Dissertations / Theses on the topic 'Melania G'
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Keuper, Melanie [Verfasser], and Klaus G. [Akademischer Betreuer] Nickel. "Transformationskinetik der Niedertemperaturumwandlung von Zirkoniumdioxid / Melanie Keuper ; Betreuer: Klaus G. Nickel." Tübingen : Universitätsbibliothek Tübingen, 2015. http://d-nb.info/1197058257/34.
Full textKnospe, Melanie [Verfasser]. "Molekularbiologie und Pharmakologie neuer G-Protein-gekoppelter Purin-Rezeptoren / Melanie Knospe. Mathematisch-Naturwissenschaftliche Fakultät." Bonn : Universitäts- und Landesbibliothek Bonn, 2012. http://d-nb.info/1021605433/34.
Full textStolzenberg, Melanie [Verfasser]. "Retrospektive Analyse der laparoskopisch assistierten suprazervikalen Hysterektomie (LASH) bei großen Uteri (≥ 500 g) / Melanie Stolzenberg." Greifswald : Universitätsbibliothek Greifswald, 2015. http://d-nb.info/1073591166/34.
Full textNeyra, Jennifer Eliana Montoya. "Modulação dos efeitos citotóxicos dos vemurafenibe pela cloroquina em células de melanoma maligno G-361: papel da dermicidina." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-30012018-101101/.
Full textIn this study we evaluated the pharmacological effects of vemurafenib ( inhibitor BRAFV600E) and chloroquine (autophagy inhibitor) in cell viability and tumor growth of two melanoma cell lines identified as G-361 pLKO, which expresses dermcidin, and G361 IBC I which silenced DCD expression. G-361 melanoma cells responded to vemurafenib (1-2 μM) and chloroquine (50-100 μM) alone or combined, with increased apoptosis rates, while decreasing senescent cells. Vemurafenib (50 mg/kg / 21 days) inhibited melanoma growth in immunodeficient mice independent of dermicidin. Chloroquine (30 mg/kg) in combination with vemurafenib, accelerated (at 24 hour interval), and reduced (at 72 hours interval), melanoma growth. Tumor tissues showed atypical cell morphology and nuclear histological patterns and melanocytic differentiation biomarkers S100, HMB-45, Melan-A or pancytokeratins were not. This work confirms the efficacy of vemurafenib and suggests potential adjuvant effect of chloroquine. It also confirms the role of dermcidin as growth factor and oncogene for melanoma cells.
Castillo, Miguel Angel Zuñiga. "Expressão do antígeno leucocitário humano G, interleucina 10 e macrófagos M2 no melanoma lentiginoso acral." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5133/tde-31072017-125708/.
Full textBACKGROUND: Acral lentiginous melanoma (ALM) is an uncommon cutaneous tumor that usually has an aggressive behavior and results in an unfavorable prognosis. The pathogenic mechanism related to the clinical evolution remains unknown. Currently, evasion mechanisms related to the melanoma microenvironment, which can inhibit the anti-tumor immune response allowing disease progression, are the focus of numerous studies. The expression of human leukocyte antigen-G (HLA-G), Interleukin- 10 (IL-10) and M2-Macrophages (MM2) at the tumor site represents one of these immunosuppressive strategies developed for some neoplasms. However, those factors have not been studied specifically in ALM. OBJECTIVES: In order to verify if HLAG and IL-10 tumoral expression as well as MM2 population in the melanoma microenvironment are related to the histopathological features predictive of unfavorable prognosis in melanoma and metastasis, we compared those markers and cells between ALM and superficial spreading melanoma (SSM) groups. METHODS: We analyzed 67 ALM and 67 SSM cases. The tumors were classified in groups according thickness, ulceration, mitosis and metastasis. HLA-G, IL-10 and MM2 (CD163+ and CD206+) expression were evaluated using immunohistochemistry. The expression (tumoral positive area fraction) of HLA-G and IL-10, as well as the number of MM2 in the intratumoral and peritumoral area was compared between the groups of melanomas using Kruskal-Wallis and Wilcoxon\'s tests. The Pearson\'s test was used to establish the correlation between HLA-G and IL-10, as well as between CD163 and CD206. Also, a binary logistic regression model was used to analyze all variables in relation to metastasis. RESULTS: HLA-G and IL-10 tumoral expression as well as the number of MM2 in the intratumoral and peritumoral area was increased in ALM compared with SSM (p < 0.05). There was positive correlation between HLA-G and IL-10 tumoral expression, as well as between the number of MM2 marked by CD163 and CD206. In the binary logistic regression model, the MM2 CD206+ of the intratumoral area was significantly associated with metastasis. CONCLUSIONS: The HLA-G and IL-10 melanoma expression likewise the high number of MM2 in the tumoral microenvironment must be considered as features associated with the increased aggressiveness of the ALM
Oliveira, Cristiane de 1985. "Influência dos polimorfismos P53 ARG72PRO, MDM2 T309G, BCL2 C(-938)A e BAX G(-248)A, relacionados com apoptose celular, na susceptibilidade ao melanoma cutâneo = Influence of the polymorphisms P53 ARG72PRO, MDM2 T309G, BCL2 C (-938) A and BAX G (-248) A, involved with cellular apoptosis, incutaneous melanoma susceptibility." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308612.
