Relevant bibliographies by topics / MEL cells

Journal articles
Dissertations / Theses
Books
Book chapters
Conference papers
Reports

Academic literature on the topic 'MEL cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'MEL cells.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "MEL cells"

Lomovsky, Alexey, Yulia Baburina, Irina Odinokova, Margarita Kobyakova, Yana Evstratova, Linda Sotnikova, Roman Krestinin, and Olga Krestinina. "Melatonin Can Modulate the Effect of Navitoclax (ABT-737) in HL-60 Cells." Antioxidants 9, no. 11 (November 18, 2020): 1143. http://dx.doi.org/10.3390/antiox9111143.

Full text

Abstract:

Melatonin (N-acetyl-5-methoxytryptamine MEL) is an indolamine that has antioxidant, anti-inflammatory and anti-tumor properties. Moreover, MEL is capable of exhibiting both anti-apoptotic and pro-apoptotic effects. In the normal cells, MEL possesses antioxidant property and has an anti-apoptotic effect, while in the cancer cells it has pro-apoptotic action. We investigated the combined effect of MEL and navitoclax (ABT-737), which promotes cell death, on the activation of proliferation in acute promyelocytic leukemia on a cell model HL-60. The combined effect of these compounds leads to a reduction of the index of mitotic activity. The alterations in the level of anti- and pro-apoptotic proteins such as BclxL, Bclw, Mcl-1, and BAX, membrane potential, Ca2+ retention capacity, and ROS production under the combined action of MEL and ABT-737 were performed. We obtained that MEL in combination with ABT-737 decreased Ca2+ capacity, dropped membrane potential, increased ROS production, suppressed the expression of anti-apoptotic proteins such as BclxL, Bclw, and Mcl-1, and enhanced the expression of pro-apoptotic BAX. Since, MEL modulates autophagy and endoplasmic reticulum (ER) stress in cancer cells, the combined effect of MEL and ABT-737 on the expression of ER stress and autophagy markers was checked. The combined effect of MEL and ABT-737 (0.2 μM) increased the expression of protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), leading to a decrease in the level of binding immunoglobulin protein (BIP) followed by an increase in the level of C/EBP homologous protein (CHOP). In this condition, the expression of ERO1 decreased, which could lead to a decrease in the level of protein disulfide isomerase (PDI). The obtained data suggested that melatonin has potential usefulness in the treatment of cancer, where it is able to modulate ER stress, autophagy and apoptosis.

APA, Harvard, Vancouver, ISO, and other styles

Qi, Chen, James A. Wheeler, Ashlie Pruett, and Phillip H. Pekala. "Expression of the RNA binding proteins, Mel-N1, Mel-N2, and Mel-N3 in adipose cells." Biochemical and Biophysical Research Communications 294, no. 2 (June 2002): 329–33. http://dx.doi.org/10.1016/s0006-291x(02)00472-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Tolksdorf, Beatrice, Sina Zarif, Jürgen Eberle, Ahmet Hazini, Babette Dieringer, Franziska Jönsson, Florian Kreppel, Jens Kurreck, and Henry Fechner. "Silencing of Mcl-1 overcomes resistance of melanoma cells against TRAIL-armed oncolytic adenovirus by enhancement of apoptosis." Journal of Molecular Medicine 99, no. 9 (May 24, 2021): 1279–91. http://dx.doi.org/10.1007/s00109-021-02081-3.

Full text

Abstract:

Abstract Arming of oncolytic viruses with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown as a viable approach to increase the antitumor efficacy in melanoma. However, melanoma cells may be partially or completely resistant to TRAIL or develop TRAIL resistance, thus counteracting the antitumor efficiency of TRAIL-armed oncolytic viruses. Recently, we found that TRAIL resistance in melanoma cells can be overcome by inhibition of antiapoptotic Bcl-2 protein myeloid cell leukemia 1 (Mcl-1). Here, we investigated whether the cytotoxicity of AdV-TRAIL, an oncolytic adenovirus, which expresses TRAIL after induction by doxycycline (Dox), can be improved in melanoma cells by silencing of Mcl-1. Two melanoma cell lines, the TRAIL-resistant MeWo and the TRAIL-sensitive Mel-HO were investigated. Treatment of both cell lines with AdV-TRAIL resulted in a decrease of cell viability, which was caused by an increase of apoptosis and necrosis. The proapoptotic effects were dependent on induction of TRAIL by Dox and were more pronounced in Mel-HO than in MeWo cells. SiRNA-mediated silencing of Mcl-1 resulted in a further significant decrease of cell viability and a further increase of apoptosis and necrosis in AdV-TRAIL-infected MeWo and Mel-HO cells. However, while in absolute terms, the effects were more pronounced in Mel-HO cells, in relative terms, they were stronger in MeWo cells. These results show that silencing of Mcl-1 represents a suitable approach to increase the cytotoxicity of a TRAIL-armed oncolytic adenovirus in melanoma cells. Key messages • Cytotoxicity of TRAIL-expressing adenovirus can be enhanced by silencing of Mcl-1. • The effect occurs in TRAIL-sensitive and TRAIL-resistant melanoma cells. • Increase of apoptosis is the main mechanism induced by Mcl-1 silencing.

APA, Harvard, Vancouver, ISO, and other styles

Shih, I., T. Wang, T. Wu, R. J. Kurman, and J. D. Gearhart. "Expression of Mel-CAM in implantation site intermediate trophoblastic cell line, IST-1, limits its migration on uterine smooth muscle cells." Journal of Cell Science 111, no. 17 (September 1, 1998): 2655–64. http://dx.doi.org/10.1242/jcs.111.17.2655.

Full text

Abstract:

An immortalized implantation site intermediate trophoblastic cell line, IST-1, was established from a human placenta of 7 weeks gestation. IST-1 cells phenotypically resembled the implantation site intermediate trophoblastic cells in situ and expressed Mel-CAM (MUC 18 or CD146). Mel-CAM is a cell adhesion molecule belonging to the immunoglobulin gene superfamily. It is involved in heterophilic cell-cell adhesion and plays a role in several biological processes including tumor progression. We have previously shown that Mel-CAM was highly expressed in the intermediate (extravillous) trophoblast in the human implantation site. In this study we determined the function of Mel-CAM in the interaction of trophoblast and uterine smooth muscle in the implantation site. IST-1 cells failed to adhere to immobilized recombinant Mel-CAM in solid phase whereas the uterine smooth muscle cells did. The presence of the putative Mel-CAM ligand in smooth muscle cells was further supported by the finding that Mel-CAM-transfected but not the mock-transfected U937 leukemia cells bind to the confluent monolayer of uterine smooth muscle cells. IST-1 cells attached efficiently to the monolayer of the uterine smooth muscle cells and acquired a spindle-shaped morphology simulating smooth muscle cells. The cell binding was only marginally affected by Mel-CAM blocking antibodies. However, Mel-CAM blocking antibodies and recombinant Mel-CAM promoted cell migration from IST-1 cell spheroids on the smooth muscle monolayer. Taken together, our results suggest that IST-1 cells express Mel-CAM but not the putative Mel-CAM ligand. In contrast, the uterine smooth muscle cells express the putative Mel-CAM ligand which binds to Mel-CAM on the surface of the IST-1 cells. The interaction between Mel-CAM and its putative ligand confers a stationary phenotype for trophoblastic cells. These observations are consistent with an important role for Mel-CAM in limiting trophoblastic migration within the myometrium in the implantation site.

APA, Harvard, Vancouver, ISO, and other styles

Ulmer, J. B., E. D. Dolci, and G. E. Palade. "Glycophorin expression in murine erythroleukaemia cells." Journal of Cell Science 92, no. 2 (February 1, 1989): 163–71. http://dx.doi.org/10.1242/jcs.92.2.163.

Full text

Abstract:

We have identified mature and putative precursor forms of glycophorins expressed in a virus-transformed murine erythroleukaemia (MEL) cell line and compared them with their normal erythroblast counterparts. The following differences were found: (1) the two major MEL cell glycophorins (apparent Mr values 29–30 and 43(x10(3] have greater mobility on polyacrylamide gels than their normal gp-3 and gp-2 counterparts, due at least in part to differences in their oligosaccharide sidechains; (2) MEL cell gp-3 consists of two discrete proteins; and (3) there are more potential glycophorin precursors in MEL cells than in normal mouse erythroblasts. Four proteins, with apparent Mr values of 21, 23, 26 and 27(x10(3], have tentatively been identified as glycophorin precursors, based on the following findings: (1) they are immunologically related to the glycophorins; and (2) their synthesis was induced by dimethyl sulphoxide coincidentally with that of gp-3 and gp-2. They do not appear to be glycoproteins, as evidenced by their lack of incorporation of [3H]galactose, [3H]glucosamine or [3H]mannose. In contrast, gp-3 and gp-2 incorporated [3H]galactose and [3H]glucosamine but not [3H]mannose. Partial characterization of the glycan moieties of MEL cell glycophorins indicates that they consist mostly of tri- and tetrasaccharides, with no indication of any N-linked chains. Hence, the glycans of MEL cell glycophorins are mostly (if not all) O-linked. Furthermore, treatment with N-glycanase did not change their electrophoretic mobility on polyacrylamide gels. MEL cell glycophorins were also shown to be modified by phosphoryl and fatty acyl groups.

