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PubMed1981

Surface topography and other characteristics of non-transformed and carcinogen transformed C3H/10T 1/2 cells in mitosis, as revealed by quantitative scanning electron microscopy.

Scanning electron microscopy (SEM) has been used for the characterization of the different phases of mitosis in normal and transformed C3H/10T 1/2 cells after the stages had been confirmed by light microscopy. Our findings suggest that it is only possible to separate the different phases of mitosis by SEM after having evaluated a great number of cells and after having established the SEM features for the light microscopically identified mitotic phases (Feulgen staining). The main finding in the study is that both the normal and all three types of transformed cells, type I, II and III, have the same shape in the different stages of mitosis but that transformed cells seem to exhibit a larger number of pleomorphic microvilli than do non-transformed cells. We also found that in contrast to the other mitotic phases, prophase cells have a very low concentration of microvilli in the nuclear area.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1994

[A cytogenetic analysis of the cells of spontaneously transformed LREC rat cell lines. I. Chromosomal rearrangements detected in the early stages of rat embryonic cell transformation in vitro].

Seven spontaneously transformed cell lines LREC of rat embryo fibroblasts were obtained by an originally elaborated cloning technique (method 2T7). Six lines (1-6) were obtained from Rattus norvegicus cells, and one line (LREC-7) from Wistar rats. Method 2T7 was based on a serial propagation of rat embryo cells, brought to a "crisis" stage under conditions of a higher cell density and followed by the appearance of actively proliferating cell clones. These lines were analysed cytogenetically at the earliest stages using the Giemsa G-banding technique. In the karyotypes of six LREC (1-6) lines two abnormal chromosomes 7 were revealed: one marker chromosome M1-t(7; 19) results from translocation between chromosomes 7 and 19, the other marker chromosome M2--del(7) is a result of deletion of the second homolog of chromosome 7 in the q11.2 q22.1 loci; besides an extra normal homolog of chromosome 7 was revealed. There are only two marker chromosomes M2 in the LREC-7 line karyotype. Cells of LREC (1-3) lines could be transformed from the immortalized stage to the malignant one by the 30-45th passages. The cells of LREC (4, 7) lines became malignant at the 10-8th passages, resp. The rearrangements of chromosome 7 are supposed to be specific for LREC lines obtained by our method. A hypothesis is put forward that the translocation of chromosome 7 may play an important role for the immortalization of the rat embryo cells. The deletion of chromosome 7 may be associated with a malignant transformation of cells, as it is possible that the deleted loci have a recessive oncogene. Method 2T7 allows to obtain constantly spontaneously transformed cell lines of rat embryo cells with the least abnormal karyotype.

Animals↗
PubMedDate not supplied

Actions and interactions of nickel and magnesium on the transformation response of transformed cells in culture.

Nickel (Ni) and magnesium (Mg) exert separate and interacting effects on cells: Ni is toxic while Mg enhances the transformation response of transformed cells and protects from heavy metal-induced toxicity. Transformed rat liver epithelial cells were used in the soft agar (SA) assay to measure the effect of Ni and/or Mg on the expression of anchorage independence. Cells were exposed to +/- Ni and +/- Mg in a single passage of growth medium (GM) prior to assay in SA. The cells were then treated with +/- Ni and +/- Mg in the SA resulting in a 4 x 4 treatment matrix yielding 16 Ni/Mg combinations. Nickel was expected to decrease the transformation frequency (TF) and did so in 6 of the 16 cases. Magnesium was expected to enhance the TF independently of Ni; Mg increased TF values in 7 of 16 cases. The Ni-Mg interaction occurred in 11 of 16 cases. In general, Mg and Ni effects were observed more in GM than is SA. It is not evident from this study why the Ni, Mg, and Ni-Mg effects are not observed universally, but it is evident that metal-metal interactions are not simply defined or analyzed in biological systems. A refined factorial design may be useful in further separating such interactions. From the point of view of the implementation of the SA assay, in which test substances are typically dose previous to the implementation of putting the exposed cells in SA, it is clear that assay results can be markedly altered by the presence of the test compound in the soft agar.

Animals↗
PubMed1996

Malignant transformation induced by cytokine genes: a comparison of the abilities of germline and mutated interleukin 3 genes to transform hematopoietic cells by transcriptional and posttranscriptional mechanisms.

