Non-DNA microarrays, such as protein, peptide and small molecule microarrays, can potentially revolutionize the high-throughput screening tools currently used in basic and pharmaceutical research. However, fundamental obstacles remain that limit their rapid and widespread implementation as an alternative bioanalytical approach. These include the prerequisite for numerous proteins in active and purified form, ineffectual immobilization strategies and inadequate means for quality control of the considerable numbers of multiple reagents. This study describes a simple yet efficient strategy for the production of non-DNA microarrays, based on the tenacious affinity of a carbohydrate-binding module (CBM) for its three-dimensional substrate, i.e., cellulose. Various microarray formats are described, e.g., conventional and single-chain antibody microarrays and peptide microarrays for serodiagnosis of human immunodeficiency virus patients. CBM-based microarray technology overcomes many of the previous obstacles that have hindered fabrication of non-DNA microarrays and provides a technically simple but effective alternative to conventional microarray technology.
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http://dx.doi.org/10.1002/pmic.200401078 | DOI Listing |
Arch Toxicol
February 2018
In Vitro Toxicology Group, Institute of Life Science 1, Singleton Campus, Swansea University Medical School, Swansea University, Swansea, SA2 8PP, UK.
Human exposure to carcinogens occurs via a plethora of environmental sources, with 70-90% of cancers caused by extrinsic factors. Aberrant phenotypes induced by such carcinogenic agents may provide universal biomarkers for cancer causation. Both current in vitro genotoxicity tests and the animal-testing paradigm in human cancer risk assessment fail to accurately represent and predict whether a chemical causes human carcinogenesis.
View Article and Find Full Text PDFMutat Res
December 2017
Environmental Health Science and Research Bureau, Health Canada, Ottawa, Ontario, K1A 0K9, Canada. Electronic address:
In vitro gene expression signatures to predict toxicological responses can provide mechanistic context for regulatory testing. We previously developed the TGx-28.65 genomic biomarker from a database of gene expression profiles derived from human TK6 cells exposed to 28 well-known compounds.
View Article and Find Full Text PDFInt J Mol Sci
September 2014
Developmental Research Laboratories, Shionogi & Co., Ltd., 3-1-1 Futaba-cho, Toyonaka, Osaka 561-0825, Japan.
In vitro mammalian cytogenetic tests detect chromosomal aberrations and are used for testing the genotoxicity of compounds. This study aimed to identify a supportive genomic biomarker could minimize the risk of misjudgments and aid appropriate decision making in genotoxicity testing. Human lymphoblastoid TK6 cells were treated with each of six DNA damage-inducing genotoxins (clastogens) or two genotoxins that do not cause DNA damage.
View Article and Find Full Text PDFToxicol Lett
August 2014
Computational and Systems Medicine, Surgery and Cancer, Imperial College London SW7 2AZ, UK. Electronic address:
The cooking of meat results in the generation of heterocyclic amines (HCA), the most abundant of which is 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). Data from epidemiological, mechanistic, and animal studies indicate that PhIP could be causally linked to breast cancer incidence. Besides the established DNA damaging and mutagenic activities of PhIP, the chemical is reported to have oestrogenic activity that could contribute to its tissue specific carcinogenicity.
View Article and Find Full Text PDFExp Hematol
December 2013
Department of Hematology and Rheumatology, Tohoku University Graduate School of Medicine, Sendai, Japan.
LIM-only protein 2 (LMO2) is a non-DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation.
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