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Literatura académica sobre el tema "ABCA13"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 10 de febrero de 2022

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Artículos de revistas sobre el tema "ABCA13"

Hlaváč, Viktor, Radka Václavíková, Veronika Brynychová, Renata Koževnikovová, Katerina Kopečková, David Vrána, Jiří Gatěk y Pavel Souček. "Role of Genetic Variation in ABC Transporters in Breast Cancer Prognosis and Therapy Response". International Journal of Molecular Sciences 21, n.º 24 (15 de diciembre de 2020): 9556. http://dx.doi.org/10.3390/ijms21249556.

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Breast cancer is the most common cancer in women in the world. The role of germline genetic variability in ATP-binding cassette (ABC) transporters in cancer chemoresistance and prognosis still needs to be elucidated. We used next-generation sequencing to assess associations of germline variants in coding and regulatory sequences of all human ABC genes with response of the patients to the neoadjuvant cytotoxic chemotherapy and disease-free survival (n = 105). A total of 43 prioritized variants associating with response or survival in the above testing phase were then analyzed by allelic discrimination in the large validation set (n = 802). Variants in ABCA4, ABCA9, ABCA12, ABCB5, ABCC5, ABCC8, ABCC11, and ABCD4 associated with response and variants in ABCA7, ABCA13, ABCC4, and ABCG8 with survival of the patients. No association passed a false discovery rate test, however, the rs17822931 (Gly180Arg) in ABCC11, associating with response, and the synonymous rs17548783 in ABCA13 (survival) have a strong support in the literature and are, thus, interesting for further research. Although replicated associations have not reached robust statistical significance, the role of ABC transporters in breast cancer should not be ruled out. Future research and careful validation of findings will be essential for assessment of genetic variation which was not in the focus of this study, e.g., non-coding sequences, copy numbers, and structural variations together with somatic mutations.

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Kruh, Gary D., Yanping Guo, Elizabeth Hopper-Borge, Martin G. Belinsky y Zhe-Sheng Chen. "ABCC10, ABCC11, and ABCC12". Pflügers Archiv - European Journal of Physiology 453, n.º 5 (26 de julio de 2006): 675–84. http://dx.doi.org/10.1007/s00424-006-0114-1.

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Barros, Scott A., Raymond W. Tennant y Ronald E. Cannon. "Molecular structure and characterization of a novel murine ABC transporter, Abca13". Gene 307 (marzo de 2003): 191–200. http://dx.doi.org/10.1016/s0378-1119(03)00465-7.

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Dwyer, S., H. Williams, I. Jones, L. Jones, J. Walters, N. Craddock, M. J. Owen y M. C. O'Donovan. "Investigation of rare non-synonymous variants at ABCA13 in schizophrenia and bipolar disorder". Molecular Psychiatry 16, n.º 8 (1 de febrero de 2011): 790–91. http://dx.doi.org/10.1038/mp.2011.2.

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Nymoen, Dag, Arild Holth, Thea E. Hetland Falkenthal, Claes G. Tropé y Ben Davidson. "CIAPIN1 and ABCA13 are markers of poor survival in metastatic ovarian serous carcinoma". Molecular Cancer 14, n.º 1 (2015): 44. http://dx.doi.org/10.1186/s12943-015-0317-1.

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Maeß, Marten B., Katrin Stolle, Paul Cullen y Stefan Lorkowski. "Evidence for an alternative genomic structure, mRNA and protein sequence of human ABCA13". Gene 515, n.º 2 (febrero de 2013): 298–307. http://dx.doi.org/10.1016/j.gene.2012.11.072.

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Chen, Jian-Hui, Yu-Long Zheng, Chuan-Qin Xu, Li-Zhi Gu, Zong-Li Ding, Ling Qin, Yi Wang, Ran Fu, Yu-Feng Wan y Cheng-Ping Hu. "Valproic acid (VPA) enhances cisplatin sensitivity of non-small cell lung cancer cells via HDAC2 mediated down regulation of ABCA1". Biological Chemistry 398, n.º 7 (27 de junio de 2017): 785–92. http://dx.doi.org/10.1515/hsz-2016-0307.

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Abstract Valproic acid (VPA) has been suggested to be a histone deacetylase inhibitor (HDACI). Our present study revealed that VPA at 1 mm, which had no effect on cell proliferation, can significantly increase the sensitivity of non-small cell lung cancer (NSCLC) cells to cisplatin (DDP). VPA treatment markedly decreased the mRNA and protein levels of ABCA1, while had no significant effect on ABCA3, ABCA7 or ABCB10. Luciferase reporter assays showed that VPA can decrease the ABCA1 promoter activity in both A549 and H358 cells. VPA treatment also decreased the phosphorylation of SP1, which can bind to −100 and −166 bp in the promoter of ABCA1. While the phosphorylation of c-Fos and c-Jun were not changed in VPA treated NSCLC cells. Over expression of HDAC2 attenuated VPA induced down regulation of ABCA1 mRNA expression and promoter activities. Over expression of HDAC2 also attenuated VPA induced DDP sensitivity of NSCLC cells. These data revealed that VPA can increase the DDP sensitivity of NSCLC cells via down regulation of ABCA1 through HDAC2/SP1 signals. It suggested that combination of VPA and anticancer drugs such as DDP might be great helpful for treatment of NSCLC patients.

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Besnard, Valérie, Yohei Matsuzaki, Jean Clark, Yan Xu, Susan E. Wert, Machiko Ikegami, Mildred T. Stahlman et al. "Conditional deletion of Abca3 in alveolar type II cells alters surfactant homeostasis in newborn and adult mice". American Journal of Physiology-Lung Cellular and Molecular Physiology 298, n.º 5 (mayo de 2010): L646—L659. http://dx.doi.org/10.1152/ajplung.00409.2009.

