Functional characterization of receptor-interacting serine/threonine kinase 2 (RIP2) of the goldfish ( Carassius auratus L.)
Developmental & Comparative Immunology, ISSN: 0145-305X, Vol: 48, Issue: 1, Page: 76-85
2015
- 19Citations
- 18Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations19
- Citation Indexes19
- 19
- CrossRef12
- Captures18
- Readers18
- 18
Article Description
We report on the functional characterization of RIP2 of the goldfish. Quantitative expression analysis of goldfish RIP2 revealed the greatest mRNA levels in the spleen, monocytes and splenocytes. We generated a recombinant form of the molecule (rgRIP2) and determined that anti-human RIP2 polyclonal antibody specifically recognized recombinant goldfish RIP2 (rgRIP2). Goldfish RIP2 activity was inhibited by the p38 MAPK pathway inhibitor SB203580. Treatment of goldfish macrophages with LPS, PGN, MDP, Poly I:C, heat-killed and live Mycobacterium marinum, and heat-killed Aeromonas salmonicida differentially changed the expression of RIP2 at both mRNA and protein levels. Co-immunoprecipitation assays indicated that RIP2 interacted with Nod1 and Nod2 receptors in eukaryotic cells. The results of dual luciferase reporter assay revealed that RIP2 over-expression caused the activation of the NF-κB signal pathway. In addition, RIP2 was involved in the regulation of the production of TNFα-2 and IL-1β1 in goldfish macrophages exposed to M. marinum.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0145305X14002316; http://dx.doi.org/10.1016/j.dci.2014.09.006; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84907970343&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/25242011; https://linkinghub.elsevier.com/retrieve/pii/S0145305X14002316; https://dx.doi.org/10.1016/j.dci.2014.09.006
Elsevier BV
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