Full textDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas.
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Resumo: Os genes P53 e BAX (pró-apoptóticos) e MDM2 e BCL2 (antiapoptóticos) atuam na morte de células epiteliais danificadas por raios ultravioleta (UV) da luz solar e estão relacionados com a origem do melanoma cutâneo (MC). A proteína codificada pelo alelo selvagem Arg do polimorfismo P53 Arg72Pro induz melhor a apoptose do que a do alelo variante Pro. Os alelos variantes G e A dos polimorfismos MDM2 T309G e BCL2 C(-938)A e o alelo variante A do polimorfismo BAX G(-248)A estão relacionados com maior e menor expressão proteica, respectivamente, quando comparados aos alelos selvagens T, C e G. Como são incertos os papéis desses polimorfismos no risco e manifestações clínicas do MC, estes foram os principais objetivos do presente estudo. O DNA genômico de 150 pacientes e de 150 controles foi analisado por meio da reação em cadeia da polimerase e digestão enzimática. As frequências dos genótipos P53 ArgArg (58,7% vs 44,7%, P= 0,02) e BCL2 AA (28,0% vs 15,3%, P= 0,004) foram maiores em pacientes do que em controles. Portadores dos genótipos estiveram sob riscos 1,86 e 2,87 vezes maior de MC do que os demais, respectivamente. Excessos dos genótipos combinados P53 ArgArg + BCL2 AA (36,1% vs 16,9%, P= 0,002) e P53 ArgArg + BAX AA (29,5% vs 15,3%, P= 0,008) foram observados em pacientes comparados a controles. Indivíduos com os respectivos genótipos estiveram sob riscos 3,43 e 2,71 vezes maior de ocorrência do MC do que os demais, respectivamente. Concluímos que os polimorfismos P53Arg72Pro, BCL2 C(-938)A e BAX G(-248)A alteraram o risco de ocorrência do MC em nossa amostra e indivíduos com os genótipos ArgArg, AA e AA dos respectivos polimorfismos devem receber recomendações adicionais para proteção da pele dos efeitos nocivos dos raios UV e seguimento médico com exames dermatológicos periódicos, para prevenção e diagnóstico precoce do tumor
Abstract: The P53 and BAX (proapoptotic) and MDM2 and BCL2 (antiapoptotic) genes remove cells damaged by ultraviolet (UV) rays of the sunlight and, therefore, are related to the cutaneous melanoma (CM) origin. The Arg wild allele of the P53 Arg72Pro polymorphism is more efficient in inducing apoptosis than the variant Pro allele. The variant G and A alleles of the MDM2 T309G and BCL2 C(-948)A polymorphisms, and the A allele of the BAX G(-248) A polymorphism are related to higher and lower expressions of the encoded proteins, respectively, than the wild T, C and G wild alleles. Since the roles of the referred genetic polymorphisms on the risk and clinical manifestation of the tumor are still unclear, these were the main aims of the present study. Genomic DNA from 150 patients with CM and 150 controls was analyzed by polymerase chain reaction and enzymatic digestion. The frequencies of the P53 ArgArg and the BCL2 AA genotypes were higher in patients than in controls (58.7% versus 44.7%, P= 0.02) and (28.0% versus 15.3%, P= 0.004) respectively. Carriers of these genotypes had a 1.86 and 2.87-fold increased risks for MC than others, respectively. Excesses of the P53 ArgArg + BCL2 AA and P53 ArgArg + BAX AA were seen in patients when compared to controls (36.1% versus 16.9%, P= 