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Artykuły w czasopismach na temat "RAG1 expression"
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Hnatova, Martina, Micheline Wésolowski-Louvel, Guenaëlle Dieppois, Julien Deffaud, and Marc Lemaire. "Characterization of KlGRR1 and SMS1 Genes, Two New Elements of the Glucose Signaling Pathway of Kluyveromyces lactis." Eukaryotic Cell 7, no. 8 (2008): 1299–308. http://dx.doi.org/10.1128/ec.00454-07.
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ABSTRACT The expression of the major glucose transporter gene, RAG1, is induced by glucose in Kluyveromyces lactis. This regulation involves several pathways, including one that is similar to Snf3/Rgt2-ScRgt1 in Saccharomyces cerevisiae. We have identified missing key components of the K. lactis glucose signaling pathway by comparison to the same pathway of S. cerevisiae. We characterized a new mutation, rag19, which impairs RAG1 regulation. The Rag19 protein is 43% identical to the F-box protein ScGrr1 of S. cerevisiae and is able to complement an Scgrr1 mutation. In the K. lactis genome, we identified a single gene, SMS1 (for similar to Mth1 and Std1), that encodes a protein showing an average of 50% identity with Mth1 and Std1, regulators of the ScRgt1 repressor. The suppression of the rag4 (glucose sensor), rag8 (casein kinase I), and rag19 mutations by the Δsms1 deletion, together with the restoration of RAG1 transcription in the double mutants, demonstrates that Sms1 is a negative regulator of RAG1 expression and is acting downstream of Rag4, Rag8, and Rag19 in the cascade. We report that Sms1 regulates KlRgt1 repressor activity by preventing its phosphorylation in the absence of glucose, and that SMS1 is regulated by glucose, both at the transcriptional and the posttranslational level. Two-hybrid interactions of Sms1 with the glucose sensor and KlRgt1 repressor suggest that Sms1 mediates the glucose signal from the plasma membrane to the nucleus. All of these data demonstrated that Sms1 was the K. lactis homolog of MTH1 and STD1 of S. cerevisiae. Interestingly, MTH1 and STD1 were unable to complement a Δsms1 mutation.
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Prior, C., P. Mamessier, H. Fukuhara, X. J. Chen, and M. Wesolowski-Louvel. "The hexokinase gene is required for transcriptional regulation of the glucose transporter gene RAG1 in Kluyveromyces lactis." Molecular and Cellular Biology 13, no. 7 (1993): 3882–89. http://dx.doi.org/10.1128/mcb.13.7.3882-3889.1993.
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The RAG1 gene of Kluyveromyces lactis encodes a low-affinity glucose/fructose transporter. Its transcription is induced by glucose, fructose, and several other sugars. The RAG4, RAG5, and RAG8 genes are trans-acting genes controlling the expression of the RAG1 gene. We report here the characterization of one of these genes, RAG5. The nucleotide sequence of the cloned RAG5 gene indicated that it encodes a protein that is homologous to hexokinases of Saccharomyces cerevisiae. rag5 mutants showed no detectable hexokinase or glucokinase activity, suggesting that the sugar kinase activity encoded by this gene is the only hexokinase in K. lactis. Both high- and low-affinity transport systems of glucose were affected in rag5 mutants. The defect of the low-affinity component was found to be due to a block of transcription of the RAG1 gene by the hexokinase mutation. In vivo complementation of the rag5 mutation by the HXK2 gene of S. cerevisiae and complementation of hxk1 hxk2 mutations of S. cerevisiae by the RAG5 gene showed that RAG5 and HXK2 were equivalent for sugar-phosphorylating activity but that RAG5 could not restore glucose repression in the S. cerevisiae hexokinase mutants.
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Prior, C., P. Mamessier, H. Fukuhara, X. J. Chen, and M. Wesolowski-Louvel. "The hexokinase gene is required for transcriptional regulation of the glucose transporter gene RAG1 in Kluyveromyces lactis." Molecular and Cellular Biology 13, no. 7 (1993): 3882–89. http://dx.doi.org/10.1128/mcb.13.7.3882.
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The RAG1 gene of Kluyveromyces lactis encodes a low-affinity glucose/fructose transporter. Its transcription is induced by glucose, fructose, and several other sugars. The RAG4, RAG5, and RAG8 genes are trans-acting genes controlling the expression of the RAG1 gene. We report here the characterization of one of these genes, RAG5. The nucleotide sequence of the cloned RAG5 gene indicated that it encodes a protein that is homologous to hexokinases of Saccharomyces cerevisiae. rag5 mutants showed no detectable hexokinase or glucokinase activity, suggesting that the sugar kinase activity encoded by this gene is the only hexokinase in K. lactis. Both high- and low-affinity transport systems of glucose were affected in rag5 mutants. The defect of the low-affinity component was found to be due to a block of transcription of the RAG1 gene by the hexokinase mutation. In vivo complementation of the rag5 mutation by the HXK2 gene of S. cerevisiae and complementation of hxk1 hxk2 mutations of S. cerevisiae by the RAG5 gene showed that RAG5 and HXK2 were equivalent for sugar-phosphorylating activity but that RAG5 could not restore glucose repression in the S. cerevisiae hexokinase mutants.
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Naik, Abani Kanta, Aaron T. Byrd, Aaron C. K. Lucander, and Michael S. Krangel. "Hierarchical assembly and disassembly of a transcriptionally active RAG locus in CD4+CD8+ thymocytes." Journal of Experimental Medicine 216, no. 1 (2018): 231–43. http://dx.doi.org/10.1084/jem.20181402.
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Expression of Rag1 and Rag2 is tightly regulated in developing T cells to mediate TCR gene assembly. Here we have investigated the molecular mechanisms governing the assembly and disassembly of a transcriptionally active RAG locus chromatin hub in CD4+CD8+ thymocytes. Rag1 and Rag2 gene expression in CD4+CD8+ thymocytes depends on Rag1 and Rag2 promoter activation by a distant antisilencer element (ASE). We identify GATA3 and E2A as critical regulators of the ASE, and Runx1 and E2A as critical regulators of the Rag1 promoter. We reveal hierarchical assembly of a transcriptionally active chromatin hub containing the ASE and RAG promoters, with Rag2 recruitment and expression dependent on assembly of a functional ASE–Rag1 framework. Finally, we show that signal-dependent down-regulation of RAG gene expression in CD4+CD8+ thymocytes depends on Ikaros and occurs with disassembly of the RAG locus chromatin hub. Our results provide important new insights into the molecular mechanisms that orchestrate RAG gene expression in developing T cells.
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Fisher, Megan, and Craig Bassing. "Pre-B cells suppress RAG expression in response to DNA double-strand breaks (HEM1P.225)." Journal of Immunology 194, no. 1_Supplement (2015): 50.8. http://dx.doi.org/10.4049/jimmunol.194.supp.50.8.
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Abstract The ability of the Rag1/Rag2 (RAG) endonuclease to assemble antigen receptor (AgR) genes is essential for adaptive immunity. However, aberrant induction or repair of RAG-induced DNA double strand breaks (DSBs) can lead to oncogenic AgR translocations. We have previously shown that RAG-induced DSBs in pre-B cells activate the ATM kinase to prevent RAG cleavage of the homologous allele, and to inhibit expression of Rag1 and Rag2. These breaks also suppress expression of Gadd45α, which promotes Rag1 and Rag2 transcription. Since DSBs induced by ionizing radiation (IR) signal through ATM to increase Gadd45α expression in all other cell types including mature B cells, these results indicate that RAG DSBs and/or pre-B cells use unique mechanisms to regulate Gadd45α expression. We now demonstrate that IR-induced DSBs in pre-B cells signal through the ATM kinase to down-regulate Gadd45α expression. We also demonstrate that these IR DSBs signal ATM-dependent suppression of Rag1 and Rag2 transcription, without affecting stability of Rag1 or Rag2 mRNA. Because the presence of multiple DSBs in a cell greatly increases the risk of translocation, we hypothesize that pre-B cells have developed a unique developmental stage-specific DSB response to suppress the induction of RAG DSBs in the presence of other DSBs. Our ongoing studies will determine the role of this pre-B cell specific DSB response in suppressing AgR translocations and enforcing mono-allelic assembly of immunoglobulin genes.