The effects of inheritance of germline (gIL3) and rearranged interleukin 3 (rIL3) genes on the factor dependency and tumorigenicity of a hematopoietic cell line were compared. The rIL3 gene arose after intracisternal type A particle transposition into the 3' untranslated region (UTR). The rlL3 gene efficiently transformed cells. In contrast, factor-independent cell lines were recovered only rarely from gIL3-transfected cells, and they fell into two categories. One class inherited more than one copy of the transgene and expressed moderate levels of lL-3, whereas the other group received one copy and expressed lower amounts of lL-3. Tumorigenicity was associated with the quantity of lL-3 expression because cells from the first class were malignant, whereas those from the latter set were not. To determine which portions of the rIL3 gene were responsible for cell transformation, chimeric constructs were made containing exchanged sections of the gIL3 and rIL3 genes. The transforming region was mapped to the 3' end of the rIL3 gene, and no point mutations in the promoter region were detected. RNA gel shift assays indicated that the transposition eliminated the ability of proteins to bind the 3'UTR. These results demonstrate that the mutation of the IL-3 3'UTR by intracisternal type A particle transposition results in: (a) the inability of proteins to bind the 3'UTR; (b) prolonged mRNA half life; (c) constitutive IL-3 expression; (d) cytokine independence; and (e) tumorigenicity. Inheritance of a gIL3 gene was not normally sufficient to abrogate cytokine dependency; however, rare tumorigenic cells were isolated, implicating the importance that deregulated cytokine expression can have upon malignant transformation.

Animals↗
PubMed1995

Malignant transformation by H-ras results in aberrant regulation of ribonucleotide reductase gene expression by transforming growth factor-beta 1.

Ribonucleotide reductase is a key rate-limiting and regulatory step in DNA synthesis and plays a crucial role in the coordination of DNA synthesis, DNA repair, and cell proliferation. The present study demonstrates a link between alterations in TGF-beta 1 regulation during malignant conversion and the expression of ribonucleotide reductase. H-ras-transformed mouse 10T1/2 cell lines exhibiting malignant potential were examined for possible TGF-beta 1-mediated alterations in ribonucleotide reductase expression. Selective induction of ribonucleotide reductase gene expression occurred, since only H-ras-transformed highly metastatic cells exhibited marked elevations in ribonucleotide reductase expression, whereas nontransformed normal 10T1/2 cells were unaffected by TGF-beta 1 treatment. These changes occurred without any detectable modifications in DNA synthesis rates, suggesting that these changes were regulated by a novel mechanism independent of the S-phase of the cell cycle. Furthermore, this TGF-beta 1-mediated regulation of ribonucleotide reductase expression was shown to occur through an autocrine mechanism. TGF-beta 1-modulated regulation of ribonucleotide reductase expression requires de novo protein synthesis and involves, at least in part, transcriptional and post-transcriptional events. Furthermore, evidence is presented to suggest a possible role for protein kinase C-mediated events, protein phosphatases, and G-protein-coupled events in the TGF-beta 1-mediated regulation of ribonucleotide reductase expression in H-ras-transformed malignant cells. TGF-beta 1 regulation of ribonucleotide reductase in highly malignant cells appears to be complex and multifaceted and constitutes an integral part of an altered growth regulatory program.

Animals↗
PubMed1992

Resistance of in vivo-selected spontaneously transformed cells and Rous sarcoma virus-transformed cells to macrophage-mediated cytotoxicity.

The cytotoxic activity (CTA) of activated peritoneal macrophages (MP) on variant lines of Syrian hamster embryo (HE) cells of differing malignant characteristics was studied. The target cells were a line of low-malignant cells resulting from spontaneous transformation of HE cells in vitro (STHE strain), and malignant variants selected from them in vivo (STHE-LM-4, STHE-LM-8, and STHE-75/18 strains). In addition, we used cells of the HET-SR-1 strain; these are HE cells transformed in vitro by a tumorigenic Rous sarcoma virus (Schmidt-Ruppin strain, RSV-SR), or the TU-SR strain induced by RSV-SR in vivo. Thioglycollate-elicited peritoneal MP from Syrian hamsters were activated in vitro with bacterial levan, LPS or MDP and used as effector cells. MP-mediated cytolysis was determined by means of a 42-h radioactivity release assay with 3H-thymidine-labeled target cells. We found that only the parental STHE cells were susceptible towards fully-activated MP-mediated CTA. All three of the in vivo-selected malignant variants of the STHE cell sublines, as well as the tumorigenic RSV-SR transformants, were resistant to cytolysis by activated MP. Non-activated thioglycollate-elicited MP did not lyse any of the tumor cells studied.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1991

Expression of a new type high molecular weight receptor (type V receptor) of transforming growth factor beta in normal and transformed cells.

