Relevant bibliographies by topics / Cytokinesis Genetic aspects

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Academic literature on the topic 'Cytokinesis Genetic aspects'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 January 2023

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Journal articles on the topic "Cytokinesis Genetic aspects"

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Soyano, Takashi, Masaki Ishikawa, Ryuichi Nishihama, Satoshi Araki, Mayumi Ito, Masaki Ito, and Yasunori Machida. "Control of plant cytokinesis by an NPK1–mediated mitogen–activated protein kinase cascade." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 357, no. 1422 (June 29, 2002): 767–75. http://dx.doi.org/10.1098/rstb.2002.1094.

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Cytokinesis is the last essential step in the distribution of genetic information to daughter cells and partition of the cytoplasm. In plant cells, various proteins have been found in the phragmoplast, which corresponds to the cytokinetic apparatus, and in the cell plate, which corresponds to a new cross wall, but our understanding of the functions of these proteins in cytokinesis remains incomplete. Reverse genetic analysis of NPK1 MAPKKK (nucleus– and phragmoplast–localized protein kinase 1 mitogen–activated protein kinase kinase kinase) and investigations of factors that might be functionally related to NPK1 have helped to clarify new aspects of the mechanisms of cytokinesis in plant cells. In this review, we summarize the evidence for the involvement of NPK1 in cytokinesis. We also describe the characteristics of a kinesin–like protein and the homologue of a mitogen–activated protein kinase that we identified recently, and we discuss possible relationships among these proteins in cytokinesis.
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Guertin, David A., Susanne Trautmann, and Dannel McCollum. "Cytokinesis in Eukaryotes." Microbiology and Molecular Biology Reviews 66, no. 2 (June 2002): 155–78. http://dx.doi.org/10.1128/mmbr.66.2.155-178.2002.

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SUMMARY Cytokinesis is the final event of the cell division cycle, and its completion results in irreversible partition of a mother cell into two daughter cells. Cytokinesis was one of the first cell cycle events observed by simple cell biological techniques; however, molecular characterization of cytokinesis has been slowed by its particular resistance to in vitro biochemical approaches. In recent years, the use of genetic model organisms has greatly advanced our molecular understanding of cytokinesis. While the outcome of cytokinesis is conserved in all dividing organisms, the mechanism of division varies across the major eukaryotic kingdoms. Yeasts and animals, for instance, use a contractile ring that ingresses to the cell middle in order to divide, while plant cells build new cell wall outward to the cortex. As would be expected, there is considerable conservation of molecules involved in cytokinesis between yeast and animal cells, while at first glance, plant cells seem quite different. However, in recent years, it has become clear that some aspects of division are conserved between plant, yeast, and animal cells. In this review we discuss the major recent advances in defining cytokinesis, focusing on deciding where to divide, building the division apparatus, and dividing. In addition, we discuss the complex problem of coordinating the division cycle with the nuclear cycle, which has recently become an area of intense research. In conclusion, we discuss how certain cells have utilized cytokinesis to direct development.
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Neto, Hélia, Louise L. Collins, and Gwyn W. Gould. "Vesicle trafficking and membrane remodelling in cytokinesis." Biochemical Journal 437, no. 1 (June 14, 2011): 13–24. http://dx.doi.org/10.1042/bj20110153.

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All cells complete cell division by the process of cytokinesis. At the end of mitosis, eukaryotic cells accurately mark the site of division between the replicated genetic material and assemble a contractile ring comprised of myosin II, actin filaments and other proteins, which is attached to the plasma membrane. The myosin–actin interaction drives constriction of the contractile ring, forming a cleavage furrow (the so-called ‘purse-string’ model of cytokinesis). After furrowing is completed, the cells remain attached by a thin cytoplasmic bridge, filled with two anti-parallel arrays of microtubules with their plus-ends interdigitating in the midbody region. The cell then assembles the abscission machinery required for cleavage of the intercellular bridge, and so forms two genetically identical daughter cells. We now know much of the molecular detail of cytokinesis, including a list of potential genes/proteins involved, analysis of the function of some of these proteins, and the temporal order of their arrival at the cleavage site. Such studies reveal that membrane trafficking and/or remodelling appears to play crucial roles in both furrowing and abscission. In the present review, we assess studies of vesicular trafficking during cytokinesis, discuss the role of the lipid components of the plasma membrane and endosomes and their role in cytokinesis, and describe some novel molecules implicated in cytokinesis. The present review covers experiments performed mainly on tissue culture cells. We will end by considering how this mechanistic insight may be related to cytokinesis in other systems, and how other forms of cytokinesis may utilize similar aspects of the same machinery.
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O'Connell, Kevin F., Charles M. Leys, and John G. White. "A Genetic Screen for Temperature-Sensitive Cell-Division Mutants of Caenorhabditis elegans." Genetics 149, no. 3 (July 1, 1998): 1303–21. http://dx.doi.org/10.1093/genetics/149.3.1303.