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Klemm, Lars, Srividya Swaminathan, Elli Papaemmanuil, et al. "Exposure to Inflammatory Immune Responses As Driver of Clonal Evolution in Childhood Acute Lymphoblastic Leukemia." Blood 126, no. 23 (2015): 166. http://dx.doi.org/10.1182/blood.v126.23.166.166.
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Abstract Background: Pediatric pre-B acute lymphoblastic leukemia (ALL) may develop from prenatal chromosomal translocations acquired in utero. For instance, the ETV6-RUNX1 gene rearrangement (~25% of childhood ALL) is found in the umbilical cord blood and Guthrie blood spots of 1 in 100 healthy newborns, however, only 1 in 14,000 carriers develop overt leukemia. The molecular mechanisms driving clonal evolution towards overt leukemia were not clear. Rationale: Activation Induced Cytidine Deaminase (AID) and Recombination Activation Genes 1 and 2 (RAG1-RAG2) are genetic modifiers of the immunoglobulin (Ig) genes that are expressed during normal B cell development. Although AID and RAG1/RAG2 are thought to be segregated to early (RAG1/RAG2) and late (AID) stages of B cell development, respectively, we found that the two enzymes can be concurrently expressed during early B-lymphopoiesis in the context of repeated inflammatory stimuli. Results: Our experiments identified transitional pre-B cells as the subset that is particularly vulnerable to concomitant expression of AID and RAG1-RAG2 with earlier B cells being protected by IL7 signaling.Human B cells from children lacking a functional IL-7 receptor (IL-7R) displayed both increased expression and activity of AID concurrently with RAG1-RAG2. These results demonstrated that AID activation in both mouse and human early B cell compartments increases genetic instability. Although concurrent activation of AID and RAG1-RAG2 in patient samples implicated a correlation between the two enzymes in the pathogenesis of leukemia, this as such did not prove that the enzymes causally induce overt leukemogenesis. Therefore, we next evaluated the requirement of AID and RAG1-RAG2 in leukemogenic transformation, and identified a condition that leads to massive activation of these enzymes in a pre-leukemic B cell. Importantly, AID and RAG1-RAG2 expression increased dramatically during inflammatory immune responses (e.g. infection), where both these enzymes diversify the antibody repertoire and improve its affinity to antigens from infectious pathogens. We therefore tested whether the pre-B cell subset that concurrently expresses AID and RAG1-RAG2 can respond to an inflammatory stimulus, such as LPS. We observed that pre-B cells require protection from IL7, which prevents aberrant activation of AID. In the absence of protective IL-7, these pre-B cells acquired responsiveness to LPS and strongly activated AID concurrently with RAG1-RAG2 enzymes. We developed IL7-dependent pre-B cell cultures as a disease model for ETV6-RUNX1 pre-leukemia and tested the role of AID and RAG1 in the progression of pre-leukemic clones. To this end, we expanded ETV6-RUNX1 pre-B cells from wildtype (AID and RAG1 expressing) mice, or from mice lacking AID (Aid-/-Rag1+/+) or RAG1 (Aid+/+Rag1-/-). We then challenged pre-B cell cultures by withdrawal of IL7 (loss of protection) and inflammatory stimuli (LPS) and transplanted pre-B cells that had undergone five cycles of -IL7/LPS challenge. Upon transplanting -IL7/LPS-treated Aid+/+Rag1+/+ or Aid-/-Rag1+/+ or Aid+/+Rag1-/- pre-B cells containing ETV6-RUNX1 into NOD-SCID recipient mice, we observed that loss of either Aid or Rag1 dramatically prolonged the latency and reduced the penetrance of leukemia in transplant recipients. This proved that AID and RAG1-RAG2 causally accelerate clonal evolution of a pre-leukemic B cell towards leukemia. Our findings provide a mechanism by which pre-leukemic clones carrying a prenatal genetic lesion such as ETV6-RUNX1 can evolve through infectious and inflammatory stimuli ultimately leading to full blown leukemia. Conclusion: The impact of inflammatory stimuli on leukemogenesis has been previously implicated in multiple epidemiological studies. For instance, day-care attendance primed the immune system during early childhood and is thought to protect against exacerbation of B cell responses and to prevent collateral damage driving clonal evolution towards leukemia. Although inflammation (LPS stimulation) seems to play a role in accelerating pre-B leukemogenesis in our model, further experiments testing actual infectious pathogens are needed to corroborate this concept. Moreover, it is crucial to test whether leukemogenesis is accelerated in individuals infected with restricted classes of pathogens, not all of which may activate AID in pre-B cells. Disclosures No relevant conflicts of interest to declare.
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Hao, Bingtao, Abani Kanta Naik, Akiko Watanabe, et al. "An anti-silencer– and SATB1-dependent chromatin hub regulates Rag1 and Rag2 gene expression during thymocyte development." Journal of Experimental Medicine 212, no. 5 (2015): 809–24. http://dx.doi.org/10.1084/jem.20142207.
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Rag1 and Rag2 gene expression in CD4+CD8+ double-positive (DP) thymocytes depends on the activity of a distant anti-silencer element (ASE) that counteracts the activity of an intergenic silencer. However, the mechanistic basis for ASE activity is unknown. Here, we show that the ASE physically interacts with the distant Rag1 and Rag2 gene promoters in DP thymocytes, bringing the two promoters together to form an active chromatin hub. Moreover, we show that the ASE functions as a classical enhancer that can potently activate these promoters in the absence of the silencer or other locus elements. In thymocytes lacking the chromatin organizer SATB1, we identified a partial defect in Tcra gene rearrangement that was associated with reduced expression of Rag1 and Rag2 at the DP stage. SATB1 binds to the ASE and Rag promoters, facilitating inclusion of Rag2 in the chromatin hub and the loading of RNA polymerase II to both the Rag1 and Rag2 promoters. Our results provide a novel framework for understanding ASE function and demonstrate a novel role for SATB1 as a regulator of Rag locus organization and gene expression in DP thymocytes.
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Swaminathan, Srividya, Lars Klemm, Eugene Park, et al. "Mechanisms of Clonal Evolution of Pre-Leukemic Clones in Childhood Pre-B Acute Lymphoblastic Leukemia." Blood 124, no. 21 (2014): 861. http://dx.doi.org/10.1182/blood.v124.21.861.861.