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ATP-binding cassette A3 (ABCA3) is a lipid transport protein required for synthesis and storage of pulmonary surfactant in type II cells in the alveoli. Abca3 was conditionally deleted in respiratory epithelial cells ( Abca3Δ/Δ) in vivo. The majority of mice in which Abca3 was deleted in alveolar type II cells died shortly after birth from respiratory distress related to surfactant deficiency. Approximately 30% of the Abca3Δ/Δ mice survived after birth. Surviving Abca3Δ/Δ mice developed emphysema in the absence of significant pulmonary inflammation. Staining of lung tissue and mRNA isolated from alveolar type II cells demonstrated that ∼50% of alveolar type II cells lacked ABCA3. Phospholipid content and composition were altered in lung tissue, lamellar bodies, and bronchoalveolar lavage fluid from adult Abca3Δ/Δ mice. In adult Abca3Δ/Δ mice, cells lacking ABCA3 had decreased expression of mRNAs associated with lipid synthesis and transport. FOXA2 and CCAAT enhancer-binding protein-α, transcription factors known to regulate genes regulating lung lipid metabolism, were markedly decreased in cells lacking ABCA3. Deletion of Abca3 disrupted surfactant lipid synthesis in a cell-autonomous manner. Compensatory surfactant synthesis was initiated in ABCA3-sufficient type II cells, indicating that surfactant homeostasis is a highly regulated process that includes sensing and coregulation among alveolar type II cells.

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Yoshida, Kyoko, Yasuhiro Go, Itaru Kushima, Atsushi Toyoda, Asao Fujiyama, Hiroo Imai, Nobuhito Saito, Atsushi Iriki, Norio Ozaki y Masaki Isoda. "Single-neuron and genetic correlates of autistic behavior in macaque". Science Advances 2, n.º 9 (septiembre de 2016): e1600558. http://dx.doi.org/10.1126/sciadv.1600558.

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Atypical neurodevelopment in autism spectrum disorder is a mystery, defying explanation despite increasing attention. We report on a Japanese macaque that spontaneously exhibited autistic traits, namely, impaired social ability as well as restricted and repetitive behaviors, along with our single-neuron and genomic analyses. Its social ability was measured in a turn-taking task, where two monkeys monitor each other’s actions for adaptive behavioral planning. In its brain, the medial frontal neurons responding to others’ actions, abundant in the controls, were almost nonexistent. In its genes, whole-exome sequencing and copy number variation analyses identified rare coding variants linked to human neuropsychiatric disorders in 5-hydroxytryptamine (serotonin) receptor 2C (HTR2C) and adenosine triphosphate (ATP)–binding cassette subfamily A13 (ABCA13). This combination of systems neuroscience and cognitive genomics in macaques suggests a new, phenotype-to-genotype approach to studying mental disorders.

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Chen, Zhang-qun, Tarmo Annilo, Sergey Shulenin y Michael Dean. "Three ATP-binding cassette transporter genes, Abca14 , Abca15 , and Abca16 , form a cluster on mouse Chromosome 7F3". Mammalian Genome 15, n.º 5 (1 de mayo de 2004): 335–43. http://dx.doi.org/10.1007/s00335-004-2281-8.

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Tesis sobre el tema "ABCA13"

Knight, Helen Miranda. "Candidate gene studies in psychiatric illness". Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/6508.

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Schizophrenia, bipolar disorder and major depression are common, heritable neuropsychiatric conditions and yet the source of the inherited risk remains largely unknown. This thesis focuses on two complementary strategies for identifying and characterising the genetic component of these illnesses: homozygosity mapping in consanguineous pedigrees, and genetic and neurobiological investigations of candidate genes identified by the analysis of structural chromosomal abnormalities carried by patients with psychiatric diagnoses. In a family of a cousin marriage, five of six offspring presented with a rare combination of schizophrenia, sensori-neural hearing impairment and epilepsy. Two loci were located on chromosomes 22q13 and 2p24-25 where a series of markers were homozygous by descent (HBD). Five further HBD loci were identified in a second, related family where four of five offspring had hearing loss. However, there was no overlap of the HBD intervals in the two families, and sequencing coding regions of candidate genes failed to identify causative mutations. A second study investigated the candidate gene ABCA13 identified at a breakpoint region on chromosome 7 in a patient with schizophrenia who carried a complex chromosomal rearrangement. Re-sequencing exons encoding the highly conserved functional domains identified eight potentially pathogenic, rare coding variants. Case control association studies involving cohorts of schizophrenia, bipolar disorder and major depression revealed significant associations of these variants with all three clinical phenotypes, and follow-up in relatives displayed familial inheritance patterns. Disruption of ABCA13, expressed in human hippocampus and frontal cortex, implicates aberrant lipid biology as a pathological pathway in mental illness. A third study focused on GRIK4, a candidate gene previously reported disrupted in a patient with schizophrenia who carried a chromosome abnormality. A deletion in the 3’UTR of GRIK4, encoding the kainate receptor subunit KA1, was identified as a protective factor for bipolar disorder. Using post mortem human brain tissue from control subjects, KA1 protein expression patterns were characterized in the hippocampal formation, amygdala, frontal cortex and cerebellum. KA1 expression was found significantly increased in subjects with the protective allele, supporting the hypothesis that reduced glutamatergic neurotransmission is a risk factor in major psychiatric illnesses. Together, these novel discoveries define aspects of the genetic contribution to mental illness, implicate specific dysfunctional processes and suggest new directions for research in the quest to find rationally based treatments and preventative strategies for some of the most common and disabling psychiatric disorders.