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Abstract A novel screen to isolate conditional cell-division mutants in Caenorhabditis elegans has been developed. The screen is based on the phenotypes associated with existing cell-division mutations: some disrupt postembryonic divisions and affect formation of the gonad and ventral nerve cord—resulting in sterile, uncoordinated animals—while others affect embryonic divisions and result in lethality. We obtained 19 conditional mutants that displayed these phenotypes when shifted to the restrictive temperature at the appropriate developmental stage. Eighteen of these mutations have been mapped; 17 proved to be single alleles of newly identified genes, while 1 proved to be an allele of a previously identified gene. Genetic tests on the embryonic lethal phenotypes indicated that for 13 genes, embryogenesis required maternal expression, while for 6, zygotic expression could suffice. In all cases, maternal expression of wild-type activity was found to be largely sufficient for embryogenesis. Cytological analysis revealed that 10 mutants possessed embryonic cell-division defects, including failure to properly segregate DNA, failure to assemble a mitotic spindle, late cytokinesis defects, prolonged cell cycles, and improperly oriented mitotic spindles. We conclude that this approach can be used to identify mutations that affect various aspects of the cell-division cycle.
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Ralston, Katherine S., Alana G. Lerner, Dennis R. Diener, and Kent L. Hill. "Flagellar Motility Contributes to Cytokinesis in Trypanosoma brucei and Is Modulated by an Evolutionarily Conserved Dynein Regulatory System." Eukaryotic Cell 5, no. 4 (April 2006): 696–711. http://dx.doi.org/10.1128/ec.5.4.696-711.2006.

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ABSTRACT The flagellum of Trypanosoma brucei is a multifunctional organelle with critical roles in motility and other aspects of the trypanosome life cycle. Trypanin is a flagellar protein required for directional cell motility, but its molecular function is unknown. Recently, a trypanin homologue in Chlamydomonas reinhardtii was reported to be part of a dynein regulatory complex (DRC) that transmits regulatory signals from central pair microtubules and radial spokes to axonemal dynein. DRC genes were identified as extragenic suppressors of central pair and/or radial spoke mutations. We used RNA interference to ablate expression of radial spoke (RSP3) and central pair (PF16) components individually or in combination with trypanin. Both rsp3 and pf16 single knockdown mutants are immotile, with severely defective flagellar beat. In the case of rsp3, this loss of motility is correlated with the loss of radial spokes, while in the case of pf16 the loss of motility correlates with an aberrant orientation of the central pair microtubules within the axoneme. Genetic interaction between trypanin and PF16 is demonstrated by the finding that loss of trypanin suppresses the pf16 beat defect, indicating that the DRC represents an evolutionarily conserved strategy for dynein regulation. Surprisingly, we discovered that four independent mutants with an impaired flagellar beat all fail in the final stage of cytokinesis, indicating that flagellar motility is necessary for normal cell division in T. brucei. These findings present the first evidence that flagellar beating is important for cell division and open the opportunity to exploit enzymatic activities that drive flagellar beat as drug targets for the treatment of African sleeping sickness.
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Smith, Gregory R., Scott A. Givan, Paul Cullen, and George F. Sprague. "GTPase-Activating Proteins for Cdc42." Eukaryotic Cell 1, no. 3 (June 2002): 469–80. http://dx.doi.org/10.1128/ec.1.3.469-480.2002.