APA, Harvard, Vancouver, ISO, and other styles

Foresti, M., L. Gaudio, and G. Geraci. "Selective gene mutation in MEL cells." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 265, no. 2 (February 1992): 195–202. http://dx.doi.org/10.1016/0027-5107(92)90048-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Jiang, Yi, Ming Shen, Yuanyuan Chen, Yinghui Wei, Jingli Tao, and Honglin Liu. "Melatonin Represses Mitophagy to Protect Mouse Granulosa Cells from Oxidative Damage." Biomolecules 11, no. 7 (June 30, 2021): 968. http://dx.doi.org/10.3390/biom11070968.

Full text

Abstract:

Various environmental stimuli, including oxidative stress, could lead to granulosa cell (GC) death through mitophagy. Recently, it was reported that melatonin (MEL) has a significant effect on GC survival during oxidative damage. Here, we found that MEL inhibited oxidative stress-induced mitophagy to promote GC survival. The loss of cell viability upon H2O2 exposure was significantly restored after MEL treatment. Concomitantly, MEL inhibited the activation of mitophagy during oxidative stress. Notably, blocking mitophagy repressed GC death caused by oxidative stress. However, MEL cannot further restore viability of cells treated with mitophagy inhibitor. Moreover, PTEN-induced putative kinase 1 (PINK1), a mitochondrial serine/threonine-protein kinase, was inhibited by MEL during oxidative stress. As a result, the E3 ligase Parkin failed to translocate to mitochondria, leading to impaired mitochondria clearance. Using RNAi to knock down PINK1 expression, we further verified the role of the MEL-PINK1-Parkin (MPP) pathway in maintaining GC survival by suppressing mitophagy. Our findings not only clarify the protective mechanisms of MEL against oxidative damage in GCs, but also extend the understanding about how circadian rhythms might influence follicles development in the ovary. These findings reveal a new mechanism of melatonin in defense against oxidative damage to GCs by repressing mitophagy, which may be a potential therapeutic target for anovulatory disorders.

APA, Harvard, Vancouver, ISO, and other styles

Afanasieva, D. A., M. A. Baryshnikova, T. N. Zabotina, A. A. Borunova, O. S. Burova, E. Yu Rybalkina, A. A. Nikolina, and Z. G. Kadagidze. "CHARACTERISTICS OF MULTIDRUG RESISTANCE IN HUMAN SKIN MELANOMA CELL LINES." Russian Journal of Biotherapy 14, no. 4 (December 30, 2015): 39–44. http://dx.doi.org/10.17650/1726-9784-2015-14-4-39-44.

Full text

Abstract:

MDR is the main obstacle to chemotherapy efficiency. MDR can grow in cancer cells even if only the one cytostatic agent will act. The aim of the nowadays work is to characterize MDR in metastatic human skin melanoma cell lines prepared in “N.N. Blokhin Russian Cancer Research Center”. pgpl70 expression was detected by immunofluorescence methods. mRNA of MDR gene was identified by Reverse Transcriptase- PCR( RT-PCR) method. Rhodamine 123 (Rhl23) emission has been evaluated by flow cyto- fluorimetiy, cytotoxic activity was estimated by MTT-tests. The cells sensitivity to Aianoza cytostatic effects has showed that mel Kor cells were sensitive to Aranoza acting, but mel Ibr and mel Mtp X were not. Mel Ibr cells had expressed pgpl70 from 35 to 50 per cent, it was detected by immunofluorescence reaction. Mel Kor and mel Mtp-X cells were not expressed P-glycoprotein. mRNA of genes responsible for multi-drug resistance - MDR1, BCRP, MRP1 and LRP (MVP) - were detected by PCR. mRNA of BCRP and MRP1 genes has low expression, barely visible stripes after 33 cycles in all cell lines samples. LRP (MVP) genes expression of mRNA, unfortunately, never managed to see. YB1 gene mRNA expression is well, it is typically for cancer cells. mRNA of gene was found in mel MtpX and mel Ibr subclones cell lines. Mel Kor cells didn't contain mRNA of MDR1 gene. The study of the Rhl23 emission from cells showed that mel Kor control cells had accumulated Rhl23 and didn't throw it out. Mel Ibr cell line accumulated Rhl23 and threw out the half part of it. Mel MtpX cell tine had accumulated the less part of Rhl23 and almost all were thrown out. Thus, the study shows that mel Kor cell tine that are sensitive to Aranoza doesn't express pgpl70, not contain mRNA of multi-chug resistance genes and does not throw Rhl23. Mel Ibr cells resistant to the Aranoza cytotoxic action express pgpl70 ,contain mRNA of MDR1 gene and throw out Rhl23. However, mel MtpX cell line resistant to Aranoza does not express pgpl70, but contains mRNA of MDR1 gene and actively throws out Rhl23.

APA, Harvard, Vancouver, ISO, and other styles

Kajiume, Teruyuki, Takashi Sato, and Masao Kobayashi. "The Expression of Polycomb Group Genes Products, Bmi1 and Mel-18, Regulate the Function of Murine Primitive Hematopoietic Cells." Blood 110, no. 11 (November 16, 2007): 1261. http://dx.doi.org/10.1182/blood.v110.11.1261.1261.

Full text

Abstract:

Abstract The Polycomb group (PcG) genes (bmi1 and mel-18) known as negative control factors of the Hox gene is thought to regulate the differentiation and self-renewal of hematopoietic stem cells (HSCs). The loss of mel-18 results in the promotion of HSC self-renewal, and the increase of mel-18 expression inversely leads to the differentiation of HSCs. On the other hand, the loss of bmi1 does not lead to self-renewal activity of HSCs. In this study we examined the effect of expression of bmi1 and mel-18 on the role of function in murine HSCs. Lineage-negative, Sca1-positive, and cKit-positive primitive hematopoietic cells were purified and the expression of PcG protein was evaluated from the intra-nuclear distribution of PcG proteins. The Bmi1-positive hematopoietic cells barely contained Mel-18, and the Mel-18-positive cells barely contained Bmi1. the frequency of positive cells for both Bmi1 and Mel-18 was less than 0.5% of purified primitive hematopoietic cells. The expression levels of the PcG genes, bmi1 and mel-18, in HSCs were knocked down by siRNA and then gene expression was assessed by quantitative real-time PCR. The introduction of siRNA against bmi1 or mell-18 resulted in approximate 50 to 60% decrease of each gene expression without affecting another gene expression. Primary colony-forming activity of knocked down cells in response to stem cell factor, thrombopoietin and the ligand for flt3 was not affected by the induction of siRNA. However, secondary colony-forming activity from primary colony-forming cells in bmi1-knockdown cells was significantly decreased when compared with that of control cells. Conversely, the mel-18-knockdown cells significantly increased, suggesting that mel-18-knockdown cells are capable of proliferating activity. Finally, bone marrow reconstitutive activity was examined by using Ly5.1 and Ly5.2 system. While the bmi1-knockdown marrow cells decreased the reconstitutive activity, the mel-18-knockdown marrow cells showed the increase of engraftment activity after 6 months of transplantation. From these results, we consider that mel-18 and bmi1 have reciprocal functions in HSCs. Mammalian PcG protein complexes can be classified into two distinct types, Polycomb repressive complexes 1 and 2 (PRC1 and PRC2). The Mel-18 protein is a constituent of mammalian PRC1 together with M33, Bmi1 or rae28, and Scmh1. The Mel-18 protein is composed of 342 amino acids and the N-terminal region of the 102 amino acid, which includes the RING finger motif, shares 93% homology with Bmi1 protein. In addition, its secondary structure shows high homology with the Mel-18 and Bmi1 proteins. We hypothesized that the opposite function is expressed in HSCs because Mel-18 and Bmi1 share the same structure and compete when in the complex form. These results suggest that mel-18 and bmi1 have inverse function in HSCs and that the balance of Bmi1 and Mel-18 may regulate the fate of self-renewal and differentiation in HSCs.