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Abstract Background and hypothesis: Childhood pre-B acute lymphoblastic leukemia (ALL) can frequently be retraced to a pre-leukemic clone carrying a prenatally acquired genetic lesion (e.g. ETV6-RUNX1gene rearrangement). After birth, pre-leukemic clones can acquire secondary mutations and, hence, evolve towards overt leukemia. While this concept is well established, the mechanism(s) driving clonal evolution are not known. Epidemiological findings hint to a role of delayed childhood infections and chronic inflammation as etiologic factors of childhood ALL, but do not illuminate mechanism of clonal evolution of pre-leukemic cells. In this study, we demonstrate that cooperation between the AID cytosine deaminase and the RAG1/RAG2 V(D)J recombinase promotes acquisition of secondary genetic lesions that promote progress of pre-leukemic B cell precursors towards full-blown leukemia. Results: The enzymatic activity of RAG1/RAG2 (VDJ recombination) and AID (somatic hypermutation, class-switch recombination) are strictly segregated to early and late stages of B cell development, respectively. While RAG1 and RAG2 are actively expressed at stages of early B cell development (bone marrow and fetal liver) that give rise to pre-B ALL, little is known about the function of AID in early B-lymphopoesis. As the involvement of AID in pre-B leukemic clonal evolution is incumbent on its expression during early stages of B-lymphopoesis, we tested CD19+ pre-B cells isolated from human bone marrow (BM) for indicators of AID activity, namely, somatic hypermutation (SHM) and class switch recombination (CSR). Interestingly, most pre-B cell clones carry rearranged Ig VH region genes that are mutated at low levels (average mutation frequency 26 x 10-3 bp). Likewise, pre-B cells isolated from fetal liver tissues (three donors; 10-19 weeks of gestation) carried Ig VH region genes mutated at low levels (average mutation frequency 14 x 10-3 bp). In addition, about one third of fetal liver pre-B cells had undergone CSR to Cγ3, Cγ1 and Cα regions. These findings highlight the previously unknown function of AID in two important sites of early human B-lymphopoesis. Based on these results, we hypothesized that a specific B cell subset during early pro- and pre-B cell differentiation can concomitantly express both AID and the RAGs and, hence, would be particularly susceptible to clonal evolution of cells that carry a pre-leukemic lesion. Our subsequent studies identified late pre-B cells (Fraction D) as a natural subset of increased genetic vulnerability. Late pre-B cells downregulate IL7 receptor/Stat5 signaling, which enables expression of RAG1 and RAG2 and immunoglobulin light chain gene rearrangement. Loss of IL7 receptor/Stat5 signaling also removes an important safeguard against premature expression of AID. Therefore, late pre-B cells are poised to express AID at high levels in response to inflammatory stimuli (e.g. LPS) in concurrence with RAG1 and RAG2. Studying clonal evolution of patient-derived pre-B ALL cells, we found evidence for concomitant AID and RAG1/RAG2 activity. Further studying a genetic mouse model for pre-leukemic pre-B cells carrying ETV6-RUNX1, we found that repeated exposure to LPS can cause overt leukemia but not in the absence of either AID or Rag1. Additionally, whole exome sequencing of human B cell clones that were engineered to express AID, RAG1/RAG2 alone or in combination revealed that concurrent expression of AID with RAG1/RAG2 dramatically increased the frequency of structural chromosomal lesions. Conclusion: Consistent with epidemiological findings on the etiology of childhood ALL, we conclude that reduced cytokine signaling (here, IL7R) in late pre-B cells renders pre-leukemic clones distinctively vulnerable to genetic lesions that can be acquired in the context of repeated exposure to inflammatory stimuli (e.g. chronic and recurrent infections during childhood). Our results support a role for AID and RAGs cooperation for the generation of secondary lesions in leukemia subgroups that require additional leukemogenic events, and therefore, provide the genetic and molecular basis to support the Delayed Infections Hypothesis for leukemia progression in children. Disclosures No relevant conflicts of interest to declare.
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Lee, Baeck-seung, Joseph D. Dekker, Bum-kyu Lee, et al. "The BCL11A Transcription Factor Directly Activates RAG Gene Expression and V(D)J Recombination." Molecular and Cellular Biology 33, no. 9 (2013): 1768–81. http://dx.doi.org/10.1128/mcb.00987-12.
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Recombination-activating gene 1 protein (RAG1) and RAG2 are critical enzymes for initiating variable-diversity-joining (VDJ) segment recombination, an essential process for antigen receptor expression and lymphocyte development. The transcription factor BCL11A is required for B cell development, but its molecular function(s) in B cell fate specification and commitment is unknown. We show here that the major B cell isoform, BCL11A-XL, binds the RAG1 promoter and Erag enhancer to activate RAG1 and RAG2 transcription in pre-B cells. We employed BCL11A overexpression with recombination substrates in a cultured pre-B cell line as well as Cre recombinase-mediated Bcl11a lox/lox deletion in explanted murine pre-B cells to demonstrate direct consequences of BCL11A/RAG modulation on V(D)J recombination. We conclude that BCL11A is a critical component of a transcriptional network that regulates B cell fate by controlling V(D)J recombination.
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Bories, JC, JM Cayuela, P. Loiseau, and F. Sigaux. "Expression of human recombination activating genes (RAG1 and RAG2) in neoplastic lymphoid cells: correlation with cell differentiation and antigen receptor expression." Blood 78, no. 8 (1991): 2053–61. http://dx.doi.org/10.1182/blood.v78.8.2053.2053.
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Abstract Regulation of V-(D)-J recombinations that occur in antigen receptor encoding genes remains poorly understood. Recently, two genes, RAG1 and RAG2, that are able to activate rearrangement of synthetic recombination substrates were cloned in mouse and a human gene homologous to RAG1 was described. To define the differentiation stages corresponding to RAG1 and RAG2 RNA expression, we have studied a large number of B- and T-lymphoid neoplasias. First, we show that a human gene homologous to the murine RAG2 is transcribed in humans. Moreover, using a polymerase chain reaction approach, we have shown that RAG are expressed not only in T-cell receptor (TCR)-negative T-cell acute lymphoblastic leukemias (T-ALLs), but also in some cases in which a significant percentage of cells expressed surface TCR. Absence of RAG expression was shown in certain T-ALLs at variable stages of thymic differentiation. Data obtained in B-lineage ALLs show that RAG RNAs are expressed in almost all slg- B-lineage ALLs but are not transcribed in the slg+ B-cell proliferations tested, including Burkitt's ALLs, follicular center cell lymphomas, and chronic leukemias. These findings are consistent with the involvement of RAG in the control of in vivo V- (D)-J recombinations. These findings are also of interest in the delineation of potential regulatory factors acting on RAG transcription and in the understanding of the mechanisms of specific chromosomal abnormalities occurring in immature lymphoid cells.
Rozprawy doktorskie na temat "RAG1 expression"
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Braga, Aécio Assunção. "Polimorfismos dos genes CD40, ICAM-1, VCAM, E-selectina, LIGHT, RAGE e CX3CR1 relacionados com inflamação e sua associação à obesidade." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-26052015-143307/.