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ABSTRACT The Rho-type GTPase, Cdc42, has been implicated in a variety of functions in the yeast life cycle, including septin organization for cytokinesis, pheromone response, and haploid invasive growth. A group of proteins called GTPase-activating proteins (GAPs) catalyze the hydrolysis of GTP to GDP, thereby inactivating Cdc42. At the time this study began, there was one known GAP, Bem3, and one putative GAP, Rga1, for Cdc42. We identified another putative GAP for Cdc42 and named it Rga2 (Rho GTPase-activating protein 2). We confirmed by genetic and biochemical criteria that Rga1, Rga2, and Bem3 act as GAPs for Cdc42. A detailed characterization of Rga1, Rga2, and Bem3 suggested that they regulate different subsets of Cdc42 function. In particular, deletion of the individual GAPs conferred different phenotypes. For example, deletion of RGA1, but not RGA2 or BEM3, caused hyperinvasive growth. Furthermore, overproduction or loss of Rga1 and Rga2, but not Bem3, affected the two-hybrid interaction of Cdc42 with Ste20, a p21-activated kinase (PAK) kinase required for haploid invasive growth. These results suggest Rga1, and possibly Rga2, facilitate the interaction of Cdc42 with Ste20 to mediate signaling in the haploid invasive growth pathway. Deletion of BEM3 resulted in cells with severe morphological defects not observed in rga1Δ or rga2Δ strains. These data suggest that Bem3 and, to a lesser extent, Rga1 and Rga2 facilitate the role of Cdc42 in septin organization. Thus, it appears that the GAPs play a role in modulating specific aspects of Cdc42 function. Alternatively, the different phenotypes could reflect quantitative rather than qualitative differences in GAP activity in the mutant strains.
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Hanaei, Sara, Sina Abdollahzade, Alireza Khoshnevisan, Christopher K. Kepler, and Nima Rezaei. "Genetic aspects of intervertebral disc degeneration." Reviews in the Neurosciences 26, no. 5 (October 1, 2015): 581–606. http://dx.doi.org/10.1515/revneuro-2014-0077.

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AbstractIntervertebral disc degeneration (IVDD) is one of the common causes of low back pain. Similar to many other multifactorial diseases, it is affected by environmental and genetic factors. Although not completely understood, genetic factors include a wide spectrum of variations, such as single nucleotide polymorphisms, which could play a significant role in the etiology of this disease. Besides, the interactions with environmental factors could make the role of genetic factors more complicated. Genetic variations in disc components could participate in developing degenerative disc disease through altering the normal homeostasis of discs. Gene polymorphisms in disc proteins (collagens I, II, III, IX, and XI), proteoglycans (aggrecan), cytokines (interleukins I, VI, and X), enzymes (matrix metalloproteinases II, III, and IX), and vitamin D receptor seem to play considerable roles in the pathology of this disease. There are also many other investigated genes that could somehow take part in the process. However, it seems that more studies are needed to clarify the exact role of genetics in IVDD.
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Hold, Georgina L., and M. Emad El-Omar. "Genetic aspects of inflammation and cancer." Biochemical Journal 410, no. 2 (February 12, 2008): 225–35. http://dx.doi.org/10.1042/bj20071341.

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Chronic inflammation is involved in the pathogenesis of most common cancers. The aetiology of the inflammation is varied and includes microbial, chemical and physical agents. The chronically inflamed milieu is awash with pro-inflammatory cytokines and is characterized by the activation of signalling pathways that cross-talk between inflammation and carcinogenesis. Many of the factors involved in chronic inflammation play a dual role in the process, promoting neoplastic progression but also facilitating cancer prevention. A comprehensive understanding of the molecular and cellular inflammatory mechanisms involved is vital for developing preventive and therapeutic strategies against cancer. The purpose of the present review is to evaluate the mechanistic pathways that underlie chronic inflammation and cancer with particular emphasis on the role of host genetic factors that increase the risk of carcinogenesis.
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Bellini, Marilanda Ferreira, Rosana Silistino-Souza, Marileila Varella-Garcia, Maria Tercília Vilela de Azeredo-Oliveira, and Ana Elizabete Silva. "Biologic and Genetics Aspects of Chagas Disease at Endemic Areas." Journal of Tropical Medicine 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/357948.