A new type high molecular weight receptor (type V receptor) of transforming growth factor beta (TGF-beta) was recently purified from bovine liver plasma membranes and appears not to be related to receptors previously described for TGF-beta (Pauline O'Grady, Ming-Der Kuo, Joseph J. Baldassare, Shuan Shian Huang and Jung San Huang [1991] J. Biol. Chem. 266:8583-8589). This type V receptor may be important in the regulation of cell growth by TGF-beta. We examined its distribution in a wide range of normal and transformed cells. The type V receptor was found to be expressed in many normal cells including cells of epithelial, endothelial, fibroblastic and chondrocytic origins. However, a number of human epithelial tumor cells (5 out of 6 examined) did not express detectable levels of the type V TGF-beta receptor. These results suggest that loss of the type V receptor may potentially contribute to the transformed state of certain epithelial tumor cells.

Animals↗
PubMed1989

Transformation of mouse mammary epithelial cells with the Ha-ras but not with the neu oncogene results in a gene dosage-dependent increase in transforming growth factor-alpha production.

An enhanced expression of transforming growth factor-alpha (TGF alpha) was demonstrated in two clones of NOG-8 mouse mammary epithelial cells, NOG-8 SR1 and NOG-8 SR2, that have been transformed by a v-Ha-ras oncogene. The amount of TGF alpha production in NOG-8 SR1 and NOG-8 SR2 cells was dependent on the level of p21ras expression in these clones, which directly correlated with their cloning efficiency in soft agar. There was also a decrease in the number of epidermal growth factor (EGF) receptors on the NOG-8 SR1 and NOG-8 SR2 cells that is proportional to the amount of TGF alpha secreted. These effects were specific for ras because neu-transformed NOG-8 cells grew in soft agar at a comparable level to NOG-8 SR2 cells yet did not show any increase in TGF alpha production or change in EGF receptor expression.

Animals↗
PubMed2000

Caveolin-1 expression is down-regulated in cells transformed by the human papilloma virus in a p53-dependent manner. Replacement of caveolin-1 expression suppresses HPV-mediated cell transformation.

Squamous cell carcinomas of the lung and cervix arise by neoplastic transformation of their respective tissue epithelia. In the case of cervical carcinomas, an increasing body of evidence implicates the human papillomavirus, HPV (types 16 and 18), as playing a pivotal role in this malignant transformation process. The HPV early genes E6 and E7 are known to inactivate the tumor suppressors p53 and Rb, respectively; this leads to disruption of cell cycle regulation, predisposing cells to a cancerous phenotype. However, the role of caveolin-1 (a putative tumor suppressor) in this process remains unknown. Here, we show that caveolin-1 protein expression is consistently reduced in a panel of lung and cervical cancer derived cell lines and that this reduction is not due to hyperactivation of p42/44 MAP kinase (a known negative regulator of caveolin-1 transcription). Instead, we provide evidence that this down-regulation event is due to expression of the HPV E6 viral oncoprotein, as stable expression of E6 in NIH 3T3 cells is sufficient to dramatically reduce caveolin-1 protein levels. Furthermore, we demonstrate that p53-a tumor suppressor inactivated by E6-is a positive regulator of caveolin-1 gene transcription and protein expression. SiHa cells are derived from a human cervical squamous carcinoma, harbor a fully integrated copy of the HPV 16 genome (including E6), and show dramatically reduced levels of caveolin-1 expression. We show here that adenoviral-mediated gene transfer of the caveolin-1 cDNA to SiHa cells restores caveolin-1 protein expression and abrogates their anchorage-independent growth in soft agar. Taken together, our results suggest that the HPV oncoprotein E6 down-regulates caveolin-1 via inactivation of p53 and that replacement of caveolin-1 expression can partially revert HPV-mediated cell transformation.