0.002) and (29.5% versus 15.3%, P= 0.008), and carriers of these genotypes had a 3.43 and 2.71-fold increased risks for CM than others, respectively. We concluded that the P53 Arg72Pro, BCL2 C(-938)A and BAX G(-248)A polymorphisms alter the risk for CM in our sample. We believe that carriers of the ArgArg wild genotype and the variant AA genotypes of the respective genetic polymorphisms should receive additional recommendation to avoid exposition to sunlight and should be frequently evaluated by a dermatologist with the purpose of preventing and performing an early diagnosis of the disease, respectively
Mestrado
Biologia Estrutural, Celular, Molecular e do Desenvolvimento
Mestre em Fisiopatologia Médica
Regler, Melanie [Verfasser], and Werner G. [Akademischer Betreuer] Daniel. "Antiatherosklerotische Eigenschaften von Resveratrol: Molekulare und funktionale Effekte auf humane Endothelzellen und Monozyten / Melanie Regler. Betreuer: Werner G. Daniel." Erlangen : Universitätsbibliothek der Universität Erlangen-Nürnberg, 2012. http://d-nb.info/1025963849/34.
Full textCadan, Fellipe Magioli. "Otimização da síntese de nitreto de carbono grafítico e a formação de heteroestruturas com trióxido de tungstênio." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/75/75135/tde-29092017-172815/.
Full textThis study proposed an assessment of the role of the three major classical parameters for synthesizing graphitic carbon nitride: final temperature, residence time at the final temperature and heating rate. The synthesis was optimized, via response surface methodology, using the photocatalytic degradation of a model pollutant (tatrazine) as the response-variable. The statistical significance of the factors was confirmed, within 95% confidence level. Afterwards, a second-order model was adjusted to the better responses and, at the maximum degradation point, the conditions were: 605oC for 183 min, with heating rate of 5oC min-1. The degradation rate with the synthetized photocatalyst was approximately three times greater than the photolytic one. The samples from the better response region were analyzed in a series of characterization experiments: X ray diffractometry, mid-infrared spectrometry, specific surface area, scanning electron microscopy (SEM and FEG-SEM), zeta potential, and ultraviolet-visible diffuse reflectance spectroscopy. The most active photocatalyst showed smaller band gap energy and greater specific surface area than the ones reported in literature (2.59 eV and 29.5 m2 g-1, respectively). Heterostructures were formed between the synthetized photocatalyst and tungsten trioxide. A series of basic characterization techniques confirmed the heterostructure formation. Using this heterostructure, the degradation rate was approximately five times greater than the one with graphitic carbon nitride.
Nash, Kevin T. "KISS1 matastasis suppressor secretion is required for metastasis suppression." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2006. https://www.mhsl.uab.edu/dt/2008r/nash.pdf.
Full textSosa, Nancy Marcela perez. "Análise da expressão de genes regulados pela proteína Dermicidina nas células do melanoma maligno G-361 pelo método de DNA-microarray." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-24102014-124556/.