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The etiologic agent of Chagas Disease is theTrypanosoma cruzi, transmitted through blood-sucking insect vectors of the Triatominae subfamily, representing one of the most serious public health concerns in Latin America. There are geographic variations in the prevalence of clinical forms and morbidity of Chagas disease, likely due to genetic variation of theT. cruziand the host genetic and environmental features. Increasing evidence has supported that inflammatory cytokines and chemokines are responsible for the generation of the inflammatory infiltrate and tissue damage. Moreover, genetic polymorphisms, protein expression levels, and genomic imbalances are associated with disease progression. This paper discusses these key aspects. Large surveys were carried out in Brazil and served as baseline for definition of the control measures adopted. However, Chagas disease is still active, and aspects such as host-parasite interactions, genetic mechanisms of cellular interaction, genetic variability, and tropism need further investigations in the attempt to eradicate the disease.
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Drutskaya, M. S., E. O. Gubernatorova, E. A. Gorshkova, K. S. N. Athertkhany, M. A. Nosenko, V. S. Gogoleva, O. A. Namakanova, R. V. Zvartsev, A. A. Kruglov, and S. A. Nedospasov. "Cytokines, reverse genetics and anti-cytokine therapy." Bulletin of Siberian Medicine 18, no. 1 (May 16, 2019): 38–48. http://dx.doi.org/10.20538/1682-0363-2019-1-38-48.

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Cytokines comprise the molecular language of communication between the cells, which is needed to maintain the homeostatic functions of the body (including the immune system) and mediate various diseases. Many aspects of inflammation, autoimmune diseases and neoplasia are associated with cytokine signaling through specific receptors. The establishment of new physiological functions of “old” cytokines and understanding the molecular and cellular mechanisms of their involvement in disease pathogenesis, as well as the search for new therapeutic targets and development of innovative approaches to anti-cytokine therapy, present a fundamental problem. When assessing the tremendous success of anti-cytokine therapy in treatment of certain autoimmune diseases, we should not forget that (a) this treatment does not eliminate the causes of the disease:autoreactive T-cell clones; and that (b) less than half of the patients respond to this therapy; and that (c) anti-cytokine therapy has serious side effects.
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Dissertations / Theses on the topic "Cytokinesis Genetic aspects"

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O'Keefe, Louise. "Genetic analysis of the role of pebble during cytokinesis in Drosophila." Title page, contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09pho415.pdf.

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Errata pasted onto back page. Bibliography: p. 133-149. The RhoGEF activity of PBL is shown to be acting predominantly by the activation of Rho1 and downstream signaling pathways required for contractile ring function during cytokinesis. Genetic evidence suggests this could be through the activation of Diaphanous (an FH protein) to reorganize the actin cytoskeleton, as well as through the activation of Rho-kinase which results in the phosphorylation, and activation of myosin. Highlights a possible role for PBL during contractile ring function at a later stage that previously thought. Genetic interaction screens were employed to identify regulators of PBL activity during cytokinesis. CDK1 was identified genetically as a candidate for regulating PFB activity, but functional studies in vivo showed that this regulation was not by direct phophorylation of the PBK consensus CDK1 suites tested. Further screening has identified other possible components pf PBL signaling pathways, but a role during cytokinesis for these interactors remains to be confirmed. The eye phenotypes described provide ideal systems for the identification of components of PBL signaling pathways in Drosophila. The high level of conservation in the mechanism of cytokinesis from yeast to mammals would also suggest that the identified interactors would most likely represent components of cytokinesis pathways in all eukaryotes.
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Prior, Leanne Michelle. "Characterization of pebble : a gene required for cytokinesis in Drosophila melanogaster /." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09php9578.pdf.

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Mok, Ka-pun Chris, and 莫家斌. "Avian influenza A viral genetic determinants of cytokine hyper-induction in primary human macrophages." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43941539.

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Huang, Fung-yu. "Pathogenetic aspects of helicobacter pylori infection in gastric cancer : a study on the role of inflammatory cytokine and gene methylation /." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B4370363X.

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Guo, Hong, and 郭紅. "Effects of anti-DNA antibodies on pleural mesothelial cells: in vitro studies to explore thepathogenetic mechanism of pulmonary lupus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B26631945.