APA, Harvard, Vancouver, ISO, and other styles

Vartanian, A. A., O. S. Burova, Kh S. Vishnyakova, I. V. Samoylenko, V. A. Misyurin, E. E. Egorov, O. O. Ryabaya, and M. A. Baryshnikova. "Vemurafenib resistant melanoma cells acquire mesenchymal stem cell-like properties." Advances in molecular oncology 6, no. 4 (December 15, 2019): 47–57. http://dx.doi.org/10.17650/2313-805x-2019-6-4-47-57.

Full text

Abstract:

Background. Activating mutations in the BRAF gene leads to a constitutive activation of the MAPK signaling. The highly selective BRAFV600E inhibitor, vemurafenib, improves the overall survival of BRAF-mutant melanoma patients. However, despite the excellent results of response rate, the average duration of the response was short and acquired resistance develops in most BRAF mutated melanoma patients within a few months. Objective: to derive melanoma cell lines from surgical species of patients with BRAF mutant melanomas resistant to vemurafenib and to elucidate the mechanisms involved in acquired drug resistance.Materials and methods. Mel Ki and Mel F1702 melanoma cells were obtained from metastases of disseminated melanoma patients with BRAFV600E mutation. 2D tumor cell culture, MTT test, immunicytochemistry, flow cytometry, real-time polimerase chain reaction and osteogenic and adipocytic differentiation were used in the study.Results. We have derived two melanoma cell lines Mel Ki and Mel F1702 from tumor samples of patients with BRAFV600E mutation resistant to vemurafenib. These cells were homogenous and had fibroblastic morphology. The IC50 values for Mel Ki and Mel F1702 were 4.7 and 6.3 μM, respectively. The expression of cancer-testis antigens was not detected in both types of cells suggesting the stemness of Mel Ki and Mel F1702 melanoma cells. The immunophenotypic profile of the vemurafenib resistsant melanoma cells showed the expression of typical mesenchymal stem cells markers such as CD90, CD105 and CD44. In addition, we found that the melanoma cell lines derived from tumor resistant to vemurafenib differentiated into osteoblastand adipocyte-like cells. Conclusion. In this study we are offering an experimental evidence of the phenotypic transition of the vemurafenib-resistant melanoma cells into mesenchymal stem-like cells.

APA, Harvard, Vancouver, ISO, and other styles

More sources

Dissertations / Theses on the topic "MEL cells"

Clements, Andrew R. N. "The regulation of globin gene expression." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365687.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Moka, Nagaishwarya, Kelley cross, Marianne Brannon, Janet Lightner, Megan Dycus, William Stone, Victoria Palau, and Koyamangalath Krishnan. "Delta-tocotrienol and simvastatin induces differential cytotoxicity and synergy in BRAF wild-type SK-MEL-2 and mutant BRAF SK-MEL-28 melanoma cancer cells." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/215.

Full text

Abstract:

Targeting the mutant BRAF and immunotherapy are new approaches to the treatment of metastatic malignant melanoma that has significantly improved survival but is associated with significant toxicity and cost. Potent and specific BRAF inhibitors like vemurafenib and dabrafenib are superior to chemotherapy in treatment of BRAF mutant melanomas which represent nearly 50% of all melanomas. A less toxic approach to treatment of malignant melanoma is hence appealing. Delta-tocotrienol (DT3), an unsaturated vitamin E isoform, and simvastatin, an HMG-CoA reductase inhibitor have been shown to have anti-neoplastic properties. We studied the effects of these chemicals in both BRAF-mutated SK-MEL-28 and BRAF-wild type SK-MEL-2 melanoma cells. MTS assays were used to analyze cytotoxicity. SK-MEL-28 and SK-MEL-2 cells were cultured in MEM media containing 10% serum and plated in 96-well culture plates for 48 hours then treated with DT3 (0-80 µM), simvastatin (0-10 µM), or a combination and dosed again at 72 hours. SK-MEL-28 and SK-MEL-2 cells were grown in 60 mm plates and treated with DT3 at concentrations of 30 µM, simvastatin at concentrations of 10 µM and combination of DT3 and simvastatin at concentrations of 10 µM and 2 µM. Cell were lysed with RIPPA buffer with protease and phosphatase inhibitor after 6 hours of treatment. Protein concentration of cell lysates was measured spectrophotometrically (GLO Max Multi+, Promega), using a BCA protein assay kit. The samples were run in SDS PAGE and blotted onto nitrocellulose membranes. Membranes were incubated with antibodies against Hsp 70 (Enzo Life Sciences, Farmingdale, NY), Hsp 90 (Santa Cruz, Dallas, TX), pS6 and pERK (Cell Signaling, Danvers, MA) and pAKT. Using MTS assay, we found that DT3 (IC50 75.2 μM) and simvastatin (IC50 8.3μM) have cytotoxic effects on melanoma cell line SK-MEL-2, but not on the SK-MEL-28 cells DT3 and simvastatin at the concentrations studied (10-80 μM DT3) and (0.625- 10 μM simvastatin). Further studies determined that simvastatin decreased expression of pS6, pERK on SK-MEL-2 and not DT3. However, these effects are different in SK-MEL-28 cells where there is only decrease in expression of pS6; treated SK-MEL-2 cells also show over-expression of Hsp70 suggestive of a rescue effect leading to lesser cytotoxic activity. The selective cytotoxicity observed in wild type BRAF melanoma cell lines by DT3 and simvastatin warrants further research into the potential therapeutic use of these drugs. A differential cytotoxicity is shown by DT3 and simvastatin in malignant melanoma cells with selective more potency in wild type BRAF melanoma compared to mutant BRAF melanoma cells. Further studies will be undertaken to dissect the mechanistic basis of this differential response.

APA, Harvard, Vancouver, ISO, and other styles

Garcia-Alonso, Monica. "Evaluation of the potential of murine erythroleukemia (MEL) cells as an expression system for nicotinic acetylcholine receptors." Thesis, University of Reading, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389643.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Passos, Débora Cristina Silva dos. "Ação biológica in vitro de tiossemicarbazonas derivadas de canfeno e limoneno em células de melanoma humano (SK-MEL-37)." Universidade Federal de Goiás, 2013. http://repositorio.bc.ufg.br/tede/handle/tede/3426.

Full text

Abstract:

Submitted by Erika Demachki (erikademachki@gmail.com) on 2014-10-22T16:44:26Z No. of bitstreams: 4 Tese - Débora Cristina Silva dos Passos - 2013 - Parte 01.pdf: 10357491 bytes, checksum: 1678b4aad93bca319ee5ddb93d3808bc (MD5) Tese - Débora Cristina Silva dos Passos - 2013 - Parte 02.pdf: 9533486 bytes, checksum: ad5e21870e09f4f46a3045a69996aed3 (MD5) Tese - Débora Cristina Silva dos Passos - 2013 - Parte 03.pdf: 8695341 bytes, checksum: 5f8d696c0a73f923cb129f3c0aa1e4b7 (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5)
Approved for entry into archive by Jaqueline Silva (jtas29@gmail.com) on 2014-10-22T19:00:24Z (GMT) No. of bitstreams: 4 Tese - Débora Cristina Silva dos Passos - 2013 - Parte 01.pdf: 10357491 bytes, checksum: 1678b4aad93bca319ee5ddb93d3808bc (MD5) Tese - Débora Cristina Silva dos Passos - 2013 - Parte 02.pdf: 9533486 bytes, checksum: ad5e21870e09f4f46a3045a69996aed3 (MD5) Tese - Débora Cristina Silva dos Passos - 2013 - Parte 03.pdf: 8695341 bytes, checksum: 5f8d696c0a73f923cb129f3c0aa1e4b7 (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5)
Made available in DSpace on 2014-10-22T19:00:24Z (GMT). No. of bitstreams: 4 Tese - Débora Cristina Silva dos Passos - 2013 - Parte 01.pdf: 10357491 bytes, checksum: 1678b4aad93bca319ee5ddb93d3808bc (MD5) Tese - Débora Cristina Silva dos Passos - 2013 - Parte 02.pdf: 9533486 bytes, checksum: ad5e21870e09f4f46a3045a69996aed3 (MD5) Tese - Débora Cristina Silva dos Passos - 2013 - Parte 03.pdf: 8695341 bytes, checksum: 5f8d696c0a73f923cb129f3c0aa1e4b7 (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5) Previous issue date: 2013-05-16
Melanoma is a type of cancer that arises from melanocytes and is notoriously resistant to radiation and chemotherapy. The thiosemicarbazones are synthetic compounds with marked biological properties such as antibacterial, antiviral, antiprotozoal and antitumor and previous studies have demonstrated cytotoxic activity against the human melanoma cells, so in this study, we evaluated the antiproliferative activity, the enzymatic activity of Caspases 2, 3, 6, 8, 9, the effect on the cell cycle gene expression levels of caspases 2, 3, 6, 8, 9, Apaf-1 and microscopic morphological changes in human melanoma cells (SK -MEL-37) twenty one monoterpene derived from natural thiosemicarbazone (-) - camphene: camphene, benzaldehyde, benzophenone, menthone, ethyl pyruvate, p-nitroacetophenone, pchloroacetophenone, p-methoxyacetophenone, p-methylacetophenone, p fluoracetofenona-phidroxiacetofena, furan, 3-methoxy-4-hydroxybenzaldehyde, p-fluorbenzaldehyde, 2- hydroxybenzaldehyde, cinnamic aldehyde, thiophene-2-carboxaldehyde, 1-H-imidazole-4- carboxaldehyde, tiossemicaroazida and six montoterpeno natural R-(+)-limonene: benzaldehyde, thiosemicarbazide, o-nitro, m-nitro, p-nitro, p-hydroxy and p-dimethylamino. The values found for the inhibitory concentration for 50% of cells (IC50) were between 12 μM and 55 μM. The percentage of cells in phase and in phase G0/G1 decreased SG2 / M increased after forty-eight hours of incubation with benzaldehyde thio-camphene, limonene thio-benzaldehyde, m-nitro, p-hydroxy and thiosemicarbazide increased indicating that the growth inhibitory effect might be also due to arrest of cells at S-G2/M phase. We observed increased activity of caspase 3 (m-nitro thio-limonene), 6 (camphene thio-benzaldehyde and p-hydroxy thio-limonene) and 8 (thio-benzaldehyde limonene). Late apoptotic features were detected in 62% of cells treated with benzaldehyde thio-camphene and morphological changes typical of apoptosis were visualized by fluorescence microscopy and scanning electron microscopy (SEM) after treatment with benzaldehyde thio-camphene chosen due to their low IC50 value (12 mM). It was observed gene expression of caspases 2, 3, 6, 8 and Apaf-1 in cells treated with benzaldehyde thio-camphene indicating the participation of these enzymes in the anti-proliferative effect observed. Our results indicate that the thiosemicarbazones derivatives can inhibit proliferation, regulate cell cycle, induce apoptosis of human melanoma cells (SK-MEL-37) and could be an candidate for future preclinical in vivo studies.
O melanoma é um tipo de câncer que surge nos melanócitos e é notoriamente resistente à radioterapia e quimioterapia. As tiossemicarbazonas são compostos sintéticos com marcantes propriedades biológicas tais como antibacteriana, antiviral, antiprotozoária e antitumoral e em estudos anteriores demonstraram ação citotóxica frente à celulas de melanoma humano, por isso, neste estudo, foi avaliada a atividade anti-proliferativa, a atividade enzimática das caspases 2, 3, 6, 8, 9, o efeito no ciclo celular, os níveis de expressão gênica das caspases 2, 3, 6, 8, 9, Apaf-1 e as alterações morfológicas por microscopia em células de melanoma humano (SK-MEL-37) de vinte e uma tiossemicarbazonas derivadas do monoterpeno natural (-)- canfeno: canfeno, benzaldeído, benzofenona, mentona, etil piruvato, acetofenona, pnitroacetofenona, p-cloroacetofenona, p-metoxiacetofenona, p-metilacetofenona, pfluoracetofenona, p-hidroxiacetofena, furano, 3-metóxi-4-hidroxibenzaldeído, pfluorbenzaldeído, 2-hidroxibenzaldeído, aldeído cinâmico, tiofeno-2-carboxialdeído, 1-Himidazol- 4-carboxialdeído, tiossemicaroazida, bem como seis do montoterpeno natural R-(+)- limoneno: benzaldeído, tiossemicarbazida, o-nitro, m-nitro, p-nitro, p-dimetilamino e phidróxi . Os valores encontrados para a concentração inibitória para 50% das células (IC50) situaram-se entre 12 μM e 55 μM. A porcentagem de células na fase G0/G1diminuiu e na fase SG2/M aumentou após quarenta e oito horas de incubação com o benzaldeído tio-canfeno, benzaldeído tio-limoneno, m-nitro, p-hidróxi e tiossemicarbazida, indicando que o efeito antiproliferativo observado pode ser devido a uma interrupção das células na fase SG2/M. Observou-se uma maior atividade de caspase 3 (m-nitro tio-limoneno), 6 (benzaldeído tiocanfeno e p-hidróxi tio-limoneno) e 8 (benzaldeído tio-limoneno). Características apoptóticas tardias foram detectados em 62% das células tratadas com benzaldeído tio-canfeno e as alterações morfológicas típicas de processo de apoptose foram visualizadas através da microscopia de fluorescência e de microscopia eletrônica de varredura (MEV) após tratamento com o benzaldeído tio-canfeno escolhido devido ao seu baixo valor de IC50 (12 μM). Observou-se a expressão gênica das caspases 2, 3, 6, 8 e o apaf-1 nas células tratadas com benzaldeído tio-canfeno indicando a participação dessas enzimas no efeito antiproliferativo observado. Os resultados indicam que as tiossemicarbazonas derivadas de canfeno e limoneno podem inibir a proliferação celular, regular o ciclo celular e induzir apoptose nas células de melanoma humano (SK-MEL-37), portanto, podem ser considerados candidatos para futuros ensaios pré-clínico in vivo.

APA, Harvard, Vancouver, ISO, and other styles

Hawke, David H. "Quantitative mass spectrometry: Proteomic analysis of differentiation of MEL cells treated with hexamethylene bisacetamide and 7-[N-(3-aminopropyl)amino] heptan-2-one." Scholarly Commons, 2004. https://scholarlycommons.pacific.edu/uop_etds/2691.

Full text

Abstract:

Polyamines are small, polycationic molecules required for growth and development and found in all living cells. In this study, the effects of two polyamine analogues, hexamethylene bisacetamide (HMBA), a differentiation inducer, and 7-[N-(3-aminopropyl)amino] heptan-2-one (APAH), an inhibitor of N8-acetylspermidine deacetylase, were studied using quantitative proteomics and stable-isotopes. Two new technologies, isotope-coded affinity tags (ICAT) and quantification in fragment spectra using isobaric stable isotope reagents (iTRAQ) were employed and compared. Quantitative results of these experiments showed few changes in the type and level of proteins detected in whole-cell extracts. Proteins from three populations of cells were studied, control (untreated), HMBA-treated, and HMBA plus APAH treated cells. Some of the proteins that were differentially expressed in response to these agents include pyruvate kinase (PK), lactate dehydrogenase (LDH), mini-chromosome maintenance protein 3 (MCM3), and poly-rC binding protein. The proteins PK and LDH have been reported as possible cancer markers. Histone protein levels were significantly reduced on HMBA treatment, and substantially recovered with the addition of APAH. This finding was very convincing in the iTRAQ work, but invisible to the ICAT experiment, because of the lack of cysteine residues required for quantification in the ICAT methodology. Two proteins were elevated in the HMBA-APAH experiment compared to the other two, heterogeneous nuclear ribonuclear protein C1/C2 (HNRP C1/C2) and ubiquitin. Considering their unique functions, the up-regulation of these proteins suggests the involvement of internal ribosome entry and protein degradation in response to APAH. The results of the two technologies, ICAT and iTRAQ, were found to overlap, but were partly complementary.

APA, Harvard, Vancouver, ISO, and other styles

Morgado, Ana Sofia João. "Analysis of the intranuclear life of nonsense transcripts." Doctoral thesis, Faculdade de Ciências e Tecnologia, 2013. http://hdl.handle.net/10362/8798.