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Tomioka, Maiko. "Expression of ABCA13 in the brain and the effect of neurological disorder-related SNPs on the function". Kyoto University, 2013. http://hdl.handle.net/2433/175051.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(農学)
甲第17622号
農博第1984号
新制||農||1010(附属図書館)
学位論文||H25||N4743(農学部図書室)
30388
京都大学大学院農学研究科応用生命科学専攻
(主査)教授植田和光, 教授植田充美, 教授阪井康能
学位規則第4条第1項該当

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Davids, Muneera. "Single nucleotide polymorphism association studies of ABCA13 and ABHD11 genes and the bioinformatics analysis of the autism candidate genes localized on chromosome 7". University of the Western Cape, 2016. http://hdl.handle.net/11394/4977.

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Magister Scientiae - MSc
Autism, Aspergers Syndrome and Pervasive Developmental Delay-Not Otherwise Specified (PDD-NOS), among others, fall under an umbrella of disorders known as Autism Spectrum Disorder. Twin studies show that autism is a highly heritable disorder. More than 100 genes have been implicated in the aetiology of autism, each of which is involved in numerous biological processes and a variety of molecular interactions. William-Beuren syndrome is a multisystem developmental disorder caused by the deletion of contiguous genes at the 7q11.23 position. The aims of this study were (i) to genotype three SNPs (rs10279013, rs2293484 and rs17060) in the ABHD11 and ABCA13 genes, respectively, using Taqman® SNP Genotyping assays to detect association with autism in three distinct South African (SA) ethnic groups (Black, Caucasian and Mixed), and (ii) to ascertain common pathways or regulating transcription factors for genes on chromosome 7 that may attribute to it being an “autism hotspot”. Chapter 3 objectives were to identify potential candidate genes using STRING analysis and the Gene Cards database. The Taqman® study indicated significant association for SNP rs2293484 in the South African Caucasian group, as well as for the G allele in the South African Mixed group, where p<0.001. STRING analysis yielded 2 new candidate genes, FZD1 and FZD9. It was also found that the Wnt pathway in mammals plays a significant role in both ASDs and cancer, and there is a definite link between genes regulating cancer, and genes implicated in autism. The study provides evidence for not only the association of the investigated SNP in a South African population, but also provides evidence for the co-morbidity of several neurological and psychological disorders such as depression and bipolar disorder with autism.

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Teixeira, Mayza Dalcin. "Estudo da associação de polimorfismos dos genes FTO, ABCA1, ABCA7 e ABCG1 com marcadores de obesidade e perfil lipídico em mulheres obesas". reponame:Repositório Institucional da UFPR, 2017. http://hdl.handle.net/1884/47563.