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INTRODUÇÃO: A obesidade é um grave problema de saúde pública, sendo definida como o acúmulo excessivo de gordura, possivelmente decorrente do desequilíbrio, por um longo período, entre a quantidade de energia ingerida e o gasto energético. OBJETIVO: Investigar a contribuição dos polimorfismos dos genes CD40, ICAM-1, VCAM, E-selectina, LIGHT, RAGE e CX3CR1 na associação com a obesidade. CASUÍSTICA E MÉTODOS: O estudo foi realizado no Instituto Dante Pazzanese de Cardiologia (IDPC) e no Hospital Universitário da Universidade de São Paulo (HU/USP), com 199 indivíduos (40 com peso normal, 55 com sobrepeso e 104 obesos) brasileiros, sem vínculo genético, de etnias branca, parda, negra e amarela, de ambos os sexos (55 homens e 144 mulheres), com idade entre 30 e 68 anos. Foi realizado o estudo dos polimorfismos dos genes CD40 (rs1883832) C>T, CX3CR1 (rs3732379) C>T, CX3CR1 (rs3732378) G>A, E-selectina (rs5368) C>T, ICAM-1 (rs1799969) G>A, ICAM-1 (rs281432) C>G, LIGHT (rs344560) G>A, LIGHT (rs2291668) C>T, RAGE (rs2070600) G>A, RAGE (rs2236493) C>T e VCAM (rs3176878) C>T, por pirossequenciamento, a análise da expressão dos genes LIGHT, CX3CR1, RAGE e ICAM-1, pela PCR em tempo real, e as dosagens das formas solúveis de PAI-1, IL-6, TNF-α, resistina, adiponectina e leptina, utilizando o sistema LUMINEX. RESULTADOS: As frequências alélica e genotípica dos polimorfismos estudados CD40 (rs1883832) C>T, CX3CR1 (rs3732379) C>T, CX3CR1 (rs3732378) G>A, E-selectina (rs5368) C>T, ICAM-1 (rs1799969) G>A, ICAM-1 (rs281432) C>G, LIGHT (rs344560) G>A, LIGHT (rs2291668) C>T, RAGE (rs2070600) G>A, RAGE (rs2236493) C>T e VCAM (rs3176878) C>T não apresentaram associação significativa com a obesidade. Foi encontrada associação na análise da expressão do CX3CR1 com a obesidade e também foi encontrada associação do polimorfismo ICAM-1 (rs281432) G>C com a expressão do gene RAGE em indivíduos com peso normal. CONCLUSÕES: Não houve associação dos polimorfismos CD40 (rs1883832) C>T, CX3CR1 (rs3732379) C>T, CX3CR1 (rs3732378) G>A, E-selectina (rs5368) C>T, ICAM-1 (rs1799969) G>A, ICAM-1 (rs281432) C>G, LIGHT (rs344560) G>A, LIGHT (rs2291668) C>T, RAGE (rs2070600) G>A, RAGE (rs2236493) C>T e VCAM (rs3176878) C>T com a obesidade, mas houve associação da expressão do gene CX3CR1 com a obesidade. Houve, também, associação do polimorfismo ICAM-1 (rs281432) G>C com a expressão do gene RAGE em indivíduos de peso normal.<br>Background: Obesity is a serious health problem and it is defined as an excessive fat accumulation which is caused by an imbalance between the amount of energy intake and energy expenditure over a long period. Objective: The main objective of this study was to investigate the contribution of CD403 ICAM-1, VCAM, E-selectin, LIGHT, RAGE e CX3CR1 gene polymorphisms and its association with obesity. Material and Methods: The study was realized at Dante Pazzanese Institute of Cardiology and University Hospital of São Paulo University. There were included 199 individuals (40 normal weight, 55 overweight and 104 obese), all Brazilian, with no genetic link, from all ethnics in both genders (55 men and 144 women), aged between 30 and 68 years. The study of CD40 (rs1883832) C>T, CX3CR1 (rs3732379) C>T, CX3CR1 (rs3732378) G>A, E-selectin (rs5368) C>T, ICAM-1 (rs1799969) G>A , ICAM-1 (rs281432) C>G, LIGHT (rs344560) G>A, LIGHT (rs2291668) C>T, RAGE (rs2070600) G>A, RAGE (rs2236493) C>T and VCAM (rs3176878) C>T were conducted by pyrosequencing. The analysis of LIGHT, CX3CR1, RAGE and ICAM-1 gene expression were performed by real-time PCR and the measurements of PAI-1, IL- 6, TNF-a, resistin, leptin and adiponectin soluble forms using LUMINEX system. Results: The allele and genotype frequency of CD40 (rs1883832) C>T, CX3CR1 (rs3732379) C>T, CX3CR1 (rs3732378) G>A, E-selectin (rs5368) C>T, ICAM-1 (rs1799969) G>A , ICAM-1 (rs281432) C>G, LIGHT (rs344560) G>A, LIGHT (rs2291668) C>T, RAGE (rs2070600) G>A, RAGE (rs2236493) C>T and VCAM (rs3176878) C>T gene polymorphisms showed no significant association with obesity. There was found association in the analysis of CX3CR1 expression with obesity and it was found association of ICAM-1 gene polymorphism (rs281432) G>C with RAGE gene expression in the normal weight group. Conclusion: There was no association of CD40 (rs1883832) C>T, CX3CR1 (rs3732379) C>T, CX3CR1 (rs3732378) G>A, E-selectin (rs5368) C>T, ICAM-1 (rs1799969) G>A , ICAM-1 (rs281432) C>G, LIGHT (rs344560) G>A, LIGHT (rs2291668) C>T, RAGE (rs2070600) G>A, RAGE (rs2236493) C>T and VCAM (rs3176878) C>T gene polymorphisms with obesity. However, it was found association of CX3CR1 gene expression with obesity and an association of ICAM-1 (rs281432) G>C gene polymorphism with RAGE gene expression in normal weight individuals.
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Lovejoy, Elizabeth A. "RAGE-based strategies for the control of gene expression." Thesis, University of Edinburgh, 1999. http://hdl.handle.net/1842/26699.
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The Cre/loxP site-specific recombinase system evolved within bacteriophage PI as a mechanism to maintain correct unit copy segregation of the prophage within host cells. This thesis reports the application of this system to regulate gene expression in murine cells. To regulate gene expression via RAGE (Recombination Activated Gene Expression) a novel floxed STOP cassette was designed, constructed and tested in murine embryonic fibroblasts (EF) and embryonic stem (ES) cells. When the floxed STOP cassette was used to regulate the expression of the Enhanced Green Fluorescent Protein (EGFP) marker gene a two-fold upregulation of EGFP transcription was observed after Cre mediated excisive recombination. However, no expression of the EGFP gene could be detected at the protein level and several reasons for this observation are discussed. The floxed STOP cassette was also utilised in RAGE-based strategies to achieve conditional expression of the tumour suppressor gene p53. A complex array of biological functions has been assigned to p53. For example, p53 is known to be involved in the regulation of apoptosis, multiple cell cycle checkpoints and the onset of replicative cellular senescence. The development of new approaches to achieve conditional p53 expression should be a valuable tool and permit further investigation into the pleiotropic nature of p53 function. Therefore, the floxed STOP cassette was used to regulate the expression of a p53 cDNA in p53 null primary EF cells <I>in vitro. </I>The upregulation of p53 expression after Cre administration was detected, but at a low frequency, by immunohistochemistry. The response of EF cells to the expression of p53 in terms of replicative cellular senescence was also characterised, including the first description of senescence-associated β-galactosidase expression in any murine cell. The floxed STOP technology was also used in an attempt to generate tools that will allow regulated expression of the endogenous murine p53 gene.
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Carvalho, Vanessa Isabel Dias Ribeiro de. "C. albicans Cek1 and Ras1: cloning, expression and purification." Master's thesis, Universidade de Aveiro, 2012. http://hdl.handle.net/10773/9526.
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Mestrado em Biologia Aplicada - Biologia Molecular e Celular<br>Candida albicans é um fungo polimórfico e patogénico que reside de forma
comensal nas superfícies mucosas humanas. Este fungo apresenta um código
genético ambíguo, uma vez que, o codão universal leucina CUG é
predominantemente traduzido como serina (97%), mas também como leucina
(3%). A análise de proteínas de C. albicans que contêm resíduos CUG em
importantes posições funcionais, revela que a ambiguidade do codão modela a
função da proteína e poderá ter um papel determinante nas vias de sinalização
associadas a mudanças morfológicas e patogénicas.
Com o presente estudo pretende-se investigar o efeito da leucina e da serina
nas posições CUG (ambiguidade CUG) na estrutura e função de duas
proteínas chave nas vias de sinalização de C. albicans, a Ras1 (GTPase) e a
Cek1 (Cinase). Estas regulam a transcrição dos genes associados com
mudanças morfológicas, patológicas e, por outro lado, contêm resíduos CUG
numa posição estritamente conservada e com relevo funcional.
Neste contexto foi possível clonar com sucesso genes sintéticos para os
centros ativos da Ras1 e Cek1 (variantes de serina e de leucina para o codão
CUG) em vetores que apresentam diferentes caudas de solubilidade (MBP,
NusA, Trx, ZTag2 e Gb1). Foram desenvolvidos protocolos de alta expressão
bacteriana e de purificação para os domínios ativos Ras1 (ligado à Gb1) e
Cek1 (ligado à MBP). A análise dos resultados de purificação analítica e de
“Dynamic Light Scaterring” demonstraram que as proteínas recombinantes se
apresentam na forma monomérica.
Ensaios de cristalização estão a ser realizados esperando-se determinar as
estruturas tridimensionais das proteínas por cristalografia de raio-X. As
estruturas da Cek1 e Ras1 com leucina e serina nas posições CUG,
conjuntamente com uma análise meticulosa da sua estabilidade e função in
vitro, irão fornecer informações importantes sobre o papel estratégico da
ambiguidade natural do codão.<br>The polymorphic fungal pathogen Candida albicans has an ambiguous genetic
code, as the universal leucine CUG codon is predominantly translated as
serine (97%) but also as leucine (3%). Analysis of the rare C. albicans proteins
containing CUG-encoded residues in functionally relevant positions reveals that
codon ambiguity shapes protein function and might have a pivotal role in
signaling cascades associated with morphological changes and pathogenesis.