Full text

Abstract:

Dissertação para obtenção do Grau de Doutor em Biologia, Especialidade de Biologia Molecular
Nonsense-mediated mRNA decay (NMD) is a quality control mechanism that detects and rapidly degrades mRNAs carrying premature translation-termination codons (PTCs). Mammalian NMD depends on both splicing and translation, and requires recognition of the premature stop codon by the cytoplasmic ribosomes. Surprisingly, some published data have suggested that nonsense codons may also affect the nuclear metabolism of the nonsense-mutated transcripts. Therefore, we hypothesized that human β-globin transcripts sensitive to NMD could have a singular subcellular localization and processing state in mammalian cells nuclei. To determine if PTCs could influence nuclear events, we have established mouse erythroleukemia (MEL) cell lines stably transfected with wild-type or PTC-containing human β-globin genes. Subsequently, we analyzed the accumulation of NMD-competent β-globin transcripts versus wild-type counterparts using two different approaches: visualization of transcripts localization by fluorescence in situ hybridization (FISH); and quantification of pre-mRNA steady-state levels by ribonuclease protection assays (RPA) and reverse transcription-coupled quantitative polymerase chain reaction (RT-qPCR). FISH analysis shows that MEL cells stably expressing PTC-containing β-globin transcripts present a marked tendency to display an abnormal speckled-like pattern of localization in the nucleus. However, in addition to the presence of the PTC, other effectors may act on the β-globin transcripts localization, as some wild-type β-globin MEL cells presented this abnormal FISH phenotype as well. On the other hand, our analyses by RPA and RT-qPCR clearly show that β- -globin pre-mRNAs carrying NMD-competent PTCs, but not those containing a NMD-resistant PTC, exhibit a significant decrease in their steady-state levels relatively to the wild-type or to a missense-mutated β-globin pre-mRNA. Conversely, in non-erythroid HeLa cells, human β-globin pre-mRNAs carrying NMD-competent PTCs accumulate at normal levels. Half-life analysis of these pre-mRNAs in MEL cells demonstrate that their low steady-state levels do not reflect significantly lower pre-mRNA stabilities when compared to the normal control. Furthermore, our results also provide evidence that the relative splicing efficiencies of intron 1 and 2 are unaffected. In conclusion, our set of data highlights potential nuclear pathways that induce a selective downregulation of PTC-containing β-globin pre-mRNA in MEL cells, albeit not affecting their stability or splicing effectiveness. These specialized nuclear pathways, which may act in concert with the general NMD mechanism, might discriminate the NMD-sensitive transcripts as abnormal in a promoter- and/or cell line-specific manner, probably to obtain optimal NMD activity.
Fundação para a Ciência e Tecnologia - (SFRH/BD/31920/2006); financial support [Centro de Investigação em Genética Molecular Humana (CIGMH) and Center for Biodiversity, Functional and Integrative Genomics (BioFIG)]

APA, Harvard, Vancouver, ISO, and other styles

Valente, Sabrina <1980&gt. "Vascular wall stem cells. Selection and conditioning of progenitors useful for cell therapy. A pathological case study." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/2857/.

Full text

Abstract:

The arterial wall contains MSCs with mesengenic and angiogenic abilities. These multipotent precursors have been isolated from variously-sized human adult segments, belying the notion that vessel wall is a relatively quiescent tissue. Recently, our group identified in normal human arteries a vasculogenic niche and subsequently isolated and characterized resident MSCs (VW-MSCs) with angiogenic ability and multilineage potential. To prove that VW-MSCs are involved in normal and pathological vascular remodeling, we used a long-term organ culture system; this method was of critical importance to follow spontaneous 3-D vascular remodeling without any influence of blood cells. Next we tried to identify and localize in situ the VW-MSCs and to understand their role in the vascular remodeling in failed arterial homografts. Subsequently, we isolated this cell population and tested in vitro their multilineage differentiation potential through immunohistochemical, immunofluorescence, RT-PCR and ultrastructural analysis. From 25-30cm2 of each vascular wall homograft sample, we isolated a cell population with MSCs properties; these cells expressed MSC lineage molecules (CD90, CD44, CD105, CD29, CD73), stemness (Notch-1, Oct-4, Sca-1, Stro-1) and pericyte markers (NG2) whilst were negative for hematopoietic and endothelial markers (CD34, CD133, CD45, KDR, CD146, CD31 and vWF). MSCs derived from failed homografts (H-MSCs) exhibited adipogenic, osteogenic and chondrogenic potential but scarce propensity to angiogenic and leiomyogenic differentiation. The present study demonstrates that failed homografts contain MSCs with morphological, phenotypic and functional MSCs properties; H-MSCs are long-lived in culture, highly proliferating and endowed with prompt ability to differentiate into adipocytes, osteocytes and chondrocytes; compared with VW-MSCs from normal arteries, H-MSCs show a failure in angiogenic and leiomyogenic differentiation. A switch in MSCs plasticity could be the basis of pathological remodeling and contribute to aneurysmal failure of arterial homografts. The study of VW-MSCs in a pathological setting indicate that additional mechanisms are involved in vascular diseases; their knowledge will be useful for opening new therapeutic options in cardiovascular diseases.

APA, Harvard, Vancouver, ISO, and other styles

Curradi, Giacomo <1977&gt. "Airway Basal Cell Vascular Endothelial Growth Factor-mediated Cross-Talk Regulates Endothelial Cell Dependent Growth Support of Human Airway Basal Cells." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5925/.

Full text

Abstract:

The human airway epithelium is a pseudostratified heterogenous layer comprised of cili-ated, secretory, intermediate and basal cells. As the stem/progenitor population of the airway epi-thelium, airway basal cells differentiate into ciliated and secretory cells to replenish the airway epithelium during physiological turnover and repair. Transcriptome analysis of airway basal cells revealed high expression of vascular endothelial growth factor A (VEGFA), a gene not typically associated with the function of this cell type. Using cultures of primary human airway basal cells, we demonstrate that basal cells express all of the 3 major isoforms of VEGFA (121, 165 and 189) but lack functional expression of the classical VEGFA receptors VEGFR1 and VEGFR2. The VEGFA is actively secreted by basal cells and while it appears to have no direct autocrine function on basal cell growth and proliferation, it functions in a paracrine manner to activate MAPK signaling cascades in endothelium via VEGFR2 dependent signaling pathways. Using a cytokine- and serum-free co-culture system of primary human airway basal cells and human endothelial cells revealed that basal cell secreted VEGFA activated endothelium to ex-press mediators that, in turn, stimulate and support basal cell proliferation and growth. These data demonstrate novel VEGFA mediated cross-talk between airway basal cells and endothe-lium, the purpose of which is to modulate endothelial activation and in turn stimulate and sustain basal cell growth.
I risultati preliminari dello studio suggeriscono che il vascular endothelial growth factor A(VEGFA) e’ attivamente secreto dalle cellule basali dell’epitelio bronchiale e svolge una funzione paracrina nell’attivazione della cascata delle mitogen-activated protein kinases (MAPKs) nelle cellule endoteliali mediata dal VEGF receptor type 2. Utilizzando un sistema di co-coltura di cellule basali primarie delle vie aeree umane con cellule endoteliali umane, abbiamo mostrato come il VEGFA secreto dalle cellule basali sia in grado di attivare le cellule endoteliale che a loro volta, esprimono mediatori capaci di stimolare e sostenere la proliferazione delle cellule basali stesse. Questi dati dimostrano un cross-talk mediato dal rilascio di VEGFA tra le cellule basali dell’epitelio bronchiale e l’endotelio, il cui scopo è di modulare l'attivazione endoteliale e, a sua volta stimolare e sostenere la crescita delle cellule basali.

APA, Harvard, Vancouver, ISO, and other styles

Avanzi, Simone <1982&gt. "Cell Host-Microbe Interactions: Turning Pathogen Mechanisms Into Cell's Advantages." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5759/.

Full text

Abstract:

Host-Pathogen Interaction is a very vast field of biological sciences, indeed every year many un- known pathogens are uncovered leading to an exponential growth of this field. The present work lyes between its boundaries, touching different aspects of host-pathogen interaction: We have evaluate the permissiveness of Mesenchimal Stem cell (FM-MSC from now on) to all known human affecting herpesvirus. Our study demonstrate that FM-MSC are full permissive to HSV1, HSV2, HCMV and VZV. On the other hand HHV6, HHV7, EBV and HHV8 are susceptible, but failed to activate a lytic infection program. FM-MSC are pluripotent stem cell and have been studied intensely in last decade. FM-MSC are employed in some clinical applications. For this reason it is important to known the degree of susceptibility to transmittable pathogens. Our atten- tion has then moved to bacterial pathogens: we have performed a proteome-wide in silico analy- sis of Chlamydiaceae family, searching for putative Nuclear localization Signal (NLS). Chlamy- diaceae are a family of obligate intracellular parasites. It’s reasonably to think that its members could delivered to nucleus effector proteins via NLS sequences: if that were the case the identifi- cation of NLS carrying proteins could open the way to therapeutic approaches. Our results strengthen this hypothesis: we have identified 72 protein bearing NLS, and verified their func- tionality with in vivo assays. Finally we have conceived a molecular scissor, creating a fusion protein between HIV-1 IN protein and FokI catalytic domain (a deoxyexonuclease domain). Our aim is to obtain chimeric enzyme (trojIN) which selectively identify IN naturally occurring target (HIV LTR sites) and cleaves subsequently LTR carrying DNA (for example integrated HIV1 DNA). Our preliminary results are promising since we have identified trojIN mutated version capable to selectively recognize LTR carrying DNA in an in vitro experiments.