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Orientadora : Profª. Drª. Lupe Furtado-Alle
Coorientadora : Drª Luciane Viater Tureck
Dissertação (mestrado) - Universidade Federal do Paraná, Setor de Ciências Biológicas, Programa de Pós-Graduação em Genética. Defesa: Curitiba, 31/03/2017
Inclui referências : f. 85-88
Resumo: A maioria dos casos de obesidade e de dislipidemias possui origem complexa, pois é resultante da interação entre fatores genéticos e ambientais. Diversos genes têm sido relacionados com a susceptibilidade a estas doenças, incluindo variantes alélicas dos genes FTO, ABCA1, ABCA7 e ABCG1. Desse modo, o objetivo deste trabalho foi verificar se há influência de polimorfismos de nucleotídeo único (SNPs) destes genes em variáveis relacionadas à obesidade e ao perfil lipídico em mulheres obesas e avaliar o efeito destes SNPs na mudança destas variáveis em resposta a uma dieta de restrição calórica. Para isso, foi coletado sangue de 211 mulheres obesas para análises bioquímicas (níveis de triglicerídeos - TG, colesterol total - CT, HDL-c, LDL-c e VLDL) e genotípicas, além de medidas antropométricas (índice de massa corporal - IMC, circunferência da cintura - CC, e circunferência abdominal - CA), antes e depois de uma dieta com redução de 600Kcal por dia. As amostras foram genotipadas por ensaio de discriminação alélica TaqMan® e posteriormente foram feitas análises estatísticas. Como resultado, as mulheres portadoras do alelo A do SNP rs9939609 (FTO) apresentaram uma menor redução de CA e maior redução dos níveis de HDL-c em resposta à dieta. As portadoras do alelo A do SNP rs1800977 (ABCA1) perderam menos IMC após a intervenção do que as não portadoras. As portadoras do genótipo TT do SNP rs2230806 (ABCA1) reduziram mais seus níveis de CT em resposta a dieta do que as portadoras do genótipo GG. Além disso, o alelo T foi mais frequente que o alelo C no grupo de mulheres com níveis de HDL-c maiores e níveis de LDL-c menores. As portadoras do genótipo GG do SNP rs2279796 (ABCA7) apresentaram níveis de CT e LDL-c maiores. Além disso, o alelo G foi mais frequente no grupo de mulheres com nível de CT e LDL-c maiores. Na resposta a intervenção dietética, as portadoras do genótipo GG aumentaram os níveis de TG e VLDL. As portadoras do alelo G do SNP rs692383 (ABCG1) apresentaram IMC maior, menor redução da CA em resposta a dieta e, em contrapartida, níveis de TG e VLDL menores e uma redução menor nos níveis de HDL-c. As portadoras do alelo A do SNP rs3827225 (ABCG1) tiveram uma maior redução de CA que as não portadoras, porém apresentaram um aumento maior nos níveis de LDL-c após a intervenção dietética. Esses resultados são indicativos de que possivelmente o alelo T do SNP rs2230806 (ABCA1) está associado com o efeito de proteção contra doenças cardiovasculares, pelos seus efeitos nos níveis de lipídeos séricos. Outrossim, o alelo G do SNP rs2279796 (ABCA7) pode estar conferindo um risco para doenças cardiovasculares, assim como o alelo A do SNP rs9939609 (FTO) sobre uma maior dificuldade em reduzir a CA e pela maior perda de HDL-c. Palavras-chave: Obesidade. Mulheres obesas. Intervenção dietética. Perfil lipídico. Gene FTO. Transportadores ABC. Estudo de associação.
Abstract: Obesity and dyslipidemias, in the majority of cases, have complex origin, as they result from the interaction between genetic and environmental factors. Many genes have been related to the susceptibility for these diseases, including FTO, ABCA1, ABCA7 and ABCG1 gene variants. Thus, the aim of this study was to verify if single nucleotide polymorphisms (SNPs) of these genes influence variables related to obesity and lipid profile in obese women and evaluate the effect of these SNPs in the variation of the variables in response to a calorie restriction diet. Thereunto, blood of 211 obese women was collected for biochemical (triglycerides - TG, total cholesterol - TC, HDL-c, LDL-c and VLDL levels) and genotypic analyses, besides anthropometric measures (body mass index - BMI, waist circumference - WC and abdominal circumference - AC), before and after a dietetic intervention with reduction of 600kcal per day. The samples were genotyped by allelic discrimination assay TaqMan® and analyzed statistically. As result, women carrying rs9939609 SNP (FTO) allele A had a lower AC reduction and a greater reduction of HDL-c levels in response to diet. A allele carriers of rs1800977 SNP (ABCA1) lost less BMI after intervention than non-carriers. TT genotype carriers of rs2230806 SNP (ABCA1) reduced more their TC levels than GG genotype carriers in response to diet. In addition, the T allele was more frequent than C allele in the group of women with higher HDL-c levels and lower LDL-c levels. GG genotype carriers of rs2279796 SNP (ABCA7) had higher TC and LDL-c levels. In addition, the G allele was more frequent in the group of women with higher TC and LDL-c levels. In response to dietary intervention, GG genotype carriers increased TG and VLDL levels. G allele carriers of rs692383 SNP (ABCG1) had higher BMI and lower AC reduction in response to diet but, on the other hand, lower TG and VLDL levels and a lower reduction in HDL-c levels. A allele carriers of SNP rs3827225 SNP (ABCG1) had a greater reduction in AC than non-carriers, but they had a higher increase in LDL-c levels after dietary intervention. These results are indicative that possibly T allele of rs2230806 SNP (ABCA1) is associated with the protective effect against cardiovascular diseases by their effects on serum lipid levels. In addition, the G allele of rs2279796 SNP (ABCA7) possibly is conferring a risk for cardiovascular diseases, as well as the A allele of rs9939609 SNP (FTO) on a greater difficulty in reducing AC and the greater loss of HDL-c. Keywords: Obesity. Obese women. Dietetic intervention. Lipid profile. FTO gene. ABC transporters. Association study.

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Matsuda, Akihiro. "(24S)-Hydroxycholesterol efflux from neuronal cells by ABC proteins". Kyoto University, 2014. http://hdl.handle.net/2433/185211.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(農学)
甲第17986号
農博第2033号
新制||農||1019(附属図書館)
学位論文||H26||N4811(農学部図書室)
80830
京都大学大学院農学研究科応用生命科学専攻
(主査)教授植田和光, 教授植田充美, 教授三芳秀人
学位規則第4条第1項該当

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Nascimento, Gabrielle Araújo do. "Avaliação do efeito de polimorfismos nos genes FTO, ABCA1, ABCA7 e ABCG1 sobre indicadores de obesidade e dislipidemias em crianças e adolescentes submetidos a treinamentos físico". reponame:Repositório Institucional da UFPR, 2017. http://hdl.handle.net/1884/47393.