3T3 Cells↗
PubMed2001

Double-stranded RNA-dependent protein kinase, PKR, down-regulates CDC2/cyclin B1 and induces apoptosis in non-transformed but not in v-mos transformed cells.

The interferon (IFN)-induced, double stranded RNA (dsRNA)-activated serine/threonine kinase, PKR, is a potent negative regulator of cell growth when overexpressed in yeast or mammalian cells. Paradoxically, while it can function as a tumor suppressor and inducer of apoptosis, it is overexpressed in a variety of human cancers. To resolve this enigma, we established cell-lines that overexpress PKR in non-transformed and in v-mos transformed CHO cells. Overexpression of PKR suppressed the proliferation of CHO cells by inducing a transient G0/G1 arrest, followed by a delayed G2/M arrest, which attenuated cell cycle progression. These effects were accompanied by early induction of p21/WAF-1 and delayed downregulation of CDC2 and cyclin B1. Induction of proapoptotic activity of the ectopic PKR paralleled the onset of G2/M arrest in CHO cells. However, while transiently inducing p21/WAF-1, PKR did not impose G2/M arrest or apoptosis in v-mos-transformed cells, nor was CDC2 or cyclin B1 down-regulated in those cells. These findings link the proapoptotic activity of PKR to the arrest of cell cycle at the G2/M phase. Consequently, the apoptotic activity of PKR could be counter-acted by an oncogene-like v-mos that overrides the G2/M arrest induced by PKR.

Animals↗
PubMed1991

Loss of transforming growth factor beta 1 receptors and its effects on the growth of EBV-transformed human B cells.

Transforming growth factor-beta (TGF-beta) is a potent negative regulator of normal human B cell growth mediated by exogenous signals, including IL-2 and low m.w. B cell growth factor 12 kDa (BCGF-12 kDa). In the present study, we investigated the regulatory linkage between viral or nonviral transformation of human B cells and the growth inhibitory effects of TGF-beta 1. A panel of EBV+ and EBV- B cell lines, derived either by in vitro EBV B cell transformation, or from cases of lymphoma was used to quantitate the negative growth effects of TGF-beta 1. The proliferative response of three EBV- B cell lines to rBCGF-12 kDa or serum was inhibited by low concentrations of TGF-beta 1 (0.2-0.5 ng/ml for 50% maximal effect), as measured by tritiated thymidine uptake and viable cellular recovery. In contrast, rBCGF-12 kDa or serum mediated proliferation of three EBV+ B cell lines was refractory to the growth inhibitory effects of TGF-beta 1. In an attempt to understand the mechanism(s) for this differential growth control in EBV+ and EBV- B cells, we studied the expression of TGF-beta 1, c-myc, and TGF-beta 1 receptors. No correlation was observed between the expression of TGF-beta 1 or c-myc gene and growth inhibition by TGF-beta 1 in the cell lines studied. Our results indicate that sensitivity or resistance to TGF-beta 1 correlated with the presence or absence (loss) of high affinity receptors for TGF-beta 1. EBV- B cell lines expressed levels of high affinity receptors similar to those found on activated normal B or T cells. In contrast, EBV+ B cell lines showed no detectable high affinity receptors. Chemical cross-linking studies with a bifunctional reagent, dissuccinimidyl suberate revealed a normal expression of type I (65-70 kDa), type II (85-90 kDa), and type III (280-300 kDa) TGF-beta 1 high affinity receptors on EBV- B cell lines. In contrast, EBV+ B cell lines did not express type I and type II receptors, whereas type III receptors were expressed but could not be inhibited by unlabeled TGF-beta 1.(ABSTRACT TRUNCATED AT 400 WORDS)

B-Lymphocytes↗
PubMed1999

Accuracy of stereotactic coordinate transformation using a localisation frame and computed tomographic imaging. Part II. Analysis of matrix-based coordinate transformation.