The present study investigates the effect of leucine or serine at CUG positions
(CUG ambiguity) in the structure and function of two key effectors of signaling
cascades in C. albicans, Ras1 (GTPase) and Cek1 (protein kinase), which
regulate the transcription of genes associated with morphological changes and
pathogenesis. These two proteins contain a CUG residue in a strictly
conserved and functionally relevant position.
Synthetic genes coding for the active domains of Ras1 and Cek1 (serine and
leucine variants for the CUG codon) were successfully cloned into expression
vectors carrying different solubility partners (MBP, NusA, Trx, ZTag2 and Gb1).
Furthermore, using an incomplete factorial approach, high level bacterial
expression and purification protocols for the active domains of Ras1 (in fusion
with Gb1) and Cek1 (in fusion with MBP) were developed. Analytical size
exclusion chromatography (SEC) and dynamic light scattering (DLS) results
indicate that both recombinant proteins are monomeric.
Crystallization trials must be done aiming for the determination of their threedimensional
structures by X-ray crystallography. The structures of Ras1 and
Cek1 with serine or leucine at CUG positions, together with a thorough analysis
of their stability and function in vitro, will provide valuable insights into a
possible strategic role of natural codon ambiguity.
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Kim, Sun. "HAPLOINSUFFICIENCY OF RAI1 AND ITS EFFECT ON BDNF EXPRESSION." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/165.
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Smith-Magenis Syndrome (SMS) [OMIM, #182290] is a congenital anomaly and mental retardation (MCA/MR) syndrome associated with deletion of chromosome17p11.2 [1]. The clinical phenotype has been well described and includes minor craniofacial anomalies, self-injurious behaviors as well as sleep disturbances, speech delays, and obesity [1,2,3]. The incidence of SMS is estimated to be ~ 1:15,000 - 25,000 births [2,6]. Among SMS patients, ~90% are comprised of 17p11.2 deletions, while ~10% have RAI1 mutations [8]. All 17p11.2 deletions associated with SMS include RAI1 deletion [10]. RAI1 is thought to function as a transcriptional factor although its cellular role is still unclear. First, in order to better understand the role of RAI1 as a transcriptional factor and its relation to SMS, we confirmed that RAI1 regulates BDNF within an intronic region. This sequence was further narrowed down by utilizing the luciferase reporter assay. This test confirmed what was previously found using ChIP-chip assay and microarray analysis of Rai1+/- mice hypothalami. Next, in order to evaluate the role of Bdnf, an ampakine drug was administered to the Rai1+/- mouse model. A mouse model is a powerful tool for studying a specific gene. Rai1+/- mice exhibit the SMS phenotypes of obesity, craniofacial abnormalities, reduced pain sensitivities, seizures and others. Many physical, neurological, and behavioral tests were performed on the mice to see if any of the phenotypes can be rescued. Interestingly, twice-daily injections of ampakine CX1837 restored the pain sensitivities in Rai1+/- mice. The hot plate data suggest that BDNF potentially has a role in regulating the SMS phenotype of decreased pain sensitivity. In order to evaluate other genes that are altered as a result of the CX1837 ampakine drug, the whole brain's global gene expression was evaluated via microarray analysis. Two potential pain-related genes were identified to be upregulated due to drug administration, which could account for the pain phenotypes observed. One of the genes upregulated in treated mice was Osm, which is interesting because Osm is responsible for pain sensitivity. Further analysis is needed to confirm that an ampakine drug can potentially be used to treat SMS patients.
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Chen, Suzi Su-Hsin, and suzi chen@med monash edu au. "Cyclooxygenase Expression in Human Diabetes." RMIT University. Medical Sciences, 2007. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080206.121439.
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Cyclooxygenase (COX) is the rate limiting enzyme that catalyses the production of prostanoids, which are crucial to vascular homeostasis. Evidence suggests that endothelial dysfunction and inflammation play a role in vascular complications in aging and diabetes. Previous animal studies by our laboratory at RMIT University reported enhanced COX expression with aging in rat aortas, platelets and monocytes. Potentially, alteration in COX expression may result in an imbalanced prostanoid production favoring the synthesis of vasoconstrictors and hence increase the risk of cardiovascular events in the aging population. The regulation of altered COX expression in aging, however, is not clear. It has been suggested that histone hyperacetylation may be an important mechanism that regulates COX levels during the aging process as increased histone acetylation has been shown to occur with aging. Thus, we hypothesized that COX expression is modulated by histone hyperacetylati on. This was investigated by measuring COX expression in histone hyperacetylated cultured endothelial cells. In the case of diabetes, studies have reported that the development of diabetes and its complications is associated with persistent inflammatory activity, evident with increased inflammatory markers in the circulation. COX-mediated pathways may be involved in this inflammatory process in diabetes. Furthermore, the formation of advanced glycation end products (AGEs) is accelerated in diabetes. AGEs can bind to receptors for AGEs (RAGE), which has also been suggested to play a role in inflammation in diabetes. We hypothesized that COX- and RAGE-mediated pathways contribute to increased inflammation in diabetes and potentiate the development of diabetic vascular complications. This was investigated by measuring changes in COX-mediated pathways in both rat and human diabetic models. The current thesis reports: 1) in cultured endothelial cells, histone hyperacetylation was associated with increased COX expression; 2) an overall increase in inflammation was observed in diabetes involving COX- and RAGE-mediated pathways. This was supported by increased platelet COX-1 and monocyte COX-2 levels in Zucker rats, increased monocyte COX-2 in human Type 1 diabetes and elevated plasma TXB2 and PGE2 levels in both human Type 1 and Type 2 diabetic subjects. Up-regulation of RAGE expression was further found in platelets and monocytes in both human diabetes types. When treated with NSAIDs, plasma prostanoid levels, COX and RAGE expression were reduced significantly in both platelets and monocytes in human diabetic subjects. 3) It is unclear how COX and RAGE expression was regulated, but histone modifications may be one of the mechanisms. Data from cultured cells indicated that increased COX expression was associated with increased histone acetylation levels induced by TSA. Concurrent increases in histone acetylation and COX-2 levels were also observed in human Type 1 diabetes, but similar findings were not observed in human Type 2 diabetes. In addition, we failed to find an age-dependent increase in monocyte histone H4 acetylation in human Type 2 diabetes despite an age-dependent increase in monocyte COX-2 expression. Thus, whether histone hyperacetylation modulates COX expression and in what conditions require further investigation.
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Sikora, Kristin [Verfasser]. "RAGE-abhängige S100A8- und S100A9-Expression in humanen THP-1 Zellen / Kristin Sikora." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1023749920/34.
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Gonçalves, Carolina de Souza. "Expressão de proteínas RAP1 recombinantes e produção de anticorpos anti- RAP1: potencial uso como biomarcador no diagnóstico de tumores." s.n, 2014. https://www.arca.fiocruz.br/handle/icict/9945.