APA, Harvard, Vancouver, ISO, and other styles

Wang, Aibo. "Phosphorylation of Nur77 by MEK-ERK-RSK cascade induces mitochondrial translocation and apoptosis in T cells." Amherst, Mass. : University of Massachusetts Amherst, 2009. http://scholarworks.umass.edu/dissertations/AAI3372283/.

Full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Books on the topic "MEL cells"

1949-, Lumsden Charles J., and Woolridge Nicholas, eds. In silico: Cell biology art and science with MAYA and MEL. Amsterdam: Morgan Kaufmann, 2008.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Nat, Roxana, and Andreas Eigentler. Cell Culture, iPS Cells and Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0013.

Full text

Abstract:

Somatic reprogramming technology, which enables the conversion of adult human non-neural cells into neurons, has progressed rapidly in recent years. The derivation of patient-specific induced pluripotent stem (iPS) cells has become routine. The inherent broad differentiation potential of iPS cells makes possible the generation of diverse types of human neurons. This constitutes a remarkable step in facilitating the development of more appropriate and comprehensive preclinical human disease models, as well as for high throughput drug screenings and cell therapy. This chapter reviews recent progress in the human iPS cell culture models related to common and rare NDDs, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, spinal muscular atrophy, and degenerative ataxias. It focuses on the pathophysiological features revealed in cell cultures, and the neuronal subtypes most affected in NDDs. The chapter discusses the validity, limitation, and improvements of this system in faithfully and reproducibly recapitulating disease pathology.

APA, Harvard, Vancouver, ISO, and other styles

Watts, Christine. Mel Bay Cello Method. Mel Bay Publications, Inc., 1998.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Watts, Christine. Mel Bay presents Cello Method. Mel Bay Publications, Inc., 2002.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Elger, Marlies, and Wilhelm Kriz. The renal glomerulus. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0043.

Full text

Abstract:

The glomerulus performs its functions with three major cell types. Endothelial cells and visceral epithelial cells (podocytes) lie on the inside and outside of the glomerular basement membrane, and together these three structures form the glomerular filtration barrier. Mesangial cells sit in the axial region. Pathologies of all these regions and cell types can be identified. Parietal epithelial cells lining Bowman’s capsule participate in crescent formation, and at the tubular pole some of these cells seem to represent a stem cell population for tubular cells and podocytes. The extraglomerular mesangium and juxtaglomerular apparatus complete the description of the glomerular corpuscle. The structure of these elements, and how they relate to function, are illustrated in detail.

APA, Harvard, Vancouver, ISO, and other styles

Dörner, Thomas, and Peter E. Lipsky. Cellular side of acquired immunity (B cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0050.

Full text

Abstract:

B cells have gained interest in rheumatoid arthritis (RA) beyond being the precursors of antibody-producing plasma cells since they are also a broader component of the adaptive immune system. They are capable of functioning as antigen-presenting cells for T-cell activation and can produce an array of cytokines. Disturbances of peripheral B-cell homeostasis together with the formation of ectopic lymphoid neogenesis within the inflamed synovium appears to be a characteristic of patients with RA. Enhanced generation of memory B cells and autoreactive plasma cells producing IgM-RF and ACPA-IgG antibodies together with formation of immune complexes contribute to the maintenance of RA, whereas treatment with B-cell-directed anti-CD20 therapy provides clinical benefit.

APA, Harvard, Vancouver, ISO, and other styles

Bay, Bill. Mel Bay Fun With the Cello. Mel Bay Publications, Inc., 1993.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Norgaard, Martin. Mel Bay Jazz Cello Wizard Junior. Mel Bay Publications, 2002.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Read, Nick D. Fungal cell structure and organization. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0004.

Full text

Abstract:

Human pathogenic fungi produce three basic ‘cell’ types: hyphae, yeast cells, and spores. The organization and subcellular structure of these different cell types and their modes of growth and formation are reviewed. Growth and form is the consequence of how new cell surface is formed. This is generated by the delivery of vesicles to the surface which provides new membrane and the enzymes for cell wall synthesis. To generate these various cell types, the pathway of vesicle secretion to the surface has to be carefully regulated. These vesicles have to be transported through the cell by the cytoskeleton, and in filamentous cells these vesicles accumulate at a supply centre called the Spitzenkörper before docking and fusion with the hyphal apex. Ultimately, membrane is also endocytosed and recycled behind actively expanding regions of the fungal surface. These various processes are described and particular emphasis is given to the structural and organizational features of fungal cells that play roles in their pathogenesis and virulence.

APA, Harvard, Vancouver, ISO, and other styles

Eljaafari, Assia, and Pierre Miossec. Cellular side of acquired immunity (T cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0049.

Full text

Abstract:

The adaptive T-cell response represents the most sophisticated component of the immune response. Foreign invaders are recognized first by cells of the innate immune system. This leads to a rapid and non-specific inflammatory response, followed by induction of the adaptive and specific immune response. Different adaptive responses can be promoted, depending on the predominant effector cells that are involved, which themselves depend on the microbial/antigen stimuli. As examples, Th1 cells contribute to cell-mediated immunity against intracellular pathogens, Th2 cells protect against parasites, and Th17 cells act against extracellular bacteria and fungi that are not cleared by Th1 and Th2 cells. Among the new subsets, Th22 cells protect against disruption of epithelial layers secondary to invading pathogens. Finally these effector subsets are regulated by regulatory T cells. These T helper subsets counteract each other to maintain the homeostasis of the immune system, but this balance can be easily disrupted, leading to chronic inflammation or autoimmune diseases. The challenge is to detect early changes in this balance, prior to its clinical expression. New molecular tools such as microarrays could be used to determine the predominant profile of the immune effector cells involved in a disease process. Such understanding should provide better therapeutic tools to counteract deregulated effector cells.

APA, Harvard, Vancouver, ISO, and other styles

More sources

Book chapters on the topic "MEL cells"

Liu, Shujuan, and Ahmed Ashour Ahmed. "Growth factors and uncontrolled proliferation." In Oxford Textbook of Oncology, 11–22. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199656103.003.0002.

Full text

Abstract:

A mandatory requirement of normal growth and development is the tight spatial and temporal synchronization of cellular proliferation within a specific tissue type and between tissue types that make up an organ, a process that is governed by intrinsic and extrinsic regulatory pathways. For a cell to synchronize its growth with that of other cells it requires a network of proteins that can sense external cues, send internal messages, and produce extracellular messengers that feed back information to neighbouring cells. Growth factors act as cellular messengers to feed back regulatory signals that modulate the cell’s own behaviour (autocrine signals) and that of other adjacent cells (paracrine signals). These proteins regulate a myriad of other cellular activities. In this chapter we discuss how different growth factors relay messages to cells and describe how their deregulation contributes to the development of uncontrolled proliferation and cancer.

APA, Harvard, Vancouver, ISO, and other styles

Full text

Abstract:

APA, Harvard, Vancouver, ISO, and other styles

Bullenkamp, Jessica, and Mahvash Tavassoli. "Cancer and cell death." In Oxford Textbook of Cancer Biology, edited by Francesco Pezzella, Mahvash Tavassoli, and David J. Kerr, 196–208. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0014.

Full text

Abstract:

Programmed cell death is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions. Regulated programmed cell death is one of the mechanisms by which multicellular organisms limit the growth and replication of cells. Cell death is essential to control cell growth and tissue homeostasis; it occurs in normal tissues to allow the removal of damaged cells or to maintain a constant number of cells in regenerating tissues and plays an important part in embryogenesis. In an average human adult 50–70 billion cells undergo programmed cell death every day. The abundance of literature suggests that defects in programmed cell death play a crucial role in carcinogenesis. The genetic alterations in the cancer cell not only lead to increased cellular proliferation, as discussed in other chapters of this book, but also lead to loss of programmed cell death, thus increasing tumour growth. Despite being part of the problem, cell death plays an important role in the treatment of cancer as it is an important target of many treatment strategies. Unquestionably, apoptosis is the best-characterized and the most evolutionary conserved form of programmed cell death. Recently, many studies have demonstrated the existence of several other forms of programmed cell death including autophagy, necroptosis, and pyroptosis. In this chapter we discuss several regulated forms of cell death; we outline what we know about their mechanisms and how we can exploit this knowledge to reactivate programmed cell death in tumour cells for the treatment of cancer.

