Update citations (usegalaxy-eu#1274)

Co-authored-by: bgruening <[email protected]>

_bibliography/citations-eu.bib

@@ -271,6 +271,24 @@ @article{alawi_private_2024
  year = {2024}
 }
 
+@incollection{albrecht_amplicon-based_2024,
+ abstract = {DNA methylation is an important epigenetic modification that regulates chromatin structure and the cell-type-specific expression of genes. The association of aberrant DNA methylation with many diseases, as well as the increasing interest in modifying the methylation mark in a directed manner at genomic sites using epigenome editing for research and therapeutic purposes, increases the need for easy and efficient DNA methylation analysis methods. The standard approach to analyze DNA methylation with a single-cytosine resolution is bisulfite conversion of DNA followed by next-generation sequencing (NGS). In this chapter, we describe a robust, powerful, and cost-efficient protocol for the amplification of target regions from bisulfite-converted DNA, followed by a second PCR step to generate libraries for Illumina NGS. In the two consecutive PCR steps, first, barcodes are added to individual amplicons, and in the second PCR, indices and Illumina adapters are added to the samples. Finally, we describe a detailed bioinformatics approach to extract DNA methylation levels of the target regions from the sequencing data. Combining barcodes with indices enables a high level of multiplexing allowing to sequence multiple pooled samples in the same sequencing run. Therefore, this method is a robust, accurate, quantitative, and cheap approach for the readout of DNA methylation patterns at defined genomic regions.},
+ address = {New York, NY},
+ author = {Albrecht, Claudia and Bashtrykov, Pavel and Jeltsch, Albert},
+ booktitle = {Epigenome {Editing}: {Methods} and {Protocols}},
+ doi = {10.1007/978-1-0716-4051-7_21},
+ editor = {Jeltsch, Albert and Rots, Marianne G.},
+ isbn = {978-1-07-164051-7},
+ keywords = {{\textgreater}UseGalaxy.eu},
+ language = {en},
+ pages = {405--418},
+ publisher = {Springer US},
+ title = {Amplicon-{Based} {Bisulfite} {Conversion}-{NGS} {DNA} {Methylation} {Analysis} {Protocol}},
+ url = {https://doi.org/10.1007/978-1-0716-4051-7_21},
+ urldate = {2024-07-20},
+ year = {2024}
+}
+
 @article{alcaraz_development_2021,
  abstract = {There is increasing pressure to develop alternative ecotoxicological risk assessment approaches that do not rely on expensive, time-consuming, and ethically questionable live animal testing. This study aimed to develop a comprehensive early life stage toxicity pathway model for the exposure of fish to estrogenic chemicals that is rooted in mechanistic toxicology. Embryo-larval fathead minnows (FHM; Pimephales promelas) were exposed to graded concentrations of 17α-ethinylestradiol (water control, 0.01\% DMSO, 4, 20, and 100 ng/L) for 32 days. Fish were assessed for transcriptomic and proteomic responses at 4 days post-hatch (dph), and for histological and apical end points at 28 dph. Molecular analyses revealed core responses that were indicative of observed apical outcomes, including biological processes resulting in overproduction of vitellogenin and impairment of visual development. Histological observations indicated accumulation of proteinaceous fluid in liver and kidney tissues, energy depletion, and delayed or suppressed gonad development. Additionally, fish in the 100 ng/L treatment group were smaller than controls. Integration of omics data improved the interpretation of perturbations in early life stage FHM, providing evidence of conservation of toxicity pathways across levels of biological organization. Overall, the mechanism-based embryo-larval FHM model showed promise as a replacement for standard adult live animal tests.},
  author = {Alcaraz, Alper James G. and Potěšil, David and Mikulášek, Kamil and Green, Derek and Park, Bradley and Burbridge, Connor and Bluhm, Kerstin and Soufan, Othman and Lane, Taylor and Pipal, Marek and Brinkmann, Markus and Xia, Jianguo and Zdráhal, Zbyněk and Schneider, David and Crump, Doug and Basu, Niladri and Hogan, Natacha and Hecker, Markus},
@@ -5673,6 +5691,23 @@ @article{kohler_msstatsshiny_2023
  year = {2023}
 }
 
+@article{kojima_cytochrome_nodate,
+ abstract = {Austocystin D is a natural compound that induces cytochrome P450 (CYP) monooxygenase-dependent DNA damage and growth inhibition in certain cancer cell lines. Cancer cells exhibiting higher sensitivity to austocystin D often display elevated CYP2J2 expression. However, the essentiality and the role of CYP2J2 for the cytotoxicity of this compound remain unclear. In this study, we demonstrate that CYP2J2 depletion alleviates austocystin D sensitivity and DNA damage induction, while CYP2J2 overexpression enhances them. Moreover, the investigation into genes involved in austocystin D cytotoxicity identified POR and PGRMC1, positive regulators for CYP activity, and KAT7, a histone acetyltransferase. Through genetic manipulation and analysis of multiomics data, we elucidated a role for KAT7 in CYP2J2 transcriptional regulation. These findings strongly suggest that CYP2J2 is crucial for austocystin D metabolism and its subsequent cytotoxic effects. The potential use of austocystin D as a therapeutic prodrug is underscored, particularly in cancers where elevated CYP2J2 expression serves as a biomarker.},
+ author = {Kojima, Yukiko and Fujieda, Saki and Zhou, Liya and Takikawa, Masahiro and Kuramochi, Kouji and Furuya, Toshiki and Mizumoto, Ayaka and Kagaya, Noritaka and Kawahara, Teppei and Shin-ya, Kazuo and Dan, Shingo and Tomida, Akihiro and Ishikawa, Fuyuki and Sadaie, Mahito},
+ copyright = {© 2024 The Author(s). Cancer Science published by John Wiley \& Sons Australia, Ltd on behalf of Japanese Cancer Association.},
+ doi = {10.1111/cas.16289},
+ issn = {1349-7006},
+ journal = {Cancer Science},
+ keywords = {{\textgreater}UseGalaxy.eu, DNA damage, austocystin D, cytotoxicity, gene expression, knockout screening},
+ language = {en},
+ note = {\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1111/cas.16289},
+ number = {n/a},
+ title = {Cytochrome {P450} {2J2} is required for the natural compound austocystin {D} to elicit cancer cell toxicity},
+ url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/cas.16289},
+ urldate = {2024-07-19},
+ volume = {n/a}
+}
+
 @article{kolosov_malpighian_2019,
  abstract = {Skip to Next Section
 The Malpighian tubules (MTs) and hindgut constitute the functional kidney of insects. MTs are outpouchings of the gut and in most insects demonstrate proximodistal heterogeneity in function. In most insects, such heterogeneity is confined to ion/fluid secretion in the distal portion and ion/fluid reabsorption in the proximal portion. In contrast, MTs of larval Lepidoptera (caterpillars of butterflies and moths) are composed of five regions that differ in their association with the gut, their structure and ion/fluid transport function. Recent studies have shown that several regions can rapidly and reversibly switch between ion secretion and reabsorption. The present study employed RNAseq, pharmacology and electrophysiology to characterize four distinct regions of the MT in larval Trichoplusia ni. Luminal microelectrode measurements indicate changes in [K+], [Na+] and pH as fluid passes through different regions of the tubule. In addition, the regions examined differ in gene ontology enrichment, and demonstrate robust gradients in expression of ion transporters and endocrine ligand receptors. Lastly, the study provides evidence for direct involvement of voltage- and ligand-gated ion channels in epithelial ion transport of insect MTs.},