Full textDermcidin (DCD) is a human gene mapped to chromosome 12q13 region, only identified in primates and humans, and normally expressed in the eccrine glands of skin and brain. Several studies have confirmed that DCD-derived peptides contribute to innate and immune surveillance and in the oncogenic processes of breast, prostate and skin cancers, as revealed by its role as a growth factor and cell survival. We have further explored DCD function and its tumorigenic potential on skin melanocytes by specifically knocking down its expression in G-361 malignant melanoma cells via expressing constitutively short hairpin RNA against DCD mRNA. Biological and biochemical assays showed that the \"knockdown\" in the expression of DCD in G-361-pLKO control clone and a G-361-IBC-I clone expressing constitutively short hairpin RNA against DCD mRNA decreased significantly the in vitro growth in cell culture and tumor formation in nude mice. Similar results were obtained treating nude mice bearing G-361 melanoma xenografts with rabbit polyclonal antibodies against DCD protein. Here, we present a DNA microarray-based study that identified the genes that are up- and down-regulated in a G-361-pLKO control clone and a G-361-IBC-I clone expressing constitutively short hairpin RNA against DCD mRNA. A total of 372 genes differentially expressed were identified; being 162 genes up-regulated and 212 genes down-regulated. Bioinformatic studies showed that DCD gene silencing modulates canonical pathways and signaling networks mediated APRIL/BAFF receptors and ligands and NF-kB signaling pathway as well as chromatin remodeling mediated by histone family. The mRNA expression levels of 9 genes of interest were validated by RT-qPCR assays. Next we analyzed the proteins present in nuclear extracts from G-361- pLKO and G-361-IBC-I clones by mass spectrometry. We identified 74 proteins in the G-361-pLKO clone and 31 proteins in the G-361-IBC-I. A group of 21 proteins was identified in both sublineages. Bioinformatics analyses by STRING (Search Tool for the Retrieval of Interacting Genes/Proteins) platform showed that a small portion of the proteins identified only in G-361- pLKO cells was predicted to interact directly with DCD. The network formed by these proteins is centered in the p53 protein, a key regulator of survival and cell death program in response to DNA damage and oxidative stress. On the other hand, this network was completed abrogated using the nuclear protein from G-361-IBC-I because of absence of DCD protein. Since most of the proteins identified in nuclear extracts are of the histone family, it is likely that they are acting in the chromatin-remodeling complexes which are important to remodel nucleosomes of the G-361-IBC-I cells. Our results allowed us to suggest that future studies on the expression of histones and their posttranslational modifications may help to unravel the possible role of DCD in the epigenetic regulation of melanoma and other cancers
Melo, Estêvão Azevedo 1989. "Análise do efeito inibidor de FASN orlistat sobre a produção de IL-10, IL-12, IFN-G e TGF-B em células de melanoma murino B16-F10." [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/290684.
Full textDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
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Resumo: A ácido graxo sintase (FASN) é a enzima responsável pela biossíntese endógena de ácidos graxos e apontada como uma oncoproteína metabólica, por favorecer a proliferação e sobrevivência das células tumorais nas quais sua expressão é elevada. Vários são os compostos capazes de inibir a atividade de FASN, dentre eles o orlistat (Xenical®), que possui efeitos antiproliferativos previamente mostrados em células de câncer de mama, próstata, boca e melanoma. O sistema imunológico apresenta um importante papel na prevenção e defesa do organismo contra neoplasias malignas. As células do sistema imune que se infiltram nos melanomas são produtoras de uma vasta gama de citocinas, dentre elas interleucina 12 (IL-12) e interferon gama (IFN-?) que favorecem uma resposta imune bem sucedida contra os tumores, porém, as células dos melanomas possuem capacidade de produzir interleucina 10 (IL-10) e fator de crescimento transformante beta (TGF-?), capazes de inibir as células imunocompetentes, favorecendo a progressão tumoral e disseminação metastática. O objetivo deste estudo foi avaliar a secreção das citocinas IL-10, IL-12, IFN-? e TGF-? pelas células de melanoma murino B16-F10 após tratamento com orlistat. Para isto, inicialmente determinou-se a dosagem de orlistat capaz de inibir a proliferação celular em 50% (IC50). Em seguida, as células foram tratadas por 24 e 48 horas, quando realizou-se a quantificação da secreção das citocinas por ELISA. Após 24 horas de tratamento, observou-se aumento da secreção de IL-10 e IL-12, no entanto, após 48 horas de tratamento não foi detectada diferenças estatisticamente significantes na secreção de ambas as citocinas, quando comparadas aos seus controles. IFN-? e TGF-? não foram detectáveis. Assim, os resultados desta pesquisa mostram que o tratamento com orlistat alterou a produção das citocinas IL-10 e IL-12, sugerindo que o tratamento promove um equilíbrio entre estas citocinas pró e anti-inflamatórias nas células estudadas
