2,966 research outputs found
aE Journal 2015/2016: aE/INTECTURE innovating architecture
No full textThe graduation studio of Architectural Engineering focuses on the integration of (new) technology in architecture. For this purpose, the name aE/ INTECTURE® was devised, which will be developed further as a brand in the coming years. Students start with a technical fascination and translate this into an architectural concept, finally being able to implement this within the environment in a responsible way. ‘If technology is the answer, what is the question?‘ Under the guidance of a team of enthusiastic (guest) lecturers, students search for the dot on the horizon that is necessary for coming up with solutions that improve the quality of the built environment and make it more sustainable. In addition, either the ‘making‘ (make) or ‘the energy and material flow’ (flow) is used and applied as a basis in different contexts.Architectural Engineerin
p73 and p63 regulate the expression of fibroblast growth factor receptor 3
No full textp53, p63 and p73 make a family of transcription factors that play a vital role in development and cancer. All p53 family members have more than one promoter producing Transactivating (TA) and Dominant Negative (DeltaN) isoforms and their mRNAs are subjected to extensive splicing at 3' end to produce multiple protein products. p53 is usually inactivated by point mutations during tumorigenesis, whereas the expression levels and p63 and p73 are modulated to give tumor cells a selective advantage. In this study, aiming to find novel targets of the p53 family members, we identified FGFR3 as a gene transcriptionally controlled by p63 and p73. FGFR3 has been implicated in development and tumor biology as activating mutations of this gene was described in skeletal disorders, non-invasive skin conditions and superficial bladder cancers. We found that TAp73, TAp63 and DeltaNp63 was capable of inducing FGFR3. siRNA mediated downregulation of DeltaNp63 decreased endogenous FGFR3 protein levels. Our findings of this new link between p53 family proteins and FGFR3 may help understanding the transition of superficial bladder cancers to an invasive phenotyp
Mechanism of induction of apoptosis by p73 and its relevance to neuroblastoma biology
No full textTP73, as a TP53 homologue, drew the attention of tumor biologists because it is rarely mutated in human cancers and can induce cell cycle arrest and apoptosis by activating genes also regulated by p53. However, TP73 harbors an additional promoter that produces a dominant negative p73 protein (Delta Np73) having the opposite effect of the TAp73 protein. Thus, the regulation F of p53 responsive genes in the absence of p53 relies on a critical balance I between different p73 gene-derived proteins. Recent reports have described additional complexity in the mechanism of action of transcriptionally active p73 (TAp73) in the induction of cell death. The molecular mechanism through which p73 induces apoptosis involves (i) expression and changes in subcellular localization of scotin, producing an endoplasmic reticulum (ER) stress; and (ii) transactivation of PUMA and Bax, thus determining cell fate. On the contrary, Delta Np73 inhibits apoptosis, thus contributing to the oncogenic potential of neuroblastoma cells
Cleavage of the transactivation-inhibitory domain of p63 by caspases enhances apoptosis
No full textp63 is a p53-related transcription factor. Utilization of two different promoters and alternative splicing at the C terminus lead to generation of six isoforms. The α isoforms of TAp63 and ΔNp63 contain a transactivation-inhibitory (TI) domain at the C termini, which can bind to the transactivation (TA) domain and inhibit its transcriptional activity. Consequently, TAp63α can directly inhibit its activity through an intramolecular interaction; similarly, ΔNp63α can inhibit the activity of the active TAp63 isoforms through an intermolecular interaction. In this work, we demonstrate that after induction of apoptosis, the TI domain of the p63α isoforms is cleaved by activated caspases. Cleavage of ΔNp63α relieves its inhibitory effect on the transcriptionally active p63 proteins, and the cleavage of TAp63α results in production of a TAp63 protein with enhanced transcriptional activity. In agreement with these data, generation of the N-terminal TAp63 fragment has a role in apoptosis because stable cell lines expressing wild-type TAp63 are more sensitive to apoptosis compared with cells expressing the noncleavable mutant. We also used a model system in which TAp63 expression was induced by trichostatin-A treatment in HCT116 cells. Trichostatin-A sensitized these cells to apoptosis, and this sensitization was associated with cleavage of up-regulated p63. © 2007 by The National Academy of Sciences of the USA
aE Journal 2017/2018: aE/Intecture innovating architecture