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Orientadora : Profª Drª Luciane Viater Tureck
Coorientadora : Profª Drª Lupe Furtado Alle
Dissertação (mestrado) - Universidade Federal do Paraná, Setor de Ciências Biológicas, Programa de Pós-Graduação em Genética. Defesa: Curitiba, 27/03/2017
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Resumo: A obesidade e as dislipidemias geralmente estão associadas, e na maior parte dos casos possuem origem complexa, sendo decorrentes da interação entre os fatores ambientais e fatores genéticos. Dentre os fatores genéticos já conhecidos encontram-se genes relacionados ao metabolismo, como o gene FTO (Fat Mass and Obesity Associated) e os genes dos transportadores ABC. Polimorfismos de nucleotídeo único (SNPs) no gene FTO foram associados com o ganho de peso, enquanto os transportadores ABC estão relacionados com o efluxo de colesterol, e, nesse trabalho, foram analisados SNPs dos genes ABCA1, ABCA7 e ABCG1. Visto isso, o objetivo desse estudo é avaliar se há influência de polimorfismos nesses genes sobre variáveis antropométricas (índice de massa corporal ajustado para idade e sexo (IMC escore-Z), circunferência abdominal (CA), circunferência da cintura (CC), gordura corporal (GC) e massa magra (MM)) e bioquímicas (glicose em jejum, glicose 120, insulina em jejum, insulina 120, HOMA-IR (do inglês homeostasis model assessment of insulin resistance), QUICKI (do inglês quantitative insulin sensitivity check index) e perfil lipídico) de 557 crianças e adolescentes (eutróficos, sobrepeso e obesos) estudantes de escolas de Curitiba (PR), além de verificar o efeito de tais polimorfismos nas mudanças desses marcadores em resposta a um programa de exercícios físicos. A genotipagem foi realizada por ensaio de discriminação alélica. As análises estatísticas realizadas foram contagem direta dos genótipos, cálculo de frequência alélica, comparação de médias (teste T e teste Mann Whitney), análise de regressão múltipla e predição de risco. Todos os SNPs analisados promoveram variação significativa em alguma das variáveis analisadas. Com relação ao gene FTO, o alelo A do SNP rs9939609 foi associado a um aumento da insulina e HOMA-IR, e diminuição de QUICKI. Em relação aos genes dos transportadores ABC, o alelo C do SNP rs1800977 (ABCA1) foi associado a aumento no IMC escore-Z, CA, GC, insulina 120 e redução em QUICKI; o alelo A do SNP rs2230806 (ABCA1) foi associado a aumento no IMC escore-Z, CA e redução em %MM; o alelo C do SNP rs2279796 (ABCA7) foi associado à maior IMC escore-Z; o SNP rs692383 (ABCG1) foi associado à maior IMC escore-Z, CA, HDL-C, glicose, insulina e HOMA-IR e o alelo G do SNP rs3827225 (ABCG1) foi associado à maior VLDL-C e glicose. Com relação ao efeito na resposta aos exercícios físicos, os genes FTO, ABCA7 e ABCG1 não apresentaram interação, enquanto o alelo C do SNP rs1800977 (ABCA1) foi associado à maior redução de IMC escore-Z e maior aumento de QUICKI em resposta ao exercício e o alelo A do SNP rs2230806 (ABCA1) foi associado à maior ganho de MM. Nesse trabalho nós verificamos os efeitos dos polimorfismos analisados em variáveis relacionadas ao metabolismo (adiposidade, metabolismo da glicose e de lipídeos), sendo que alguns desses polimorfismos também interagiram com os programas de exercícios físicos aplicados. Os resultados obtidos corroboram e abrem novas perspectivas de estudo quanto ao papel da interação entre fatores ambientais e genéticos na prevenção e tratamento de patologias complexas, como a obesidade e as dislipidemias, no sentido de tornar tais medidas cada vez mais individualizadas. Palavras chave: Obesidade, dislipidemias, exercício físico, FTO, ABCA1, ABCA7, ABCG1, rs9939609, rs1800977, rs2230806, rs2279796, rs692383, rs3827225.
Abstract: Obesity and dyslipidemias are usually associated, and in most cases have complex origin, resulting from interaction between environmental and genetic factors. Among these already know genetic factors there are genes related to metabolism, such as FTO (Fat Mass and Obesity Associated) and the ABC transporters genes. Single nucleotide polymorphisms (SNPs) in FTO gene are associated to weight gain, while ABC transporters are related to cholesterol efflux, and SNPs in ABCA1, ABCA7 and ABCG1 genes were analyzed in this work. The objective of this study is to evaluate the influence of polymorphisms in these genes on anthropometric (body mass index adjusted for age and sex (BMI Z-score), abdominal circumference (AC), waist circumference (WC), fat mass (FM) and lean body mass (LBM)) and biochemical variables (fasting glucose, glucose 120, fasting insulin, insulin 120, HOMA-IR (homeostasis model assessment of insulin resistance), QUICKI (quantitative insulin sensitivity check index) and lipid profile) of 557 children and adolescents (normal weight, overweight and obese) in Curitiba (PR), and verify these polymorphisms effects in the changes of these markers in response to a physical exercise program. Genotyping was carried out by allelic discrimination assay. The statistical analyzes made were direct counting of genotypes, allelic frequency calculation, comparison of means (T test and Mann-Whitney test), multiple regression analysis and risk prediction. All the analyzed SNPs promoted significant variation in some of the variables. Regarding FTO gene, the rs9939609 SNP A-allele was associated to higher insulin and HOMA-IR, and reduced QUICKI. In relation to the ABC transporter genes, SNP rs1800977 C-allele (ABCA1) was associated to higher BMI-Z score, AC, FM and insulin 120 increase and QUICKI reduction; SNP rs2230806 (ABCA1) A-allele was associated to higher BMI-Z score and AC and %LBM reduction; SNP rs2279796 (ABCA7) C-allele was associated to higher BMI Z-score; SNP rs692383 (ABCG1) was associated to higher BMI Z-score, AC, HDL-C, glucose, insulin and HOMA-IR, and SNP rs3827225 (ABCG1) G-allele was associated to higher VLDL-C and glucose. Regarding the effect on physical exercise response, FTO, ABCA7 and ABCG1 genes did not shown interaction, whereas rs1800977 (ABCAI) C-allele was associated to higher reduction of BMI Z-score and increase in QUICKI in response to physical exercise and rs2230806 SNP (ABCA1) A-allele was associated to higher gain of LBM. In this study, we verified the effects of the polymorphisms analyzed on variables related to metabolism (adiposity, glucose metabolism and lipid metabolism), and some of these polymorphisms also interacted with the applied physical exercise programs. The results obtained corroborate and open new perspectives on the role of the interaction between environmental and genetic factors in the prevention and treatment of complex pathologies, such as obesity and dyslipidemias, in order to make these measures more individualized. Key-words: Obesity, dyslipidemia, physical exercise, FTO, ABCA1, ABCA7, ABCG1, rs9939609, rs1800977, rs2230806, rs2279796, rs692383, rs3827225.