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The Best M.Phil Thesis in the Faculties of Dentistry, Engineering, Medicine and Science (University of Hong Kong), Li Ka Shing Prize, 2001-2003.
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Medicine
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Master of Philosophy
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Yim, Chi-ho Howard, and 嚴志濠. "Cytokine dysregulation by human immunodeficiency virus-1 transactivating protein." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B36987700.

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Silva, Gustavo Milson Fabricio da. "Polimorfismo genético de citocinas na população do Rio de Janeiro." Universidade do Estado do Rio de Janeiro, 2009. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=10210.

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Citocinas são moléculas que controlam e modulam a atividade de numerosas células por se ligarem a seus receptores específicos. As diferenças observadas na produção de citocinas entre indivíduos podem ser, pelo menos em parte, explicadas pelos polimorfismos genéticos como o polimorfismo de um único nucleotídeo (SNP). Em 181 indivíduos saudáveis não-aparentados da cidade do Rio de Janeiro (região Sudeste - Brasil), nós analisamos os polimorfismos de citocinas em genes que codificam para Fator de Necrose Tumoral-alfa (TNF-a), Fator de Crescimento Transformante-beta (TGF-b), Interleucina-10, Interleucina-6 e Interferon-gama (IFN-g). Reação em cadeia da polimerase utilizando-se iniciadores sequencia-específicos foi realizada com auxílio do kit comercial CytGen (One Lambda Inc. Canoga Park, CA, USA). Ao todo, 8 polimorfismos foram analisados: TNF-a (-308G/A); TGF-b (códon 10C/T, códon 25C/G); IL-10 (-1082A/G, -819T/C, -592A/C); IL-6 (-174C/G) e IFN-g (+874T/A). Os dados observados foram comparados a três grupos de população de diferentes regiões do Brasil (São Paulo, Paraná e Bahia) e a três populações de outros continentes (Itália, Eslováquia e Negros Norte-Americanos). O teste qui-quadrado foi utilizado para as comparações. Nossa análise da população do Rio de Janeiro mostrou que os as freqüências alélicas em IL-10, IL-6 e IFN-g são desigualmente distribuídos entre Brancos, Mulatos e Negros (p<0,05). A comparação com populações de outras regiões do Brasil revelou que Rio de Janeiro e Bahia possuem freqüências alélicas e genotípicas de TGF-b (códon 25) estatisticamente diferentes (p=0,004 e p=0,002, respectivamente). Ainda, a freqüência alélica na população do Rio de Janeiro é significativamente diferente quando comparada à população da Itália [IL-6 (-174), p=0,0092; e IFN-g (+874) p=0,0418)]; Eslováquia [IL-10(-1082), p=0,006; IL-6(-174), p=0,0002; e IFN-g(+874), p=0,0335]; e Afro-Americanos [IL-10(-819), p=0,0446; IL-6(-174), p<0,0001; e IFN-g(+874), p<0,0001]. Adicionalmente, observamos que a diferença na distribuição dos haplótipos em IL-10 (-1082/-819/-592) na população do Rio de Janeiro em comparação com a da Itália (p=0,0293) e Afro-Americanos (p=0,0025) é significativa. Portanto, concluímos que os polimorfismos em IL-10, IL-6 e IFN-g estão distribuídos de acordo com a etnia na população do Rio de Janeiro. A população do Rio de Janeiro possui freqüências de polimorfismos diferentes das populações de Bahia, Itália, Eslováquia e Afro-Americanos, mas semelhantes à população de São Paulo/Paraná. Nossas observações poderão ser úteis para futuros estudos e associação entre polimorfismos genéticos de citocinas e doenças na população do Rio de Janeiro.
Cytokines are molecules that control and modulate the activities of numerous target cells via binding to specific receptors. The observed differences in the cytokine production among individuals can be, at least, explained by genetic polymorphisms like single nucleotide polymorphism (SNP). In 181 unrelated healthy Brazilian individuals from Rio de Janeiro City, we investigated the polymorphisms of cytokine genes encoding Tumor Necrosis Factor-alpha (TNFA), Transforming Growth Factorbeta (TGFB), Interleukin (IL)-10, IL-6, and Interferon-gamma (IFNG). Polymerase chain reaction using sequence-specific primers genotyping was performed for these gene cytokines using the avaiable comercial kit CytGen (One Lambda Inc., CA, USA). Eight polymorphisms were tested: TNF-a (-308G/A); TGF-b (códon 10C/T, códon 25C/G); IL-10 (-1082A/G, -819T/C, -592A/C); IL-6 (-174G/C) and IFN-g (+874T/A). Chi-square test was used for comparisons. Observed data were compared to three other populations from different regions of Brazil (São Paulo, Paraná and Bahia) and three populations of other countries (Italy, Slovakia and North American Blacks). Our analysis from Rio de Janeiro population showed that the alleles frequencies in IL-10, IL-6 and IFN-g are unevenly distributed among Whites, Blacks and Mulatos (p<0.05). The comparison with populations from other regions of Brazil showed that Rio de Janeiro and Bahia have genotypic and allelic frequencies of TGF-b (códon 25) statistically different (p=0,004 and p=0,002, respectively). Also, the allelic frequency in the population of Rio de Janeiro is significantly different when compared to the population of Italy [IL-6 (-174), p=0.0092, and IFN-g (+874), p=0.0418] ; Slovak [IL-10 (-1082), p=0006; IL-6 (-174), p=0.0002, and IFN-g (+874), p=0.0335] and Afro-Americans [IL-10 (-819), p=0.0446, IL-6 (-174), p<0.0001, and IFN-g (+874), p<0.0001]. Additionally, we observed that the distribution of haplotypes in IL-10 (-1082/-819/-592) in the population of Rio de Janeiro in comparison with that of Italy (p = 0.0293) and Afro-Americans (p =0,0025) is statistically different. Therefore, we conclude that the polymorphisms in IL-10, IL-6 and IFN-g are distributed according to ethnicity in the population of Rio de Janeiro. The population of Rio de Janeiro have different frequencies of polymorphisms of the population of Bahia, Italy, Slovak and Afro-American, but similar to the population of São Paulo/Paraná. Our observations may be useful for future studies in association between genetic polymorphisms of cytokines and disease in the Rio de Janeiro population.
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Wang, Cathy Ting-Peng. "Molecular dissection of RANKL signaling pathways in osteoclasts." University of Western Australia. School of Surgery and Pathology, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0037.

