Defective lymphocyte chemotaxis in β-arrestin2- and GRK6-deficient mice

By A. Fong, R. Premont, R. Richardson, Yen-Rei Yu, R. J. Lefkowitz, D. Patel. Proceedings of the National Academy of Sciences of the United States of America, 2002

293 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/26004dccc1bbcf8679bd3606f7195e92543b2162

How researchers see this paper

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

In Immunology

1. J. Benovic
2. J. Busillo

In Molecular Biology

1. Éric Reiter
2. J. Benovic
3. R. J. Lefkowitz
4. Sudha K. Shenoy

In Oncology

1. J. Benovic
2. R. J. Lefkowitz
3. J. Busillo

Citations in the corpus

• Regulation of CXCR4 signaling. (2007, background): “Lymphocytes and neutrophils isolated from mice with a targeted disruption of GRK6 showed enhanced CXCR4 function and a lack of desensitization [95,106], which was not seen in cells isolated from mice lacking GRK5 [95].”
• GRKs and β-arrestins: roles in receptor silencing, trafficking and signaling (2006, background): “Sometimes, G proteins and b-arrestins act in concert to activate ERK: several chemokine receptors are sensitive to both pertussis toxin (implicating signaling through Gai or Gao) and siRNAmediated depletion of b-arrestin 2 [42,48, 49 ].”