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Previous issue date: 2014<br>Fundação Oswaldo Cruz. Centro de Pesquisa René Rachou. Belo Horizonte, MG, Brasil<br>Alterações imunofenotípicas qualitativas e quantitativas na expressão da proteína RAP1, uma pequena GTPase da superfamília RAS, estão presentes em diversos tipos de cânceres, tais como carcinomas de células escamosas de orofaringe, câncer papilar da tireóide, câncer de mama, carcinoma de células renais, leucemia, melanoma, neoplasias intraepiteliais e câncer cervical. Entretanto, para a utilização de RAP1 como biomarcador para auxiliar no diagnóstico imuno-histoquímico de tumores, especialmente do câncer cervical, são necessários anticorpos anti-RAP1 a baixo custo, uma vez que, atualmente, os anticorpos disponíveis no Brasil são importados e de custo elevado, tornando inviável sua utilização no diagnóstico de rotina. Assim, este trabalho tem como objetivos a expressão de proteínas RAP1 recombinantes (rRAP1) em sistema bacteriano, e a produção de anticorpos monoclonais e policlonais anti-rRAP1, visando a sua aplicação no diagnóstico de diversos tumores por imuno-histoquímica. Dois genes RAP1 sintéticos codificantes para as proteínas rRAP1A e rRAP1AB foram desenhados, sintetizados e subclonados no plasmídeo de expressão bacteriano pQE9 e sua expressões obtidas na linhagem hospedeira E.coli M15. Após indução com IPTG, as proteínas rRAP1 foram purificadas por cromatografia líquida em coluna de afinidade de quelato de níquel, obtendo-se o rendimento, por litro de cultura bacteriana, de 185,6 mg/L de rRAP1A e 103,9 mg/L de rRAP1AB. As proteínas rRAP1 purificadas foram inoculadas em animais para a produção de anticorpos monoclonais e policlonais anti-rRAP1A e antirRAP1AB. Ensaios imuno-histoquímicos foram realizados em tecidos de pacientes com neoplasia cervical para a avaliação da reatividade dos anticorpos anti-rRAP1 com a proteína RAP1 humana. Uma intensa imunorreatividade foi verificada com o anticorpo anti-rRAP1A (policlonal produzido em coelhos) considerado, até o momento, o melhor candidato para uso na detecção da expressão de RAP1 em ensaios imuno-histoquímicos, o que pode auxiliar no diagnóstico de várias neoplasias, especialmente, do câncer do colo uterino.<br>Qualitative and quantitative immunophenotypical changes in the expression of RAP1 protein, a small GTPase of the RAS superfamily, have been detected in many types of cancers such as oropharyngeal squamous cell carcinomas, papillary thyroid cancer, breast cancer, renal cell carcinoma, leukemia, melanoma, intraepithelial neoplasia and cervical cancer. However, to use RAP1 as a putative biomarker for immunohistochemical assays to support tumor diagnosis, especially cervical cancer, anti-RAP1 antibodies at low cost are essential, since here in Brazil the anti-RAP antibodies available are imported and expensive making them impractical to use in routine diagnostics. This work aims to express recombinant proteins RAP1 (rRAP1) in bacterial system for the production of monoclonal and polyclonal anti-rRAP1 to be used for diagnosis of various tumors by immunohistochemistry. Two synthetic RAP1 genes coding for rRAP1A and rRAP1AB proteins were designed, synthesized, and subcloned into the pQE9 vector for recombinant protein production in E. coli (strain M15). After IPTG induction, both rRAP1 proteins were purified by nickel chelate affinity chromatography yielding, per liter of bacterial culture, 185,6 mg/L of rRAP1A and 103,9 mg/L of rRAP1AB protein. The purified rRAP1 proteins were used to generate polyclonal and monoclonal antibodies against rRAP1A and against rRAP1AB. Immunohistochemistry experiments were performed on tissues samples from patients with cervical neoplasia to evaluate the reactivity of the anti-rRAP1 antibodies to the human RAP1. An intense immunoreactivity was observed for a rabbit polyclonal anti-rRAP1A antibody, considered so far, the best candidate to be used for RAP1 immunohistochemical testing to support tumor diagnosis, especially cervical cancer.
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Di, Candia Leonarda. "The expression and function of RAGE and HMGB1 in airway structural cells in asthma." Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/32339.
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Asthma is characterised by airway hyperresponsiveness, airflow obstruction, chronic inflammation and airway remodelling, with an increase in airway smooth muscle (ASM) mass and contractility. ASM also releases mediators that support inflammation and remodelling. High-mobility group box 1 (HMGB1) is a nuclear protein that is released by damaged/stressed cells and activated immune cells. HMGB1 signals through pattern recognition receptors (PRRs) including the receptor for advanced glycosylation end products (RAGE) to promote inflammation and tissue repair. HMGB1 binding and function are governed by its redox state. Evidence suggests HMGB1 elevation in asthma; however, the redox state of airway HMGB1 is unknown. Moreover, the expression and role of RAGE in regulating airway mesenchymal cells are unknown. We aimed to investigate HMGB1 and RAGE expression in bronchial tissue; the redox form of sputum HMGB1; the expression and role of HMGB1 and RAGE in airway structural cells. HMGB1 was 3.5-fold higher in sputa of moderate-to-severe asthmatics (n=34), and the reduced form was shown to be increased in this group (n=16) for the first time. Reduced HMGB1 was chemotactic for peripheral blood leukocytes, and sputum HMGB1 correlated with sputum total cell counts. HMGB1, but not RAGE, expression was ~3-fold higher ex vivo in ASM of severe asthmatics (n=16). ASM and human bronchial epithelial cells (HBECs) expressed both HMGB1 and cell-surface RAGE in vitro. HMGB1 expression was upregulated in ASM cells stimulated with inflammatory cytokines. HMGB1 stimulation caused increased reactive oxygen species production in ASM cells from non-asthmatics, but not in asthmatics; ASM contraction and inhibition of ASM cell migration and HBEC wound healing. These results suggest that HMGB1 promotes inflammatory cell recruitment, impairs epithelial and ASM repair, and promotes ASM contraction in asthma. Further work is required to determine whether antagonising HMGB1 or its receptors would be a viable therapeutic approach for the treatment of asthma.
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Lalk, Michael [Verfasser]. "Tumorregionen-abhängige Expression der Aminosäure-Sensoren MAP4K3, RagC und VPS34 in Glioblastomen / Michael Lalk." Magdeburg : Universitätsbibliothek, 2018. http://d-nb.info/1174626593/34.
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Rösch, Daniela. "Regulation der Expression der Rezeptoren für advanced glycation end products (RAGE) auf humanen Monozyten." [S.l. : s.n.], 2006.
Znajdź pełny tekst źródłaKsiążki na temat "RAG1 expression"
1
Gillis, L. Jane. Expression and recombinase activity of RAG 1 and two splice variants of RAG 2 in mature human primary tonsilar B lymphocytes. National Library of Canada, 1999.
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Ferrazza, Daniele de Andrade, and Hilusca Alves Leite. Mulheres e feminismo: perspectivas históricas e desafios atuais. Edufatecie, 2022. http://dx.doi.org/10.33872/edufatecie.mulheresefeminismo.
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O livro Mulheres e feminismo: perspectivas históricas e desafios atuais se propõe a apresentar, nas diferentes perspectivas adotadas pelas diversas autoras, discussões sobre as movimentações feministas de suas trajetórias históricas aos debates contemporâneos. Pretende, também, sensibilizar e mobilizar mulheres em diferentes contextos para uma única luta relacionada aos enfrentamentos contra relações patriarcais, machistas e falocêntricas que reproduzem violências de gênero e impedem a igualdade de direitos de mulheres na contemporaneidade brasileira (RAGO; PELEGRINI, 2019). A coletânea de textos, fruto de um trabalho tecido a várias mãos, é composta por sete capítulos. O primeiro capítulo, escrito por Bárbara Cossettin Costa Beber Brunini, é uma carta-convite a aventurar-se pelos debates feministas, no reconhecimento da potência das narrativas na interseccionalidade decolonial. No segundo capítulo, Daniele de Andrade Ferrazza propõe uma análise da constituição e enfrentamento dos processos de normalização do corpo da mulher. No terceiro capítulo, Bianca Valoski recorre ao feminismo marxista para tratar da acumulação originária sobre corpos femininos explorados no trabalho produtivo e reprodutivo. Seguindo a linha de discussão na perspectiva marxista, Nataly Batista de Jesus explora, no quarto capítulo, o papel das mulheres russas no período pré-revolucionário para compreender o processo de emancipação e conquistas de direitos das mulheres revolucionárias. Pautadas no materialismo histórico de constituição e desenvolvimento desujeitos, expresso pela Psicologia Histórico-Cultural, Tamires Lombardi Mezzon e Hilusca Alves Leite abordam a noção de saúde/doença do corpo feminino. No sexto capítulo, Daniele de Andrade Ferrazza e Mariana Frediani Sant’Ana analisam o fenômeno de psiquiatrização do corpo feminino em sua constituição histórica e atual. E, finalmente, no sétimo capítulo, Débora Nicolau de Oliveira e Deborah Karolina Perez discutem como as revistas brasileiras Manequim, Vogue Brasil e Marie Claire construíram representações sociais da mulher brasileira e influenciaram as mulheres no século XXI. Esperamos, com a proposta de coletânea que aqui apresentamos, somar forças a outras produções acadêmicas sobre os estudos feministas e influenciar reflexões entre leitoras e leitores dispostos a compor conosco a constituição de enfrentamentos ao massacre de direitos que vivenciamos nestes tempos sombrios. Momento no qual forças de direita e ultradireita, não só no Brasil, mas em outros países no mundo, atrasam debates favoráveis à elaboração e implementação de políticas pela garantia da igualdade de gênero. Enfim, organizar este livro significa rememorar lutas históricas feministas e acreditar na tessitura de novos horizontes mais justo, igualitário e libertário.