APA, Harvard, Vancouver, ISO, and other styles

Moser, Edvard I., Menno P. Witter, and May-Britt Moser. "Entorhinal Cortex." In Handbook of Brain Microcircuits, edited by Gordon M. Shepherd and Sten Grillner, 227–44. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190636111.003.0019.

Full text

Abstract:

While decades of study have unraveled some of the basic principles of hippocampal structure and function, the adjacent entorhinal cortex (EC) has remained terra incognita in many respects. Recent studies suggest that the medial part of the entorhinal cortex is part of a two-dimensional metric map of the animal’s changing location in the environment. A key component of this map is the grid cell, which fires selectively at hexagonally spaced positions in the animal’s environment. Grid cells colocalize with other recently discovered medial entorhinal cell types, such as head direction cells, conjunctive grid × head direction cells, border cells, and speed cells. This chapter provides an overview of these functional cell types, their possible relationship to morphological cell types, the intrinsic architecture of the system (including laminar, longitudinal, and modular organization), and the extrinsic connectivity and possible function of both the medial and lateral subdivisions of the entorhinal cortex.

APA, Harvard, Vancouver, ISO, and other styles

Dörner, Thomas, and Peter E. Lipsky. "Cellular side of acquired immunity (B cells)." In Oxford Textbook of Rheumatology, 371–78. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0050_update_001.

Full text

Abstract:

APA, Harvard, Vancouver, ISO, and other styles

"Haematological cancers." In Oxford Handbook of Cancer Nursing, edited by Mike Tadman and Dave Roberts, 413–34. Oxford University Press, 2007. http://dx.doi.org/10.1093/med/9780198569244.003.0032.

Full text

Abstract:

Introduction 414 Acute leukaemia 416 Chronic leukaemia 420 Hodgkin's lymphoma (Hodgkin's disease) 424 Non-Hodgkin's lymphoma (NHL) 428 Myeloma 432 Haematological cancers are cancers of blood cells. All blood cells are made in the bone marrow from a haemopoietic (blood forming) stem cell. The stem cell divides and gradually turns into one of the mature blood cells, passing first through several immature stages (...

APA, Harvard, Vancouver, ISO, and other styles

Vyas, Paresh, and N. Asger Jakobsen. "Cellular and molecular basis of haematopoiesis." In Oxford Textbook of Medicine, edited by Chris Hatton and Deborah Hay, 5172–81. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0511.

Full text

Abstract:

Haematopoiesis involves a regulated set of developmental stages from haematopoietic stem cells (HSCs) that produce haematopoietic progenitor cells that then differentiate into more mature haematopoietic lineages, which provide all the key functions of the haematopoietic system. Definitive HSCs first develop within the embryo in specialized regions of the dorsal aorta and umbilical arteries and then seed the fetal liver and bone marrow. At the single-cell level, HSCs have the ability to reconstitute and maintain a functional haematopoietic system over extended periods of time in vivo. They (1) have a self-renewing capacity during the life of an organism, or even after transplantation; (2) are multipotent, with the ability to make all types of blood cells; and (3) are relatively quiescent, with the ability to serve as a deep reserve of cells to replenish short-lived, rapidly proliferation progenitors. Haematopoietic progenitor cells are unable to maintain long-term haematopoiesis in vivo due to limited or absent self-renewal. Rapid proliferation and cytokine responsiveness enables increased blood cell production under conditions of stress. Lineage commitment means limited cell type production. The haematopoietic stem cell niche is an anatomically and functionally defined regulatory environment for stem cells modulates self-renewal, differentiation, and proliferative activity of stem cells, thereby regulating stem cell number. Haematopoietic reconstitution during bone marrow transplantation is mediated by a succession of cells at various stages of development. More mature cells contribute to repopulation immediately following transplantation. With time, cells at progressively earlier stages of development are involved, with the final stable repopulation being provided by long-lived, multipotent HSCs. Long-term haematopoiesis is sustained by a relatively small number of HSCs.

APA, Harvard, Vancouver, ISO, and other styles

Linch, D. C. "Haemopoietic stem cell disorders." In Oxford Textbook of Medicine, 4208–13. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.220202.

Full text

Abstract:

The term stem-cell disorder is usually understood to imply that a disease process has begun in a primitive cell with the potential to develop into cells of different lineages. Difficulties with such a definition include (1) malignant change in a very primitive cell does not necessarily lead to the production of mature cells of multiple lineages; (2) although an immature phenotype of a malignant cell may indicate transformation of a very early cell, it is possible that transformation could arise in a later cell with subsequent dedifferentiation....

APA, Harvard, Vancouver, ISO, and other styles

Law, Soi-Cheng, Pascale Wehr, Harriet Purvis, and Ranjeny Thomas. "Dendritic cells and T cells in rheumatoid arthritis." In Oxford Textbook of Rheumatoid Arthritis, 73–84. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198831433.003.0008.

Full text

Abstract:

Dendritic cells (DCs) are specialized antigen-presenting cells which link the innate and adaptive immune responses, activating and priming effector CD4+ T cells, cross-presenting antigen to CD8+ T cells, and promoting B-cell antibody production. DCs also play important roles in the maintenance of immune tolerance. DCs and T cells underpin the basis of the autoimmune response in rheumatoid arthritis. In this chapter we describe the function of DCs and the response of T cells in rheumatoid arthritis pathogenesis, introduce the DC and T-cell players and their function in the immune system, then review the evidence for their involvement in the pathogenesis of rheumatoid arthritis (RA), particularly through the presentation of antigen that triggers the differentiation of autoreactive T cells, as well as innate immune effector functions. Finally, the emerging prospects for DC targeting for immunotherapy are covered.

APA, Harvard, Vancouver, ISO, and other styles

Sun, Dong. "Stem Cell Studies in Traumatic Brain Injury." In Neurotrauma, edited by Dafin Muresanu, Codruta Barle, Ioana Muresanu, Cezara Costin, Johannes Vester, Alexandru Rafila, Olivia Rosu, and Dana Slavoaca, 373–86. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190279431.003.0030.

Full text

Abstract:

Traumatic brain injury (TBI) is a global public health concern, with limited treatment options available. Despite improving survival rates after TBI, there is no effective treatment to improve the neural structural repair and functional recovery of patients. Neural regeneration through neural stem cells, either by stimulating endogenous neural stem cells or by stem cell transplantation, has gained increasing attention as a potential strategy to repair and regenerate the injured brain. This chapter summarizes strategies that have been explored to enhance endogenous neural stem cells-mediated regeneration and recent developments in cell transplantation studies for post-TBI brain repair with varying types of cell sources.

APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "MEL cells"

Yoo, T., and TK Hyun. "Cytotoxic effect of white forsythia (Abeliophyllum distichum Nakai) extracts on human melanoma SK-MEL-2 cells." In 67th International Congress and Annual Meeting of the Society for Medicinal Plant and Natural Product Research (GA) in cooperation with the French Society of Pharmacognosy AFERP. © Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-3400138.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Cross, Kelley, Victoria Palau, Marianne Brannon, Janet Lightner, Megan Dycus, William Stone, and Koyamangalath Krishnan. "Abstract 3568: Delta-tocotrienol and simvastatin induce cytotoxicity and synergy in BRAF mutant SK-MEL-28 but not in wild type BRAF SK-MEL-2 melanoma cancer cells." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3568.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Siddiqui, Imtiaz A., Rohinton S. Tarapore, Vaqar M. Adhami, Dhruba J. Bharali, Zeinab Mohamud, Shaker A. Mousa, and Hasan Mukhtar. "Abstract 5708: Anti-proliferative and pro-apoptotic effects of (−)-epigallocatechin-3-gallate encapsulated in chitosan nanoparticles on human melanoma Mel 928 cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5708.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Kudugunti, Shashi, Helen Thorsheim, Mohammad Yousef, Lan Guan, and Majid Moridani. "Abstract 3241: The selective inhibition of GST by CAPE enhances the cytotoxicity of doxorubicin and camptotechin in SK-MEL-28 melanoma cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3241.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Balyan, Rajiv, Shashi Kudugunti, Nikhil Vad, and Majid Moridani. "Abstract 1345: Bioactivation of luteolin as a prodrug by tyrosinase inhibits human glutathione S-transferase and induces toxicity in SK-MEL-28 melanoma cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1345.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Cambier, P., F. van de werf, and D. collen. "CORONARY THROMBOLYSIS IN DOGS WITH A NONGLYCOSYLATED VARIANT OF HUMAN TISSUE-TYPE PLASMINOGEN ACTIVATOR LACKING THE FINGER AND GROWTH FACTOR DOMAINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643794.