The accuracy of coordinate transformation from a CT image to a stereotactic frame was investigated for stereotactic systems using a localisation frame and matrix-based coordinate transformation. The main source of error influencing calculation was input data, due to inaccurate calculation of the centres of the rods of the localisation frame in the CT image, and the propagation of this input error during subsequent matrix calculation. Systemic errors during matrix calculation do not exist, and rounding off errors were of subordinate importance compared to the input data error. The influence of input data error on coordinate transformation was studied by geometric methods, computer simulation, and numerical analysis. In the geometric model, input data errors affected the calculation of the centres of the three oblique rods in the frame space and shifted them three points upwards or downwards on the axis of each rod. The three centres of the oblique rods defined the "CT plane" in the 3D space of the stereotactic frame. Displacements of these three centres caused a characteristic tilting of the CT plane. The positions of the correct and tilted CT planes defined the spatial error properties for all target points on the CT plane. The computer simulation investigated the effects on matrix-based transformation of all possible displacement combinations on the three oblique rods by 1 pixel (1. 16 mm) in the x and y directions. A characteristic, space-dependent distribution of the frame-related coordinates was obtained for each target point. In the centre of the frame, we found a maximal deviation of 1.0 mm in the xy direction and 2 mm in the z direction. This corresponded to an error amplification of 0.73 in the xy direction and 1.22 in the z direction relative to the error at the centres of the rods. The maximum deviation (found in the periphery) for all combinations on the three oblique rods was 1.7 mm in the xy direction and 3.3 mm in the z direction. This resulted in an amplification of 1.03 in the xy direction and 2.01 in the z direction. This results had to be multiplied by 2 to obtain a maximal error estimate for displacements including all nine rods of the localisation frame. Numerical analysis showed stable solutions with low error amplification for hexagonal frame arrangements.

Brain↗
PubMed1989

Anaerobic transformation of phenol to benzoate via para-carboxylation: use of fluorinated analogues to elucidate the mechanism of transformation.

Isomeric fluorophenols were used as phenol analogues to investigate the transformation of phenol to benzoate by an anaerobic, phenol-degrading consortium derived from freshwater sediment. Transformation of 2-fluorophenol and 3-fluorophenol led to the accumulation of fluorobenzoic acids. 2-Fluorophenol was transformed in the presence or absence of phenol, while 3-fluorophenol transformation was only observed in the presence of phenol. Identification of the resulting fluorobenzoate products as 3-fluorobenzoate and 2-fluorobenzoate isomers, respectively, together with the nontransformation of 4-fluorophenol indicated that the carboxyl group was introduced para to the phenolic hydroxyl group.

Anaerobiosis↗
PubMed1987

Sodium molybdate converts the RNA-associated transformed, oligomeric form of the glucocorticoid receptor into the transformed, monomeric form.

The glucocorticoid receptor from rat liver cytosol prepared in 2 ml buffer/g tissue sedimented at approximately 10 S in low salt density gradient centrifugation without molybdate. When the receptor was heated at 25 degrees C, both approximately 10 S and approximately 7 S forms were seen in low salt gradient. The approximately 10 S form was not capable of binding to DNA-cellulose and was stabilized by sodium molybdate, namely it corresponded to untransformed receptor. The approximately 7 S form was capable of binding to DNA-cellulose and regarded as transformed receptor. On the other hand, partially-purified transformed receptor labeled with [3H]dexamethasone-21-mesylate sedimented at approximately 5 S, which migrated as a approximately 94 kDa species in SDS-polyacrylamide gel electrophoresis. The reconstitution analysis of this partially-purified approximately 5 S receptor and liver cytosol, showed the shift to approximately 7 S form. RNase A or T1 converted approximately 7 S transformed form into approximately 5 S but it did not affect approximately 10 S untransformed form. 5-20 mM sodium molybdate also shifted approximately 7 S to approximately 5 S. These results indicate that the approximately 7 S transformed form of the glucocorticoid receptor observed in low salt conditions might be an oligomer, probably including both approximately 5 S steroid-binding component and RNA/ribonucleoprotein, and that molybdate dissociates these interactions in a specific manner.

Adrenalectomy↗
PubMed1989

Microbial transformations of steroids--V. Transformation of progesterone by whole cells and extracts of Botryosphaerica obtusa.