No full textDriven by the need to think differently about resources, energy, power generation, the choice of materials, and user involvement, we see the built environment in a new perspective. The program, Architectural Engineering, seeks for innovative and inspiring architectural solutions for social and environmental issues throughout all scales.To achieve this, innovation of the architectural challenge is high on our agenda. Innovation is more than just a technical improvement. How do you implement new current issues in modern architecture? We anticipate new energy, materials, and circularity. We also use the current environment of the metropolis and the countryside. We add new buildings, strengthen existing stock, and work on new components of buildings. From high to low tech. From digital to traditional, looking carefully to the context.Architectural Engineerin
p73 and p63 regulate the expression of fibroblast growth factor receptor 3
No full textp53, p63 and p73 make a family of transcription factors that play a vital role in development and cancer. All p53 family members have more than one promoter producing Transactivating (TA) and Dominant Negative (ΔN) isoforms and their mRNAs are subjected to extensive splicing at 3' end to produce multiple protein products. p53 is usually inactivated by point mutations during tumorigenesis, whereas the expression levels and p63 and p73 are modulated to give tumor cells a selective advantage. In this study, aiming to find novel targets of the p53 family members, we identified FGFR3 as a gene transcriptionally controlled by p63 and p73. FGFR3 has been implicated in development and tumor biology as activating mutations of this gene was described in skeletal disorders, non-invasive skin conditions and superficial bladder cancers. We found that TAp73, TAp63 and DeltaNp63 was capable of inducing FGFR3. siRNA mediated downregulation of DeltaNp63 decreased endogenous FGFR3 protein levels. Our findings of this new link between p53 family proteins and FGFR3 may help understanding the transition of superficial bladder cancers to an invasive phenotype
Main motifs in the prose of the leftist author Kang Kyŏng-ae
No full textThe subject of this bachelor thesis is the life and work of the Korean writer Kang Kyǒng-ae, with a focus on her short prose. The aim of this thesis is an analysis of two works - Salt and Darkness - with attention to the context of the author's time. Nowadays, Kang Kyǒng-ae is considered a significant author of the 1930s and her works reflect the phenomenon of Korean emigrants in Manchuria. For a long time, leftist tendencies caused her prose to be neglected, which resulted in a considerably limited number of studies concerned with her work, in comparison to the number of studies about other writers. There are virtually no Czech studies of her work. The text of the thesis initially presents the timeframe of Kang's authorship and then analyzes select works of hers. The analysis of the works focuses on recurring motifs, which are put into a historical and social context. Keywords Kang Kyǒng-ae, Korean 1930s literature, leftist literature, Sogǔm, Ǒdu
Brn-3a/POU4F1 interacts with and differentially affects p73-mediated transcription
No full textThe Brn-3a/POU4F1 POU transcription factor is critical for the survival and differentiation of specific sensory neurons during development or upon injury; by regulating expression of target genes, either directly or indirectly upon interaction with other proteins. In this study, we demonstrated the physical interaction of Brn-3a with different p73 isoforms and showed co-localization in sensory neurons arising from the neural crest. The biological effects of p73/ Brn-3a interaction depend on the particular p73 isoform, because co-expression of Brn-3a with TAp73 enhanced cell cycle arrest, whereas Brn-3a and ?Np73 cooperated to increase protection from apoptosis. Brn-3a antagonized TAp73 transactivation of pro-apoptotic Bax, but co-operated to increase transcription of the cell cycle regulator p21CIP1/Waf1. The region 425–494 amino acids within the TAp73 C terminus were critical for Brn-3a to repress Bax transactivation, but not for cooperation on the p21CIP1/Waf1 promoter. Our results suggest that co-factors binding to the p73 C terminus facilitate maximal activation on the Bax but not p21CIP1/Waf1 promoter and that Brn-3a modulates this interaction. Thus, the physical interaction of Brn-3a with specific p73 isoforms will be critical for determining cell fate during neuronal development or in injured neurons expressing both factors.<br/
Biographical Romance, or The Wonders of ihe Life of An Émigrée of Choice: Fryderyk Járosy (1889–1960) – the Author of Unwritten Memoirs of Life Among the Polish Diaspora in London
No full textEnglish version. Original issue: “Archiwum Emigracji” 2009, no. 1 (10)https://apcz.umk.pl/AE/article/view/AE.2009.01
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