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[Truncated abstract] Bone remodeling is intricately regulated by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. The elevation in osteoclast number and/or activity is a major hallmark of several common pathological bone disorders including post-menopausal osteoporosis, osteoarthritis, Paget's disease, and tumour-mediated osteolysis. Receptor activator of nuclear factor kappa B ligand (RANKL) is a key cytokine for osteoclast differentiation and activation. The association of RANKL to its cognate receptor, RANK, which is expressed on osteoclast precursors and mature osteoclasts, is essential for osteoclast formation and activation. The intimate interaction between RANKL and RANK triggers the activation of a cascade of signal transduction pathways including NF-κB, NFAT, MAPK and PI3 kinase. Although osteoclast signaling pathways have been intensively studied, the precise molecules and signaling events which underlie osteoclast differentiation and function remain unclear. In order to dissect the molecular mechanism(s) regulating osteoclast differentiation and activity, this thesis herein explores the key RANKL/RANK-mediated signaling pathways. Four truncation mutants within the TNF-like domain of RANKL [(aa160-302), (aa160-268), (aa239-318) and (aa246-318)] were generated to investigate their potential binding to RANK and the activation to RANK-signal transduction pathways. All were found to differentially impair osteoclastogenesis and bone resorption as compared to the wild-type RANKL. The impaired function of the truncation mutants of RANKL on osteoclast formation and function correlates with their reduced ability to activate crucial RANK signaling including NF-κB, IκBα, ERK and JNK. Further analysis revealed that the truncation mutants of RANKL exhibited differentially affinity to RANK as observed by in vitro pull-down assays. ... It is possible that Bryostatin 1 acts via upregulation of a fusion mechanism as the RANKL-induced OCLs are morphologically enlarged, exhibiting increased nuclei number expressing high level of DC-Stamp. Furthermore, Rottlerin was shown to inhibit NF-κB activity, whereas Bryostatin 1 showed the opposing effects. Both inhibitor and activator were also found to modulate other key osteoclastic signaling pathways including NFAT and total c-SRC. These findings implicate, for the first time, Protein Kinase C delta signaling pathways in the modulation of RANKL-induced osteoclast differentiation and activity. Taken together, the studies presented in this thesis provide compelling molecular, biochemical and morphological evidence to suggest that: (1) RANKL mutants might potentially serve as peptide mimic to inhibit RANKL-induced signaling, osteoclastogenesis and bone resorption. (2) A cross talk mechanism between extracellular Ca2+ and RANKL exist to regulate on osteoclast survival. (3) TPA suppressed RANKL-induced osteoclastogenesis predominantly during the early stage of osteoclast differentiation via modulation of NF-κB. (4) Selective inhibition of Protein Kinase C signaling pathways involved in osteoclastogenesis might be a potential treatment method for osteoclast-related bone diseases. (5) Protein Kinase C delta signaling pathways play a key role in regulating osteoclast formation and function.
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Huang, Fung-yu, and 黃鳳如. "Pathogenetic aspects of helicobacter pylori infection in gastric cancer: a study on the role of inflammatorycytokine and gene methylation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B4370363X.