Members of the genus Botryosphaerica are reported 7 alpha steroid hydroxylators [1]. We found that the species B. obtusa efficiently hydroxylated progesterone in a 1-day transformation but it gave 7 beta-hydroxyprogesterone as the main product rather than the expected 7 alpha-hydroxy isomer, which was produced in only trace amounts. Also formed in minor amounts were 6 beta-, possibly 9 alpha- (see main text), 14 alpha- and 15 beta-monohydroxyprogesterones. The transformation mixtures included appreciable amounts of dihydroxylated progesterones which were mainly based on 7 beta-hydroxyprogesterone. The second hydroxyl group was at one of the minor monohydroxylation sites. The relative concentrations of the progesterone diols increased and those of the mono-alcohols concomitantly decreased when transformation was extended beyond 1 day. Monohydroxylated 6-dehydroprogesterones began to accumulate after about 3 days and these compounds seemed to have been formed by 6,7-dehydration of the dihydroxyprogesterones. We prepared mycelial cell-free extracts which were capable of transforming progesterone and retained the site-specificity of whole cells. These extracts converted 7 beta-hydroxyprogesterone to its 6-dehydro derivative, confirming that ring B desaturation occurs in this organism by dehydration. The dehydratase activity necessary for the conversion was separable from the hydroxylase activity by ultra-centrifugation. All hydroxylase activity co-sedimented with the membrane fraction, implying that steroid hydroxylation is effected by a membrane-bound enzyme(s). Dehydratase activity was present in both the pellet and the supernatant fractions, which suggests that it may involve a loosely bound, and easily removed, membrane-associated enzyme.

Biotransformation↗
PubMed2002

Studies on the accumulation and transformation of arsenic in freshwater organisms I. Accumulation, transformation and toxicity of arsenic compounds on the Japanese medaka, Oryzias latipes.

Accumulation, transformation and toxicity of arsenic compounds to Japanese Medaka, Oryzias latipes were investigated. For sodium arsenite [As(II)] and disodium arsenate [As(V)], the mean value for 7-day lethal concentration LC50 for O. latipes were 14.6 and 30.3 mg As/l, respectively. Direct accumulation of arsenic in O. latipes increased as a function of As(III) concentration in water. A small proportion of accumulated arsenic was transformed to methylated arsenic. As much as 70% of the total arsenic accumulated in tissue was depurated. Accumulation and transformation of As(III) by O. latipes in a simple freshwater food chain were also investigated. The transformation of As(III) to As(V) by organisms was more prevalent than biomethylation of accumulated arsenic in organisms of the three steps of the food chain.

Animals↗
PubMed2001

Transformation of peanut (Arachis hypogaea L.) with tobacco chitinase gene: variable response of transformants to leaf spot disease.

Fertile transgenic plants of peanut (Arachis hypogaea L.) cv. TMV-2 expressing tobacco chitinase and neomycin phosphotransferase (npt II) genes were generated using an Agrobacterium tumefaciens (LBA4404/pBI121-pBTex)-mediated transformation system. A tissue culture-independent method wherein embryo in the mature seed is inoculated and reared into single plant transformant was used for transformation. Southern blot analysis of genomic DNA isolated from T(0) transformants and progeny plants (T(1)) demonstrated that the transgenes are stably integrated in the genome of transgenic peanut plants and inherited by the offspring. The expression of the heterologous chitinase gene driven by CaMV 35S promoter led to a high level of activity in some of the transgenic plants. Small-scale field tests indicated increased ability of these plants to resist the fungal pathogen Cercospora arachidicola (the causal organism of the leaf spot or Tikka disease of peanut), which is an important peanut pathogen. These results suggest that a heterologous chitinase gene was functional in peanut and expressed in healthy plants. The study also shows that peanut plants containing transgenically increased activity of chitinase were resistant to attack by the fungal pathogen C. arachidicola to different degrees. The strategy employed may be useful for the control of other fungal diseases of the crop.

Journal Article↗
PubMed2002

Carbohydrase activities of the rolC-gene transformed and non-transformed ginseng cultures.

The levels of activity of beta-D-glucosidase, alpha-D-mannosidase, alpha- and beta-D-galactosidase, 1,3-, 1,6-, 1,4-beta-D-glucanases, 1,4-alpha-D-glucanase, fucoidanhydrolase and agarase were measured in extracts of non-transgenic and transgenic Panax ginseng cultures transformed with the rolC gene. Significantly increased levels of activity of beta- and alpha-D-galactosidases and 1,3-beta-D-glucanase were detected in rolC-gene transformed cells, compared to the control non-transformed cells, while levels of activity of other enzymes were unchanged. These, as well as the gel-permeation experiments, revealed that transformation of ginseng cells by the rolC gene could significantly affect activity of some carbohydrases and production of their molecular forms.

Cells, Cultured↗