Full text

Abstract:

A variant of human tissue-type plasminogen activator (t-PA-AΔFE3X), with deletion of the NH2-terminal fibronectin-like finger (F) and epidermal growth factor (E) domains, and with amino acid substitution of Gin for Asn at all known N-linked glycosylation sites was expressed in Chinese Hamster Ovary Cells and purified to homogeneity. The thrombolytic and pharmacokinetic properties of this variant were studied in a canine model with copper coil induced thrombosis of the left anterior descending coronary artery. Infusion of t PAΔFE3X at a rate of 5 pg/kg/min for 30 min in 3 dogs resulted in a plateau level in plasma of 0.66 ± 0.08 ug/ml and induced recanalization of the coronary artery within 24 ± 4 min (mean ± SEM). Bolus injections over 2 min of 0.15 mg/kg in 3 dogs resulted in peak antigen levels in plasma of 1.6 ± 0.72 μg/ml and caused reperfusion within 14 ± 6 min. Bolus injection of 0.075 mg/kg in 3 dogs gave plasma antigen levels of 0.81 + 0.20 μg/ml and induced lysis in 31 ±15 min. Further reduction of the bolus to 0.038 mg/kg yielded plasma peak levels of 0.43 ± 0.20 μg/ml but did not cause reperfusion within 3 hours. Bolus injection of 0.075 mg/kg of natural t-PA isolated from melanoma cell culture fluid (Mel-t-PA) resulted in plasma peak levels of 0.46 ± 0.09 μg/ml and caused recanalization within 3 hours in only 1 of 4 dogs. None of the injections was associated with systemic fibrinolytic activation and fibrinogen degradation. The disposition of t-PAΔ related antigen from plasma following bolus injection could be described by a sum of two exponential terms with t1/2α: 17 min and t1/2β: 100 min. No significant difference in disposition rates for the different bolus injections were observed. Corresponding values for t1/2α of Mel-t-PA are 3 min.It is concluded that the deletion mutant t-PAΔFE3X has a markedly slower disposition rate from plasma than intact t-PA, which renders it relatively more effective than natural t-PA after bolus injection.

APA, Harvard, Vancouver, ISO, and other styles

Shekoohi, Sahar, Santhanasabapathy Rajasekaran, Shu Yang, Sureshbabu Nagarajan, Dhaval Patel, Xiuping Yu, and Stephan N. Witt. "Abstract 896: Knocking out the gene (SNCA) that codes for the Parkinson’s disease-related protein alpha-synuclein in SK-Mel-28 melanoma cells significantly retards tumor growth in SCID mice." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-896.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Full text

APA, Harvard, Vancouver, ISO, and other styles

Singh, Ankur, Shalu Suri, Ted T. Lee, Jamie M. Chilton, Steve L. Stice, Hang Lu, Todd C. McDevitt, and Andrés J. Garcia. "Adhesive Signature-Based, Label-Free Isolation of Human Pluripotent Stem Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80044.

Full text

Abstract:

Generation of human induced pluripotent stem cells (hiPSCs) from fibroblasts and other somatic cells represents a highly promising strategy to produce auto- and allo-genic cell sources for therapeutic approaches as well as novel models of human development and disease1. Reprogramming protocols involve transduction of the Yamanaka factors Oct3/4, Sox2, Klf4, and c-Myc into the parental somatic cells, followed by culturing the transduced cells on mouse embryonic fibroblast (MEF) or human fibroblast feeder layers, and subsequent mechanical dissociation of pluripotent cell-like colonies for propagation on feeder layers1, 2. The presence of residual parental and feeder-layer cells introduces experimental variability, pathogenic contamination, and promotes immunogenicity3. Similar to human embryonic stem cells (hESCs), reprogrammed hiPSCs suffer from the unavoidable problem of spontaneous differentiation due to sub-optimal feeder cultures4, growth factors5, and the feeder-free substrate6. Spontaneously differentiated (SD)-hiPSCs display reduced pluripotency and often contaminate hiPSC cultures, resulting in overgrowth of cultures and compromising the quality of residual pluripotent stem cells5. Therefore, the ability to rapidly and efficiently isolate undifferentiated hiPSCs from the parental somatic cells, feeder-layer cells, and spontaneously differentiated cells is a crucial step that remains a bottleneck in all human pluripotent stem cell research.

APA, Harvard, Vancouver, ISO, and other styles

Gewirtz, A., W. Y. Xu, B. Rucinski, and S. Niewiarowski. "SELECTIVE INHIBITION OF HUMAN MEGAKARYOCYTOPOIESIS IN VITRO BY HIGHLY PURIFIED PLATELET FACTOR 4." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644621.

Full text

Abstract:

Platelet (plt) factor 4 (PF4) is an alpha granule protein which can modulate T lymphocyte function. T cells may help regulate megakaryocytopoiesis. Therefore, we hypothesized that T cell-PF4 interactions might play a role in autoregulating marrow megakaryocyte (MEG) production. To test this idea, we studied MEG colony formation in plasma clot cultures containing human serum derived solely from pit poor normal AB plasma, enriched hematopoietic progenitor cells (HPC), autologous T cells, and exogenous PF4. Highly purified PF4 (single band on SDS gel) was prepared from outdated human pits by a combination of heparin-agarose, Sephacryl G-200, and Sephadex G-50 column chromatography. HPC were prepared by depleting normal light density marrow mononuclear cells of adherent monocytes, and T cells. T cells were further fractionated into helper (Leu 3+) and suppressor (Leu 2+) subtypes by solid phase immunoabsorption ("panning"). MEG colonies were enumerated by indirect immunofluorescence with an anti-human platelet glycoprotein antiserum. HPC(5×105/ml) were co-cultured with Leu 3+, or Leu 2+ T cells at target;T cell ratios of 2:1 (n=3; n=4 respectively) and l:l(n=4; n=4 respectively) in the presence of 2.5 μg/ml PF4. Under these growth conditions, MEG colony formation was unchanged (p>0.5) when compared to colonies formed by HPC in the absence of PF4. When the above experiments were repeated (n=2-3/condition) at a higher PF4 concentration [25 μg/ml], MEG colony formation was markedly (>60%) inhibited. To determine if PF4 directly inhibited MEG or erythroid progenitor cell growth (CFU-Meg; CFU-E) in vitro, HPC were cloned in PF4 (25μg/ml) without added T cells. Mean ± SEM of MEG and CFU-E derived colonies formed without vs. with PF4 was as follows:These results suggest that: 1) PF4 may be a non-T cell dependent, lineage specific inhibitor of CFU-MEG, and 2) PF4 may play a role in autoregulating human megakaryocytopoiesis.

APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "MEL cells"

Ward, C. R. DWPF Melt Cell Crawler. Office of Scientific and Technical Information (OSTI), April 2003. http://dx.doi.org/10.2172/809743.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Zhu, Yimin. Engineered Nanostructured MEA Technology for Low Temperature Fuel Cells. Office of Scientific and Technical Information (OSTI), July 2009. http://dx.doi.org/10.2172/959141.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Yandrasits, Michael A. Final Report - MEA and Stack Durability for PEM Fuel Cells. Office of Scientific and Technical Information (OSTI), February 2008. http://dx.doi.org/10.2172/923720.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Conrad, Susan E. A Role for MEK-Interacting Protein 1 in Hormone Responsiveness of ER Positive Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2010. http://dx.doi.org/10.21236/ada540806.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Full text

APA, Harvard, Vancouver, ISO, and other styles

Conrad, Susan E. A Role for MEK-Interacting Protein 1 In Hormone Responsiveness of ER Positive Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada560599.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Kilejian, Lisa. The Influence of Trichinella Spiralis Infection on Heat Shock Protein 72 Production in MRL++ Mouse Intestinal Cells. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.6474.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Masamha, Chioniso P. Deciphering the Mechanism of Alternative Cleavage and Polyadenylation in Mantle Cell Lymphoma (MCL). Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada612793.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Full text

APA, Harvard, Vancouver, ISO, and other styles

Conrad, Susan E. A Role for MEK-Interacting Protein 1 (MP1) in Hormone Responsiveness of Estrogen Receptor-Positive Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2008. http://dx.doi.org/10.21236/ada491116.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

Contents

Academic literature on the topic 'MEL cells'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Journal articles on the topic "MEL cells"

Dissertations / Theses on the topic "MEL cells"

Books on the topic "MEL cells"

Book chapters on the topic "MEL cells"

Conference papers on the topic "MEL cells"

Reports on the topic "MEL cells"