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Rodrigues, Lucas Campos de Sá. "Estudo da expressão dos genes de resistência a múltiplas drogas ABCB1, ABCC1 e ABCG2, em cães com linfoma multicêntrico, submetidos a três diferentes protocolos de tratamento antineoplásico". Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/10/10136/tde-08102012-141346/.

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Um dos principais desafios no tratamento quimioterápico em seres humanos e animais é a resistência que as células neoplásicas apresentam, sendo esse mecanismo responsável por falhas no tratamento e recidivas da doença. A resistência pode ser intrínseca ou adquirida e ocorre em função da expressão de transportadores de membrana ABC, como a glicoproteína P (ABCB1/MDR), proteínas de resistência a múltiplas drogas (ABCC1/MRP) e proteína de resistência do câncer de mama (ABCG2/BCRP). O linfoma é a neoplasia hematopoiética mais comum em cães, altamente responsiva à quimioterapia, mas que recidiva durante o tratamento antineoplásico, sendo a resistência das células neoplásicas aos quimioterápicos um fator responsável pela alta taxa de recidiva e óbito dos animais. Neste estudo avaliou-se a expressão de genes relacionados à resistência a múltiplas drogas em cães com linfoma, no diagnóstico e na recidiva da doença, em três diferentes protocolos quimioterápicos utilizados na rotina clínica. A expressão dos genes ABCB1, ABCC1, ACBG2 foi determinada por RT-PCR (PCR em tempo real) em 25 animais naturalmente acometidos pela doença, divididos aleatoriamente em 3 grupos tratados com os protocolos quimioterápicos COP, VCM e Short-Madison, além de um "pool" controle constituído por linfonodos normais de oito animais. A expressão dos genes foi detectada em todas as amostras, tanto de linfonodos normais quanto de animais com linfoma. No diagnóstico da doença, a expressão do gene ABCC1 foi relacionada negativamente com idade (p=0,008) e positivamente com duração da remissão (p=0,027) e sobrevida (p=0,007), entretanto para os genes ABCB1 e ABCG2 não houve diferença estatística significante. Na recidiva, a expressão dos genes não sofreu variação estatística significante em função do tipo e duração da remissão e sobrevida. Não houve variação na expressão dos genes ABCB1, ACBC1 e ABCG2 no momento da recidiva quando comparado ao protocolo quimioterápico utilizado.
One of the main challenges of the chemotherapy treatment in human and animals is the resistance of the neoplasic cells, being this mechanism responsible for failures in the treatment and relapse of the disease. The resistance could be intrinsic or acquired and it occurs due to the expression of ABC membrane transporters, such as p-glycoprotein (ABCB1/MDR), resistance protein to multiple drugs (ABCC1/MRP) and resistance protein of breast cancer (ABCG2/BCRP). Lymphoma is the most common hematopoietic cancer disease in dogs, highly responsive to chemotherapy, but relapse during chemotherapy treatment, being the resistance of neoplastic cells to chemotherapy drugs the responsible factor for the high rate of relapse and death of animals. In this study, genes expression related to multiples drugs resistance it was evaluated in dogs with lymphoma, in the diagnosis and in the relapse of the disease in three different chemotherapy protocols used in the clinical routine. The genes expression ABCB1, ABCC1, ACBG2 was determined by RT-PCR (real time PCR) in 25 animals naturally undertaken by the illness, randomly divided into 3 groups treated with the chemotherapy protocols COP, VCM and Short-Madison, besides a "pool" control constituted by normal lymph node of eight animals. The genes expression was detected in all the samples, both in the normal lymph node and in the animals with lymphoma. In the diagnosis of the disease, the gene expression ABCC1 was negatively related with age (p=0,008) and positively with the duration of remission (p=0,027) and survival (p=0,007); however, for ABCB1 and ABCG2 there was no statiscally significant difference. In the relapse, the genes expression had no statiscally significant difference due to the type and duration of remission and survival. There was no variation in the genes expression ABCB1, ACBC1 and ABCG2 in the moment of relapse when compared to the chemotherapy protocol used.

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Plazzo, Anna Pia. "Influence of ABCA1 and ABCA7 on the lipid microenvironment of the plasma membrane". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/15953.