Części książek na temat "RAG1 expression"
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Ablin, Jason. "Rage On! Gender/Sex, Emotional, and Physical Expression in Schools." In The Gender Equation in Schools. Routledge, 2022. http://dx.doi.org/10.4324/9781003217022-8.
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Ttofa, Juliette, and Paul Greenhouse. "Rage: the shadow side of unspeakable pain." In Using the Expressive Arts with Children and Young People Who Have Experienced Trauma. Routledge, 2022. http://dx.doi.org/10.4324/9781003121411-9.
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van Lent, Anja U., Mireille Centlivre, Maho Nagasawa, et al. "In Vivo Modulation of Gene Expression by Lentiviral Transduction in “Human Immune System” Rag2−/−γc −/− Mice." In Methods in Molecular Biology. Humana Press, 2006. http://dx.doi.org/10.1007/978-1-60761-421-0_6.
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Evans, Dorinda. "5. A Challenge to International Neoclassicism." In William Rimmer. Open Book Publishers, 2022. http://dx.doi.org/10.11647/obp.0304.05.
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Rimmer's major sculptural works, such as St. Stephen, Falling Gladiator, Dying Centaur, and Osirus (destroyed), were created for exhibition and in response to the international neoclassical movement. In different ways, they are actually critiques of the rage for neoclassicism. Much of what Rimmer was trying to do is conveyed in his teaching, and he used his exhibited art as an extension of this. He wanted an art based not on copying from antique casts or from life but, rather, on the artist's own imagination so that the work is self-expressive. The fact that the man in Falling Gladiator assumes an impossible position is an instance of his insistence on the imaginative. The St. Stephen and a cast of the Falling Gladiator were exhibited in Paris at the Salon des Refusés, where the Gladiator created a stir as it seemed, wrongly, to be a cast of a live person. Rimmer broke new ground in producing fragmented human figures with an antique reference, such as his Osiris, a classical-Greek-looking nude male without parts of his arms. They resembled the broken ancient sculpture of the present rather than of the revered past. Originally Osiris had the head of a hawk. As with his pictures, Rimmer also was unusual in frankly accepting and portraying abnormalities as in his Seated Man (Despair). The late Fighting Lions, showing a male and female in vicious combat is arguably an allegory of male dominance. As an original thinker, Rimmer, more than once, explored the problem of expressing the spiritual in the material, most effectively in his relatively abstract Torso, which is an attempt to show the divine awakening or creation of a human soul. Following the Bible, the plaster cast retains the effect of a man’s torso having been crudely fashioned from clay. Perhaps just as unexpected was his plan for a colossal sculpture, Tri Mountain (never executed), which amalgamated the effect of three men and three hills as a symbol of the city of Boston. His one major public statue is the over-life-size Alexander Hamilton on Commonwealth Mall in Boston.
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Buckle, Irina, and Josephine M. Forbes. "The Role of the Receptor for Advanced Glycation Endproducts (RAGE) in Type 1 Diabetes: An Immune Cell Perspective." In Type 1 Diabetes Mellitus [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108528.
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Type 1 diabetes (T1DM) is an autoimmune disorder resulting in destruction of the insulin producing pancreatic β-cells that reside in the Islets of Langerhans. Despite significant progress in the understanding of T1DM pathogenesis, some fundamental contributing mechanisms remain to be fully elucidated. The receptor for advanced glycation end products (RAGE) and its ligands are increasingly believed to play a role in the development of T1DM, but this is not well understood. The location of RAGE gene is shared with major T1DM genetic susceptibility loci on chromosome 6 and polymorphism of this region confers risk for T1DM. Furthermore, changes in RAGE expression on and ligand binding by immune cells, in particular T cells, are associated with pro-inflammatory and autoimmune profiles key for T1DM development. Indeed, in murine models for T1DM, targeting of RAGE or its ligands decreased onset and severity of disease including favorable immune cell profiles and infiltration and improved beta cell insulin secretory function. Further understanding of RAGE expression and signaling in immune cells in T1DM will provide valuable insights into disease pathogenesis and therapy development. This chapter will discuss what is currently known about RAGE in the immune cells integral for the pathogenesis of T1DM.
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Brooks, Mary M. "“Rags of Popery”." In In-Between Textiles, 1400–1800. Amsterdam University Press, 2023. http://dx.doi.org/10.5117/9789463729086_ch08.
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This chapter examines how clerical garments became disruptive signifiers of religious and political (dis)connections in early modern England. Ritual garb, this chapter argues, became a material expression of a minority “social articulation of difference” which Bhabha positions as “a complex, on-going negotiation that seeks to authorize cultural hybridities that emerge in moments of historical transformation.” Freighted with conflicted values, vestments physically “fix[ed] cultural difference in a containable, visible object” at a time of religious flux. Their very cultural fluidity and ability to carry alternative meanings made vestments simultaneously a threat or a comfort, seen as emblems of deceit or continuity as they were rejected by reformers and claimed by believers.
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Strozier, Charles B., Konstantine Pinteris, Kathleen Kelley, and Deborah Cher. "Rage and Aggression." In The New World of Self. Oxford University PressNew York, 2022. http://dx.doi.org/10.1093/oso/9780197535226.003.0005.
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Abstract Heinz Kohut conceptualized aggression as a healthy and life-affirming aspect of the human experience, as distinct from the expression of rage at the individual or societal level. In doing so, Kohut offered a new interpretation of aggression that was not based on drive theory. That in turn led to a theory of rage that explains much about violence and its relationship to self states. This chapter discusses in detail the interplay of rage with narcissistic injury, shame, and humiliation. It delineates the sequence leading to rage, including the significance of fragmentation of the self, of which rage is a restitutional byproduct. As was often the case with Kohut, his theorizing on rage was informed by a range of sources, including his clinical work, literature, and history. Vignettes from these sources are included as well as implications for clinical practice.
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"Royal Rage and Private Anger in Ancient Egypt." In The Expression of Emotions in Ancient Egypt and Mesopotamia. BRILL, 2020. http://dx.doi.org/10.1163/9789004430761_005.
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Pedersen, Torgeir Rebolledo. "Om stillhet, raseri og rytme." In Stemma og stilla i musikk og litteratur: Festskrift til Magnar Åm. Cappelen Damm Akademisk/NOASP, 2022. http://dx.doi.org/10.23865/noasp.158.ch4.
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In this essay the poet Torgeir Rebolledo Pedersen explores the intersection of sound and silence in a text as a particular location for the creation of meaning. With reference to poems of Rolf Jacobsen and Robert Creely, Pedersen asserts the reciprocity of sound and silence as conditions for each other, and for the life-affirming musical component of rhythm. While one property of silence is that it can never be total, whether in a text or in the world at large, another is that it can hold and harbor fury. Silence can thus be ambiguous, as an expression of unreflective and automatic passivity, but also a force within creative verbal expressions of rage and resistance, for instance against the politics of a previous prime minister who went on to lead NATO. Like the African slaves of history, we might understand the power of sound and silence harnessed in rhythm, in the service of survival and the expression of resistance. Pedersen understands both rhythm and silence dialectically, proposing that a particular, perhaps world-changing imperative may be found at the point of their intersection in the words of poetic texts.
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Abdul-Ghani, Casarae Lavada. "The Inability to Compromise." In Start a Riot! University Press of Mississippi, 2022. http://dx.doi.org/10.14325/mississippi/9781496840455.003.0002.
