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2,087 results on '"Robinson A"'

14. CRISPR/Cas-based screening of long non-coding RNAs (lncRNAs) in macrophages with an NF-κB reporter

Author

Covarrubias, Sergio, Robinson, Elektra K, Shapleigh, Barbara, Vollmers, Apple, Katzman, Sol, Hanley, Nicole, Fong, Nicholas, McManus, Michael T, and Carpenter, Susan

Subjects
Biological Sciences, Medicinal and Biomolecular Chemistry, Chemical Sciences, Genetics, Biotechnology, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Animals, CRISPR-Cas Systems, Cells, Cultured, Cyclooxygenase 2, Gene Knockout Techniques, Genes, Reporter, Green Fluorescent Proteins, Humans, Immunity, Innate, Macrophages, Mice, NF-kappa B, RNA, Long Noncoding, Recombinant Fusion Proteins, Signal Transduction, CRISPR/Cas, NF-κB, inflammation, long non-coding RNA, macrophage, toll-like receptor, Medical and Health Sciences, Biochemistry & Molecular Biology, Biological sciences, Biomedical and clinical sciences, Chemical sciences
Abstract

The innate immune system protects against infections by initiating an inducible inflammatory response. NF-κB is one of the critical transcription factors controlling this complex response, but some aspects of its regulation remain unclear. For example, although long non-coding RNAs (lncRNAs) have been shown to critically regulate gene expression, only a fraction of these have been functionally characterized, and the extent to which lncRNAs control NF-κB expression is unknown. Here, we describe the generation of a GFP-based NF-κB reporter system in immortalized murine bone marrow-derived macrophages (iBMDM). Activation of this reporter, using Toll-like receptor ligands, resulted in GFP expression, which could be monitored by flow cytometry. We also established a CRISPR/Cas9 gene deletion system in this NF-κB reporter line, enabling us to screen for genes that regulate NF-κB signaling. Our deletion-based approach identified two long intergenic non-coding(linc)RNAs, lincRNA-Cox2 and lincRNA-AK170409, that control NF-κB signaling. We demonstrate a potential novel role for lincRNA-Cox2 in promoting IκBα degradation in the cytoplasm. For lincRNA-AK170409, we provide evidence that this nuclearly-localized lincRNA regulates a number of inflammation-related genes. In conclusion, we have established an NF-κB-GFP iBMDM reporter cell line and a line that stably expresses Cas9. Our approach enabled the identification of lincRNA-Cox2 and lincRNA-AK170409 as NF-κB regulators, and this tool will be useful for identifying additional genes involved in regulating this transcription factor critical for immune function.

Published
2017

23. Iron is a ligand of SecA-like metal-binding domains in vivo

Author

Cranford-Smith, Tamar, Jamshad, Mohammed, Jeeves, Mark, Chandler, Rachael A., Yule, Jack, Robinson, Ashley, Alam, Farhana, Dunne, Karl A., Aponte Angarita, Edwin H., Alanazi, Mashael, Carter, Cailean, Henderson, Ian R., Lovett, Janet E., Winn, Peter, Knowles, Timothy, and Huber, Damon

Published
2020
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36. Structural and functional analysis of Dickkopf 4 (Dkk4): New insights into Dkk evolution and regulation of Wnt signaling by Dkk and Kremen proteins

Author

Patel, Saleha, Barkell, Alice M., Gupta, Deepti, Strong, Sarah L., Bruton, Shaun, Muskett, Frederick W., Addis, Philip W., Renshaw, Philip S., Slocombe, Patrick M., Doyle, Carl, Clargo, Alison, Taylor, Richard J., Prosser, Christine E., Henry, Alistair J., Robinson, Martyn K., Waters, Lorna C., Holdsworth, Gill, and Carr, Mark D.

Published
2018
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50. Uropathogenic Escherichia coli wield enterobactin-derived catabolites as siderophores.

Author

Zongsen Zou, Robinson, John I., Steinberg, Lindsey K., and Henderson, Jeffrey P.

Subjects
*ESCHERICHIA coli, *SIDEROPHORES, *URINARY tract infections, *IRON, *IRON ions, *DEFEROXAMINE
Abstract

Uropathogenic Escherichia coli (UPEC) secrete multiple siderophore types to scavenge extracellular iron(III) ions during clinical urinary tract infections, despite the metabolic costs of biosynthesis. Here, we find the siderophore enterobactin (Ent) and its related products to be prominent components of the iron-responsive extracellular metabolome of a model UPEC strain. Using defined Ent biosynthesis and import mutants, we identify lower molecular weight dimeric exometabolites as products of incomplete siderophore catabolism, rather than prematurely released biosynthetic intermediates. In E. coli, iron acquisition from iron(III)-Ent complexes requires intracellular esterases that hydrolyze the siderophore. Although UPEC are equipped to consume the products of completely hydrolyzed Ent, we find that Ent and its derivatives may be incompletely hydrolyzed to yield products with retained siderophore activity. These results are consistent with catabolic inefficiency as means to obtain more than one iron ion per siderophore molecule. This is compatible with an evolved UPEC strategy to maximize the nutritional returns from metabolic investments in siderophore biosynthesis. [ABSTRACT FROM AUTHOR]

Published
2024
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