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Cheung, Ka-wa Benny, and 張嘉華. "Mechanism of Bacillus Calmette Guerin-induced immune response." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29488989.

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Books on the topic "Cytokinesis Genetic aspects"

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International Symposium on the Molecular Pathology and Clinical Aspects of Inflamed Liver: Alcohol and Cytokines (1st 1998 Toronto, Ont.). 1st International Symposium on the Molecular Pathology and Clinical Aspects of Inflamed Liver: Alcohol and Cytokines: June 7-9, 1998, Toronto, Canada. [Toronto: Sunnybrook Health Science Centre, University of Toronto, 1998.

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(Editor), Guido Forni, Robin Foa (Editor), Angela Santoni (Editor), and David Quinn (Editor), eds. Cytokine-Induced Tumor Immunogenicity: From Exogenous Molecules to Gene Therapy. Academic Press, 1994.

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Cytokine-Induced Tumor Immunogenicity: From Exogenous Molecules to Gene Therapy. Academic Press, 1994.

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1947-, Scherbaum W. A., ed. Autoimmune thyroiditis: Approaches towards its etiological differentiation. Berlin: Springer-Verlag, 1991.

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Book chapters on the topic "Cytokinesis Genetic aspects"

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Al Asmari, Abdulrahman, and Misbahul Arfin. "The Genetic Aspects of Behçet’s Disease: Role of Cytokine Genes Polymorphisms." In Cytokines. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.88856.

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A. Pandith, Arshad, Ina Bhat, Sheikh Mansoor, Aabid Koul, Usma Manzoor, Iqra Anwar, Fozia Mohammad, Qurat Ul Aein, Shahid M. Baba, and Carmen Vladulescu. "Cytokine Gene Polymorphism and Cancer Risk: A Promising Tool for Individual Susceptibility and Prognostic Implications." In Genetic Polymorphisms - New Insights [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99363.

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Abstract:
Cytokines are potent molecules produced mainly by specific activated immune cells to control inflammatory responses besides other biologic processes. Although active participation of cytokines provides defense against carcinogenesis on the other hand, deregulation at the genetic level influences their activity to promote tumor development. Among many aspects, constitutional polymorphic sequence variations are key factors that derange the cytokine expression to lead an individual’s propensity to risk for different cancers. Cytokine polymorphisms are now believed to alter these critical molecules that have a dual face in carcinogenesis as, when implicated in the activation of the immune response, these molecules check the cancer development while their persistent inflammatory reaction can envisage the development of malignancy and tumor growth. We have given ample evidence of case-control studies in a range of cancers where substantial evidence, as reported in this chapter, links polymorphism of cytokine gene susceptibility with numerous cancers. Cytokine gene polymorphism is vital to be significant bimolecular genetic determinants of susceptibility and prognosis of cancer. A strong need is felt for more case-control association studies in cytokine candidate genes involved in specific pathways for particular cancer in bigger powered sample sizes involving additional variables to disclose their factual risk for cancer.
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