miR-146a is a significant brake on autoimmunity, myeloproliferation, and cancer in mice

By M. Boldin, K. Taganov, D. S. Rao, Lili Yang, Jimmy L. Zhao, M. Kalwani, Y. Garcia-Flores, M. Luong, Asli Devrekanli, Jessica A. Xu and 4 more. Journal of Experimental Medicine, 2011

882 citations recorded by the source corpus.

Mice lacking miR-146a exhibit exaggerated inflammatory responses, autoimmunity, and increased rate of tumorigenesis.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/5270bd55920e202b4a5f6adff9d71eec95bdd0c1

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. David Baltimore
2. D. Rao
3. Ryan M. O’Connell
4. David P. Bartel
5. Scott M. Hammond
6. Phillip D. Zamore
7. V. Narry Kim
8. Aadel A Chaudhuri

In Molecular Biology

1. David Baltimore
2. Ryan M. O’Connell
3. D. Rao
4. David P. Bartel
5. Scott M. Hammond
6. Phillip D. Zamore
7. Yukihide Tomari
8. M. Jones-Rhoades

Citations in the corpus

• Metazoan MicroRNAs (2018, background): “miR-146 (2) miR-146a Hyperresponsive macrophages, exaggerated inflammatory response, and myeloid cell proliferation; eventual autoimmune disorders, exhaustion of hematopoietic stem cells, and hematopoietic neoplasms (Lu et al., 2010; Boldin et al., 2011; Zhao et al., 2013); altered pathology in five”
• Follicular Helper T Cells. (2016, background): “Toll-like receptor (TLR) signaling in myeloid cells is dampened by miR-146a targeting Irak1 and Traf6 (101).”
• microRNA regulation of inflammatory responses. (2012, background): “Inhibition of miR155 using an antisense oligonucleotide reduced the severity, whereas miR-146a−/− mice exhibited increased sensitivity to administration of Escherichia coli LPS (28, 39).”