Abstract: Fatty acid synthase (FASN) is the enzyme responsible for the endogenous biosynthesis of fatty acids suggested as a metabolic oncoprotein by promoting proliferation and survival of cancer cells. Several compounds are known to inhibit FASN activity, including orlistat (Xenical®), which has antiproliferative effects in breast, prostate, and oral cancer as well as melanoma cells. Melanoma is an aggressive malignant tumor of melanocytes with high propensity for metastatic spread and resistant to chemotherapy. The immune system plays an important role in the prevention and defense against malignant neoplams. In fact, immune cells that infiltrate melanomas produce a wide range of cytokines, such as interleukin 12 (IL-12) and interferon gamma (IFN-?), which favor a successful immune response against the tumor. However, melanomas cells are able to produce interleukin 10 (IL-10) and transforming growth factor beta (TGF-?) and in turn inhibit immunocompetent cells, favoring tumor progression and metastatic spread. The aim of this research was to evaluate the effect of the FASN inhibitor orlistat on the secretion of the cytokines IL-10, IL-12, IFN-? and TGF-? by B16-F10 mouse melanoma cells. For this purpose, we first searched for the IC50 Of orlistat in B16-F10 cells. Then, cells were treated for 24 and 48 hours with the drug and the secretion of cytokines quantified by ELISA. After 24 hours of treatment the secretion of IL-10 and IL-12 was increased, however, after 48 hours there were no statistically significant changes in the secretion of both cytokines, compared to their controls. IFN-? and TGF-? were not detectable. Thus, the results of this study show that the treatment with orlistat change the production of IL-10 and IL-12, suggesting a balance between the secretion of pro- and anti-inflammatory cytokines
Mestrado
Estomatopatologia
Mestre em Estomatopatologia
Sirch, Melanie Sophia Christina [Verfasser], and Sascha [Akademischer Betreuer] Meyer. "Beurteilung der parenteralen Ernährung bei Frühgeborenen unter 1500 g im Universitätsklinikum des Saarlandes im Vergleich zu publizierten Leitlinien / Melanie Sophia Christina Sirch ; Betreuer: Sascha Meyer." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2019. http://d-nb.info/1185484639/34.
Full textSirch, Melanie [Verfasser], and Sascha [Akademischer Betreuer] Meyer. "Beurteilung der parenteralen Ernährung bei Frühgeborenen unter 1500 g im Universitätsklinikum des Saarlandes im Vergleich zu publizierten Leitlinien / Melanie Sophia Christina Sirch ; Betreuer: Sascha Meyer." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2019. http://d-nb.info/1185484639/34.
Full textMeißner, Saskia Melanie [Verfasser], and G. [Akademischer Betreuer] Weiß. "Dynamik atomarer Tunnelsysteme in dünnen, ungeordneten AlOₓ-Schichten - Einzelne Tunnelsysteme in Josephson-Kontakten und Zustandsdichte in Al-AlOₓ-Al-Kondensatoren / Saskia Melanie Meißner ; Betreuer: G. Weiß." Karlsruhe : KIT-Bibliothek, 2017. http://d-nb.info/1137946547/34.
Full textHohmann, Maria Melanie [Verfasser]. "Haben die Einführung von strenger Rückenlagerung über 72 Stunden und die pränatale Steroidverabreichung Einfluss auf die Inzidenz von intraventrikulärer Hirnblutung bei Frühgeborenen unter 1500 g? / Maria Melanie Hohmann." Kiel : Universitätsbibliothek Kiel, 2017. http://d-nb.info/1144269806/34.
Full textChaushova, Aleksandra. "L'appropriation de l'art contemporain par les artistes du bloc de l'Est. Étude sur le positionnement culturel (V. Komar et A. Melamid, Z. Kulik, G. Richter)." Doctoral thesis, Universite Libre de Bruxelles, 2018. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/278723.
Full textDoctorat en Art et Sciences de l'Art
info:eu-repo/semantics/nonPublished
Guemiri, Ramdane. "Etude de l’implication du complexe eIF4F dans la réponse immune antitumorale via la régulation traductionnelle de l’axe STAT1-PD-L1 dans le mélanome métastatique." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS351.