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Der ABC-Transporter ABCA1 ist unmittelbar in die zelluläre Lipidhomeostasie einbezogen, in dem er die Freisetzung von Cholesterol an plasmatische Rezeptoren, wie ApoA-I, vermittelt. Trotz intensiver Untersuchungen ist dieser molekulare Mechanismus nicht verstanden. Verschiedene Studien deuten daraufhin, dass durch die Aktivität von ABCA1 bedingte Veränderungen in der Lipidphase der äußeren Hälfte der Plasmamembran (PM) wichtig für die Freisetzung des Cholesterols sind. In der vorliegenden Arbeit wird die Lipidumgebung von ABCA1 in der PM lebender Säugetierzellen unter Anwendung der Fluoreszenzlebenszeitmikroskopie von fluoreszierenden Lipidsonden untersucht. Es wurde eine breite Verteilung der Fluoreszenzlebenszeiten der Sonden gefunden, die sensitiv gegenüber Veränderungen der lateralen und transversalen Organisation der Lipide ist. Im Einklang mit Studien an riesengroßen unilamellaren Vesikeln und Plasmamembranvesikeln weisen unsere Ergebnisse die Existenz einer größeren Vielfalt submikroskopischer Lipiddomänen auf. Die FLIM-Untersuchungen an ABCA1 exprimierenden HeLa-Zellen weisen eine die Lipidphase destabilisierende Funktion des Transportes aus. Dieses wurde unterstützt durch die Lipidanalyse von Fraktionen der PM. Auf der Basis unserer Untersuchungen und früheren Daten stellen wir die Hypothese auf, dass die Exponierung von Phosphatidylserin (PS) auf der Zelloberfläche ein zentrales Ereignis der ABCA1 bedingten Veränderungen ist. Allerdings zeigen vergleichende Studien an ABCA7 exprimierenden Zellen, dass dies nicht ausreicht, um die ABCA1 verursachten Veränderungen in der Lipidpackung der PM zu erklären. Unsere Ergebnisse beweisen, dass die Fähigkeit von ABCA1, den Cholesterolefflux zu vermitteln, auf durch den Transporter bedingte Veränderungen in der LP der PM zurückzuführen sind, die unabhängig von der Bindung von ApoA-1 sind und dieser vorausgehen. Diese Veränderungen sind notwendig für die Lipidierung von ApoA-1 und der Generierung von HDL-Partikeln.
The ABCA1 transporter organizes cellular lipid homeostasis by promoting the release of cholesterol to plasmatic acceptors such as ApoA-I. Despite intensive investigation, the molecular mechanism of such a process has not yet been clarified. In the present study we report on the analysis of the ABCA1 lipid microenvironment at the plasma membrane of living cells, by a novel approach based on fluorescence lifetime imaging microscopy (FLIM). In the plasma membrane of mammalian cells, a broad fluorescence lifetime distribution sensitive to treatments interfering with the membrane lateral and transbilayer organization was found. In agreement with investigations in giant unilamellar vesicles and giant plasma membrane vesicles, our results are consistent with the existence of a large variety of submicroscopic lipid domains. Based on that, FLIM in HeLa cells expressing ABCA1 revealed the destabilizing function of the transporter on the lipid arrangement at the membrane, indicating that lipid packing was a primary target of ABCA1 activity. This was corroborated by the analysis of plasma membrane fractions isolated by density fractionation. On the basis of our analysis and previous data, we speculate that the exposure of phosphatidylserine on the cell surface is a central event for ABCA1-dependent modifications. However, a comparative study of cells expressing ABCA7, the member of the ABCA subfamily with the highest homology to ABCA1, revealed that exposure of PS alone cannot account for the detected effects. Collectively, our data suggest that the ability of ABCA1 to promote cholesterol efflux is independent and precedes its actual binding to ApoA-I. Rather, ABCA1-induced plasma membrane modifications are necessary for the lipidation of ApoA-I and the generation of high density lipoprotein particles.

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Brüggmann, Nina [Verfasser]. "Untersuchungen zum ABCA1-/ABCG1-vermittelten Cholesterin-Efflux in humanen Kontroll- und Tangierfibroblasten / Nina Brüggmann". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2021. http://d-nb.info/1228861153/34.

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中塔, 充宏. "ABCタンパク質による脳内脂質輸送の生理的役割". Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263711.

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Más fuentes

Libros sobre el tema "ABCA13"

Giddings, Gary. Affluent singles: Targeting the single ABC1 adult. St. Albans: Headland Business Research, 1989.

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Vernaschi, Elvira. Olhar da crítica: Arte premiada da ABCA e o Acervo Artístico dos Palácios. São Paulo, Brazil]: Acervo Artístico-Cultural dos Palácios do Governo, 2009.

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Abcar, Klara. Klara Abcar Minature Paintings 5 Vols. Eqhbal, 2001.

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Abca Baseball Directory. Sports Market Place, 1991.

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Simon, Taylor y Key Note Publications, eds. The ABC1 consumer. 2^a ed. Hampton: Key Note, 2002.

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The ABC1 consumer. 3^a ed. Hampton: Key Note, 2004.

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ABC123: Les lettres et les chiffres de 1 à 10. Chevron (Belgique): Hemma, 2007.

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Ng, Dominic S. Tangier Disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0035.

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Tangier disease is characterized by profound high-density lipoprotein (HDL) deficiency in association with accumulation of cholesterol esters in tissues, especially those of the reticuloendothelial system. Clinical signs include hyperplastic, yellow-orange colored tonsils, peripheral neuropathies, and hepatosplenomegaly. The disease is caused by two mutant alleles of the ABCA1 gene encoding ATP-binding cassette subfamily A member 1. Despite severe HDL deficiency, predisposition to accelerated coronary heart disease is highly variable in affected individuals. With the exception of tonsillectomy for severe hyperplastic tonsils and corneal transplantation in rare cases of severe corneal opacification, treatments for specific manifestations are largely ineffective.

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Elvira, Vernaschi y Bertoli Marisa, eds. ABCA: Histórico : catálogo de sócios, 2003/2009. São Paulo: ABCA, 2009.

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The ABC1 consumer 1999: Strategic market intelligence for the professional. Hampton: Market Assessment International, 1999.

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Capítulos de libros sobre el tema "ABCA13"

Biswas-Fiss, Esther E., Stephanie Affet, Malissa Ha, Takaya Satoh, Joe B. Blumer, Stephen M. Lanier, Ana Kasirer-Friede et al. "ABC1 (for ABCA1) and ABC2 (for ABCA2)". En Encyclopedia of Signaling Molecules, 21. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100025.

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Schmitz, Gerd y Wolfgang E. Kaminski. "Phospholipid transporters ABCA1 and ABCA7". En Membrane Transporter Diseases, 291–99. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9023-5_19.

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Paolini, Alessandro, Antonella Baldassarre y Andrea Masotti. "ABCA3". En Encyclopedia of Signaling Molecules, 68–74. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101533.

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Paolini, Alessandro, Antonella Baldassarre y Andrea Masotti. "ABCA3". En Encyclopedia of Signaling Molecules, 1–7. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101533-1.

