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Matthew J. Billard

Researcher at University of North Carolina at Chapel Hill

Publications -  10
Citations -  149

Matthew J. Billard is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: G protein-coupled receptor kinase & Chemokine receptor. The author has an hindex of 6, co-authored 9 publications receiving 112 citations.

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G Protein Coupled Receptor Kinase 3 Regulates Breast Cancer Migration, Invasion, and Metastasis.

TL;DR: It is demonstrated that alterations inGRK3 expression levels in tumor cells directly affect migration and invasion in vitro and the establishment of distant metastasis in vivo, and that GRK3 dysregulation may play an important part in TNBC metastasis.
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G protein-coupled receptor kinase-3-deficient mice exhibit WHIM syndrome features and attenuated inflammatory responses

TL;DR: It is concluded that the loss of GRK3‐mediated regulation of CXCL12/CXCR4 signaling contributes to some, but not all, of the complete WHIM phenotype and thatGRK3 inhibition may be beneficial in the treatment of inflammatory arthritis.
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G-protein signaling modulator-3, a gene linked to autoimmune diseases, regulates monocyte function and its deficiency protects from inflammatory arthritis.

TL;DR: The results suggest that GPSM3 is an important regulator of monocyte function involving mechanisms of differentiation, survival, and chemotaxis, and deficiency in GPSM 3 expression is protective in acute inflammatory arthritis.
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Chemerin-activated functions of CMKLR1 are regulated by G protein-coupled receptor kinase 6 (GRK6) and β-arrestin 2 in inflammatory macrophages.

TL;DR: The findings show that chemerin-activated CMKLR1 regulation in inflammatory macrophages is largely GRK6 and β-arrestin mediated, which may impact innate immunity and have therapeutic implications in rheumatic disease.

G protein signaling modulator-3: a leukocyte regulator of inflammation in health and disease.

TL;DR: G protein signaling modulator-3 has a selective tissue distribution and is highly expressed in immune system cells; genome-wide association studies (GWAS) have recently revealed that single nucleotide polymorphisms in GPSM3 are associated with chronic inflammatory diseases.