Full textThe eukaryotic translation initiation complex eIF4F is subject of an increased interest in the field of cancer. This heterotrimeric complex, comprising the RNA helicase eIF4A, the cap-binding protein eIF4E and the scaffold protein eIF4G, is known to be more abundant and active in tumor cells than non-malignant counterparts.In a previous work, we showed that this complex is implicated in the resistance to melanoma-targeted therapies (Boussemart et al, Nature 2014). Furthermore, it is implicated in the resistance to various chemotherapies. Thus, agents targeting the eIF4F complex appear as promising tools in the field of cancer therapy.On the other hand, immunotherapy, by (re)stimulating and enhancing the host immune system against tumors is giving good clinical results in oncology treatment and appears nowadays as the most promising approach to fight cancer, especially anti-PD1 treatment. Even though immunotherapy has demonstrated remarkable results in curing some established cancers, such as advanced melanoma or Hodgkin’s lymphoma, many tumors relapse or fail to respond. It is thus important to still look for a new strategy enhancing the efficacy of actual treatments. Here, we propose to study the impact of inhibiting the eIF4F complex on the tumor-specific immune response
Vollert, Seike [Verfasser], Kai-Martin [Akademischer Betreuer] Thoms, Steffen [Akademischer Betreuer] Emmert, Jochen [Akademischer Betreuer] Reiss, and Patricia [Akademischer Betreuer] Virsik-köpp. "Xeroderma-Pigmentosum-Gruppe-C- und -G-Gen-Polymorphismen: Alternatives Splicing und funktionelle DNA-Reparatur beim multiplen Melanom / Seike Vollert. Gutachter: Steffen Emmert ; Jochen Reiss ; Patricia Virsik-Köpp. Betreuer: Kai-Martin Thoms." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2011. http://d-nb.info/1042348596/34.
Full textMukherjee, Madhuparna, and Madhuparna Mukherjee. "The Role of G-Protein Coupled Receptor 56 in the Cellular Functions of Melanoma Cells." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/z84yd8.
Full text長庚大學
分子醫學全英語碩士學位學程
104
This study indicates that the melanoma cells MeWo, A375 GPR56 WT, A375 Neo and two mutant cells of A375 GPR56 WT, one is A375 GPR56 T383A having GAIN domain deficiency at GPS auto proteolytic site and another is A375 GPR56 TM1 having one transmembrane domain, allowed to crosslink with anti GPR56 mAb CG4, to observe whether they have any GPR56 specific effect on dose and time dependent cell adhesion assay. However dose dependent assay helps to detect in which concentration of antibody the phenotypic expression of the cells would be more appropriate. We clearly demonstrates that through successive time duration, CG4 after crosslinking to MeWo, A375 GPR56 WT and A375 GPR56 T383A cells, have some inhibitory responses resulting in less adhesion phenomenon compared to A375 Neo and A375 GPR56 TM1 cell lines. It’s highly considerable to distinguish GPR56 specific differences with the treatment of melanoma cells in crosslinking to control mAbs mIgG1 and CG3 (ligand binding). Besides it also indicates that GAIN domain at GPS auto proteolytic site are not necessary in cell adhesion but also N terminal and C terminal segment along with seven transmembrane domain are responsible. After that we want to reveal the signaling pathways involved in GPCR56-mediated cell adhesion, so after 3-5hrs of incubation, we are able to find out the phenotypic changes of MeWo cells treated with 5μM and 10μM of signaling molecule inhibitors such as Erk, Jnk, p38, in comparison with PI3K, ROS inhibitors. It results that GPR56 mediated signaling molecules Erk, Jnk and p38 inhibitors treated cells showed less number of adherent cells after crosslinking to CG4 mAb compared with control Abs mIgG1 and CG3.
Vollert, Seike. "Xeroderma-Pigmentosum-Gruppe-C- und -G-Gen-Polymorphismen: Alternatives Splicing und funktionelle DNA-Reparatur beim multiplen Melanom." Doctoral thesis, 2011. http://hdl.handle.net/11858/00-1735-0000-0006-B1E8-5.
Full textJayasinghe, Melany [Verfasser]. "Nachweis von δ-Opioidrezeptoren [delta-Opioidrezeptoren] auf Melanozyten der Melanomzellinie G-361 / vorgelegt von Melany Jayasinghe." 2004. http://d-nb.info/97184612X/34.
Full textKatzer, Kerstin. "Flowzytometrische Messung der intrazellulären Interferon-g-Produktion [Interferon-gamma-Produktion] peripherer T-Lymphozyten bei Patienten mit malignem Melanom /." 2005. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=014644524&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.
Full text