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Turton, James y Kevin Morgan. "ATP-Binding Cassette, Subfamily A (ABC1), Member 7 (ABCA7)". En Genetic Variants in Alzheimer's Disease, 135–58. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7309-1_7.

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Stieger, Bruno y Gerd A. Kullak-Ublick. "BSEP (ABCB11)". En Pharmacogenomics of Human Drug Transporters, 295–309. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118353240.ch13.

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Toyoda, Yu y Toshihisa Ishikawa. "MRP8 (ABCC11)". En Pharmacogenomics of Human Drug Transporters, 387–400. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118353240.ch17.

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Zahid, Sarwar, Kari Branham, Dana Schlegel, Mark E. Pennesi, Michel Michaelides, John Heckenlively y Thiran Jayasundera. "ABCA4". En Retinal Dystrophy Gene Atlas, 1–5. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-10867-4_1.

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Zarubica, Ana y Giovanna Chimini. "ABCA1, Tangier Disease, and Lipid Flopping". En Transmembrane Dynamics of Lipids, 353–77. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118120118.ch17.

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Böning, Dieter, Michael I. Lindinger, Damian M. Bailey, Istvan Berczi, Kameljit Kalsi, José González-Alonso, David J. Dyck et al. "Adenosine Triphosphate–Binding Cassette A1 (ABCA1)". En Encyclopedia of Exercise Medicine in Health and Disease, 21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2029.

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Actas de conferencias sobre el tema "ABCA13"

Oba, Takaaki, Ken-ichi Ito y Shun’ichiro Taniguchi. "Abstract 2112: ABCC11/MRP8 and ABCB1/MDR1 confer eribulin resistance to breast cancer cells". En 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.am2016-2112.

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SOUZA, M. F. D., H. L. S. NETA, H. A. MARIZ, M. J. B. M. RÊGO, M. C. PEREIRA, I. R. PITTA, C. D. L. MARQUES, A. L. B. P. DUARTE y M. G. R. PITTA. "AVALIAÇÃO DA EXPRESSÃO DOS GENES ABCB1, ABCC1, ABCG2 EM PACIENTES COM LÚPUS ERITEMATOSOSISTÊMICO". En ANAIS DO 5º ENCONTRO BRASILEIRO PARA INOVAçãO TERAPêUTICA. Galoa, 2017. http://dx.doi.org/10.17648/ebit-2017-85731.

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He, Ping-Ping, Xin-Ping OuYang, Kai Yin, Wu-Jun Chen, Qian Lu, Zhong-Cheng Mo, Guo-Jun Zhao, Yun-Cheng Lv y Chao-Ke Tang. "PDE Inhibitor Rolipram Increases Cholesterol Efflux and ABCA1 Expression: Rolipram Increases ABCA1 Expression". En 2012 International Conference on Biomedical Engineering and Biotechnology (iCBEB). IEEE, 2012. http://dx.doi.org/10.1109/icbeb.2012.292.

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Pasello, Michela, Marilù Fanelli, Valentina Mularoni, Sonia Ciotti, Piero Picci, Massimo Serra y Katia Scotlandi. "Abstract 589: Expression levels of ABCA6 or ABCA7 predict primary Ewing sarcoma progression at diagnosis". En Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-589.

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Castro, Blanca Elena, Eunice Aguilar, Lourdes Cabrera, Javier Camacho, Adriana Hernandez, Guillermo Ramón, Stanislaw Sadowinski, Manuela Orjuela y Veronica Ponce. "Abstract A26: Analysis of ABCB1, ABCC1 and ABCG2 expression and clinical parameters in 40 primary retinoblastoma cases". En Abstracts: AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; June 18-21, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-a26.

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Xu, K., D. J. Wegner, H. B. Heins, P. Yang, F. S. Cole y J. A. Wambach. "Characterization of Preferential ABCA3 Allele Expression from Lung Explants of Infants and Children with ABCA3 Deficiency". En American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3451.

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Yamada, Akimitsu, Takashi Ishikawa, Mariko Kimura, Daisuke Shimizu, Mikiko Tanabe, Takashi Chishima, Keiichi Kondo, Takeshi Sasaki y Itaru Endo. "Abstract 1695: Relationship between expression of ATP-binding cassette (ABC) transporters (ABCB1, ABCC1, ABCG2) and breast cancer subtypes". En 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.am2011-1695.

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Şişmanlar Eyuboglu, Tuğba, Tugba Ramaslı Gursoy, Ayse Tana Aslan, Zeynep Reyhan Onay, Sevgi Pekcan y Matthias Griese. "Progressive lung disease caused by ABCA3 mutation". En ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3527.

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Si, X. C. y M. Tracy. "Not All ABCA3 Mutations Are Created Equal". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5030.

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Li, Yang, Susanna Kinting, Stefanie Hoeppner y Matthias Griese. "Functional analysis of ABCA3 in phosphatidylcholine metabolism". En ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa3661.

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Informes sobre el tema "ABCA13"

Troyer, G. L. ABCASH plotting program users guide. Office of Scientific and Technical Information (OSTI), abril de 1995. http://dx.doi.org/10.2172/71321.

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Gory, Duane. ABCA FOCUS 2000 Issues Workshop. Fort Belvoir, VA: Defense Technical Information Center, marzo de 2000. http://dx.doi.org/10.21236/ada377467.

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Moon, Mike y Duane E. Gory. ABCA FOCUS 2000 Work Group US Delegation Preparation. Fort Belvoir, VA: Defense Technical Information Center, diciembre de 1999. http://dx.doi.org/10.21236/ada375430.

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