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This chapter examines Amiri Baraka's (LeRoi Jones) and Ben Caldwell's underexamined plays The Slave and Riot Sale, or Dollar Psyche Fake Out. In it, the chapter argues that BAM artists-writers like Baraka and Caldwell employ Black rage as a central component of revolts designed to protest and dismantle the systemic racism that lingers within American society. Ironically, through the seemingly chaotic and disparate expression of rage and revolution, Baraka and Caldwell reveal Black America’s derived sense of racial unity as they work toward the common goal of social and economic equality. Through its representations of rebellion (and the rage that energizes it), the 'revolutionary theatre' of Baraka and Caldwell ultimately delineates and affirms a Black political subjectivity.
Streszczenia konferencji na temat "RAG1 expression"
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Ge, zheng, Qi Han, Jinlong Ma, et al. "Abstract 5507: RAG1 high expression associated with IKZF1 dysfunction in adult B-cell acute lymphoblastic leukemia." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5507.
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de Souza Xavier Costa, Natália, Giovana Da Costa Sigrist, Marisa Dolhnikoff, and Luiz Fernando Ferraz Da Silva. "RAGE expression in lung tissue of ARDS and septic patients." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2752.
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Vieira, Paula Cristina de Vasconcelos, Adriano de Paula Sabino, Jaqueline Germano de Oliveira, Marcelo Antônio Pascoal Xavier, Annamaria Ravara Vago, and Maria Gabrielle de Lima Rocha. "Avaliação de RAP1 como biomarcador da neoplasia intraepitelial cervical." In XIII Congresso da Sociedade Brasileira de DST - IX Congresso Brasileiro de AIDS - IV Congresso Latino Americano de IST/HIV/AIDS. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/dst-2177-8264-202133p067.
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Introdução: Mundialmente, o carcinoma de colo uterino associado ao papilomavírus humano está entre as maiores causas de morte relacionadas ao câncer na população feminina. Nos últimos anos, a detecção de lesões pré-neoplásicas mediante a ação de programas consolidados de rastreamento, prevenção e acompanhamento clínico permitiram a redução das taxas de câncer de colo em diversos países. Entretanto, essa neoplasia ainda é muito frequente. Esse problema tem fortalecido a procura por biomarcadores que possam aumentar a eficiência do rastreamento. Entre esses biomarcadores está RAP1, pequena GTPase com atuação em múltiplas vias de sinalização celular e em processos neoplásicos. Objetivo: Avaliar, em biópsias de colo uterino diagnosticadas por histopatologia em cervicites, lesões pré-neoplásicas e neoplásicas, (i) a expressão de RAP1 por imuno-histoquímica nas áreas lesionadas do epitélio, (ii) a prevalência da infecção por papilomavírus humano por meio da Nested Polymerase Chain Reaction e a genotipagem dos papilomavírus humano por sequenciamento automático de ácido desoxirribonucleico. Resultados: A presença do ácido desozirribonucleico do vírus da imunodeficiência humana foi observada em 74% das amostras, e o genótipo do vírus da imunodeficiência humana 16 foi o mais prevalente, especialmente em neoplasia intraepitelial cervical grau III e câncer. Em relação a RAP1 em tecidos cervicais, observou-se a expressão da proteína em amostras de todos os grupos analisados. A marcação esteve predominantemente no núcleo e no citoplasma de células epiteliais, representando 69% das amostras cervicais. Em relação ao parâmetro intensidade da marcação, verificou-se que amostras de neoplasia intraepitelial cervical grau III exibiram maior intensidade de RAP1 do que lesões de menor gravidade (Cervicites + neoplasia intraepitelial cervical grau I). Nas amostras de carcinoma de células escamosas também se observou a imunomarcação para RAP1 predominantemente intensa, com forte marcação nuclear. Percebe-se que nas lesões mais graves, neoplasia intraepitelial cervical grau III e carcinoma de células escamosas a quantidade de núcleos marcados é mais elevada se comparado a lesões mais leves. Conclusão: Uso potencial da marcação tecidual de RAP1 como biomarcador de lesões cervicais de maior gravidade, como neoplasia intraepitelial cervical grau III e carcinoma de células escamosas.
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Perkins, Timothy, Elizabeth Oczypok, Regina Dutz, and Tim Oury. "RAGE-dependent VCAM-1 expression in the pulmonary endothelium mediates IL-33 induced asthma pathogenesis." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa4915.
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Kasahara, D. I., A. Nicholas, T. Reed, et al. "Silencing RAGE Expression with a Lung-Targeted RNAi Trigger Delivery Platform Suppresses Pulmonary Allergic Inflammation." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a5013.
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AI, Cabrera-García, M. Protschka, G. Alber, et al. "Dysregulation of gastrointestinal RAGE (receptor for advanced glycation end products) expression in dogs with inflammatory bowel disease." In 29. Jahrestagung der FG „Innere Medizin und klinische Labordiagnostik“ der DVG (InnLab) – Teil 2: Poster. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1723879.
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Mangalmurti, Nilam S., Jessica Friedman, Liang Chuan Wang, et al. "Banked RBCs Induce The Expression Of The Receptor For Advanced Glycation Endproducts (RAGE) On Lung Endothelial Cells." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5498.
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Leckelt, J., F. Thomas, A. Kott, et al. "Eine hohe RAGE Expression könnte für das frühzeitige Auftreten von Diabetes mellitus assoziierten neuropathischen Schädigungen der cornealen Nervenfasern verantwortlich sein." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641966.
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Pendyala, S., I. Gorshkova, PV Usatyuk, et al. "Nrf2 Regulation of Hyperoxia-Mediated Nox4 Expression and ROS Production in Lung Endothelium: Role of Rac1, MAP Kinases and Redox Status." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3861.
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Wan, Qiaoqiao, Eunhye Cho, Seungman Park, Bumsoo Han, Hiroki Yokota, and Sungsoo Na. "Visualizing Chondrocyte Mechanotransduction in 3D." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14484.
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Chondrocytes are the only cell type present in the articular cartilage and their response to mechanical stimuli influences the maintenance and remodeling of the cartilage. Numerous studies have shown that the balance between anabolic and catabolic responses of the chondrocytes to mechanical loading is dependent on the loading intensities (reviewed in ref. [1]). Moderate, physiological loading, for instance, increases synthetic activity of the extracellular matrix (ECM) such as collagen type II, aggrecan, and proteoglycan, while decreasing the catabolic activity of degradative enzymes such as matrix metalloproteinases (MMPs) and ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) [2,3]. In contrast to moderate loading, static or high-intensity loading has been shown to degrade the cartilage resulting from inhibition of matrix synthesis and up-regulation of catabolic activities [3,4]. Therefore, the importance of these load-dependent signaling pathways involved in the maintenance and remodeling of the cartilage is widely accepted. However, the underlying mechanisms as to how varying magnitudes of mechanical stimuli trigger differential signaling activities that consequently lead to selective gene expression are not clear. FAK and Src are considered to be the main mechanotransduction signaling proteins at the cell-ECM adhesion sites and their activities influence various structural and signaling changes within the cell, including cytoskeletal organization, migration, proliferation, differentiation, and survival [5]. Accumulating evidence has shown that Src and FAK play crucial roles in regulating cartilage maintenance and degeneration and their activation stimulates matrix catabolic genes and activity [6,7]. Rho family GTPases such as RhoA and Rac1 play critical roles in fundamental processes including morphogenesis, polarity, movement, and cell division [8]. They also contribute to cartilage development and degradation [9,10]. Despite these studies, much remains to be elucidated on how load-induced Src and FAK participate in chondrocyte functions, and how their interactions are linked and regulated in connection to the activities of RhoA and Rac1 under different loading conditions. In this study, we use fluorescence resonance energy transfer (FRET)-based biosensors to monitor activities of Src and FAK as well as individual GTPases and evaluate the potential linkage of a network of these signaling molecules under different loading conditions.
Raporty organizacyjne na temat "RAG1 expression"
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Su, Bing. The Role of mTOR Signaling in the Regulation of RAG Expression and Genomic Stability during B Lymphocyte Development. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada588301.
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