The diagnosis of diffuse goitre by ultrasound imaging in children.

In order to find an easy and accurate procedure for diagnosis of diffuse goitre in children, we examined 50 patients with diffuse goitre using fine needle aspiration biopsy cytology, thyroid antibody detection, thyroid hormone analysis and ultrasound imaging. In the meantime, 109 healthy children (control) were examined by ultrasound imaging. The results showed that thyroid imaging in health children was a smooth echo pattern with stronger homogenous echogram than surrounding muscle tissues. The patients with diffuse goitre showed an abnormally enlarged thyroid volume. In 22 (84.6%) of 26 children with chronic lymphocytic thyroiditis, a varied patch hypoechogenicity was found, of whom 18 (81.8%) had positive results of antibody testing. On the contrary, echo-pattern was normal in 17 (70.8%) of 24 patients with diffuse thyroid proliferation and only the remainder (7/24, 29.1%) had abnormal echo-pattern as well as elevated auto-antibody titers, of whom 2 were confirmed as chronic lymphocytic thyroiditis by a repeat fine needle aspiration biopsy 1 year later. By using combined ultrasound imaging and antibody determination, 92% of the cases with chronic lymphocytic thyroiditis could be diagnosed. Our study suggests that ultrasonic imaging is an easy, non-invasive, reproducible and effective procedure in the differential diagnosis of chronic lymphocytic thyroiditis in children.

Adolescent↗
PubMed1998

SKF 38393 enhances odor detection performance.

The purpose of this study was to determine the influence of the D1-selective partial agonist SKF 38393 on the odor detection performance of rats using high precision olfactometry and a go/no-go operant task. Previous studies have found that the D2 receptor partial agonist quinpirole decreases such performance, but the influences of D1 receptor activation are unknown. In experiment 1, such detection performance to the odorant ethyl acetate was enhanced by SKF 38393, relative to saline, in male rats at 7.5 and 10.0 mg/kg i.p. dose levels, but not at the lower doses of 1.0, 2.5, and 5.0 mg/kg. In experiment 2, this enhancement was replicated at the 7.5 and 10.0 mg/kg doses and was shown to occur at the 12.5 mg/kg dose as well. In experiment 3, similar enhancement was shown for the odorant eugenol in female rats at the 7.5, 10.0 and 12.5 mg/kg doses, suggesting this effect is neither sex-specific nor confined to the odorant ethyl acetate. In experiment 4, a 0.025 mg/kg dose of the D1 receptor antagonist SCH 23390 depressed the enhancement produced to ethyl acetate by 7.5 mg/kg SKF 38393 to control levels. Overall, these data demonstrate that, in contrast to quinpirole, SKF 38393 improves odor detection performance in the rat and that this phenomenon can be attenuated by the D1 receptor blocker SCH 23390.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1998

Proton inhibition of GABA-activated current in rat primary sensory neurons.

The modulation of the Cl- current activated by gamma-aminobutyric acid (GABA) by changes in extracellular pH in freshly isolated rat dorsal root ganglia (DRG) neurons was studied using the whole-cell patch-clamp technique. In the pH range of 5.0-9.0, increased extracellular pH enhanced, and decreased extracellular pH suppressed, current activated by 10 microM GABA in a reversible and concentration-dependent manner with an IC50 of pH 7.1 in these neurons. Acidification to pH 6.5 inhibited currents activated by the GABAA-selective agonist muscimol in all neurons tested. The antagonism of GABA-activated current by lowering the pH was equivalent at holding potentials between -80 and +40 mV and did not involve a significant alteration in reversal potential. Acidification shifted the GABA concentration/response curve to the right, significantly increasing the EC50 for GABA without appreciably changing the slope or maximal value of the curve. Inhibition of the GABA-activated current by protons was not significantly different when the patch-pipette solution was buffered at pH 7.4 or pH 6.5. These results suggest that extracellular protons inhibit GABAA receptor channels in primary sensory neurons by decreasing the apparent affinity of the receptor for GABA. This represents a novel mechanism of inhibition by protons of a neurotransmitter-gated ion channel. Proton inhibition of GABAA receptor channels may account in part for the modulation by protons of sensory information transmission under certain pathophysiological conditions.

Animals↗
PubMed1998

Adenomatous polyposis coli gene mutation alters proliferation through its beta-catenin-regulatory function in aggressive fibromatosis (desmoid tumor).

Aggressive fibromatosis is a monoclonal proliferation of spindle (fibroblast-like) cells. A subset of lesions contain somatic truncating adenomatous polyposis coli (APC) gene mutations, and all of the lesions contain an elevated beta-catenin protein level. A major function of APC is to regulate beta-catenin protein level. Beta-catenin has a dual function in the cell: it is a member of the adherens junction, and it binds transcription factors in the tcf-lef family, transactivating transcription. Cell cultures from aggressive fibromatoses containing an APC mutation were studied. Transient transfection of the full-length APC gene caused decreased proliferation and beta-catenin protein level in these cultures. To determine whether beta-catenin protein level was responsible for the change in proliferation rate, stable transfections of deltaN89beta-catenin (a stabilized form that is not degraded by APC, but retains all other functions) were achieved in half of the cultures derived from each tumor, whereas the other half were transfected with an empty vector. Transfection of the full-length APC gene in cultures that were stably transfected with deltaN89beta-catenin did not result in a change in proliferation. The type I promotor of p56lck contains an HMG consensus region, to which members of the tcf-lef family can bind. p56lck was expressed in cultures not transfected with the full-length APC gene and in cultures transfected with the full-length APC gene and deltaN89beta-catenin, but not in cultures transfected with only the full-length APC gene. These data show that APC truncating mutations give aggressive fibromatosis cells a proliferative advantage through beta-catenin and suggest that beta-catenin acts to transactivate transcription.

Apoptosis↗