102 research outputs found
Infinite Archives, Infinite Possibilities: Learning Research and Databases with Archive of our Own
This article will discuss the importance of acknowledging the information practices of subcultural groups within library instruction and fostering an inclusive learning environment with the implementation of a workshop by comparing research databases with the popular fanfiction website, Archive of Our Own. By incorporating AO3 into library instruction, students’ interests and prior experiences were engaged by utilizing the principles of subcultural capital. The workshop utilized students’ knowledge of information searching from their personal lives and their interests to highlight similarities with academic research using examples such as filters, keywords, and author searching. This allowed students to develop skills to search precisely for materials in a familiar environment. Further, the success of the workshop demonstrates how librarians can incorporate fan’s informational behaviors, and access practices into instructional content about research and database usage, making research less intimidating and more accessible to students
Molecular determinants and interaction data of cyclic peptide inhibitor with the extracellular domain of TrkB receptor
TrkB is a high affinity receptor for the brain derived neurotrophic factor (BDNF) and its phosphorylation stimulates activation of several intracellular signalling pathways linked to cellular growth, differentiation and maintenance. Identification of various activators and inhibitors of the TrkB receptor and greater understanding their binding mechanisms is critical to elucidate the biochemical and pharmacological pathways and analyse various protein crystallization studies. The data presented here is related to the research article entitled Brain Derived neurotrophic factor is involved in the regulation of glycogen synthase kinase 3β (GSK3β) signalling [1]. Cyclotraxin B (CTXB) is a disulphide bridge linked cyclic peptide molecule that interacts with TrkB receptor and inhibits the BDNF/TrkB downstream signalling. This article reports for the first time binding mechanism and interaction parameters of CTXB with the TrkB receptor. The molecular model of CTXB has been generated and it\u27s docking with TrkB domain carried out to determine the critical residues involved in the protein peptide interaction. © 2016 The Authors
Analyzing the regulation of metabolic pathways in human breast cancer
<p>Abstract</p> <p>Background</p> <p>Tumor therapy mainly attacks the metabolism to interfere the tumor's anabolism and signaling of proliferative second messengers. However, the metabolic demands of different cancers are very heterogeneous and depend on their origin of tissue, age, gender and other clinical parameters. We investigated tumor specific regulation in the metabolism of breast cancer.</p> <p>Methods</p> <p>For this, we mapped gene expression data from microarrays onto the corresponding enzymes and their metabolic reaction network. We used Haar Wavelet transforms on optimally arranged grid representations of metabolic pathways as a pattern recognition method to detect orchestrated regulation of neighboring enzymes in the network. Significant combined expression patterns were used to select metabolic pathways showing shifted regulation of the aggressive tumors.</p> <p>Results</p> <p>Besides up-regulation for energy production and nucleotide anabolism, we found an interesting cellular switch in the interplay of biosynthesis of steroids and bile acids. The biosynthesis of steroids was up-regulated for estrogen synthesis which is needed for proliferative signaling in breast cancer. In turn, the decomposition of steroid precursors was blocked by down-regulation of the bile acid pathway.</p> <p>Conclusion</p> <p>We applied an intelligent pattern recognition method for analyzing the regulation of metabolism and elucidated substantial regulation of human breast cancer at the interplay of cholesterol biosynthesis and bile acid metabolism pointing to specific breast cancer treatment.</p
- …