Selection of Active ScFv to G-Protein-Coupled Receptor CCR5 Using Surface Antigen-Mimicking Peptides†

Biochemistry ◽  
2004 ◽  
Vol 43 (39) ◽  
pp. 12575-12584 ◽  
Author(s):  
Ying Zhang ◽  
Chadler Pool ◽  
Kristen Sadler ◽  
He-ping Yan ◽  
Jennifer Edl ◽  
...  
Keyword(s):  
G Protein ◽  
Surface Antigen ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled ◽  
Mimicking Peptides ◽  
Receptor Ccr5 ◽  
Selection Of

scholarly journals G-Protein-Coupled Receptor Screen Reveals a Role for Chemokine Receptor CCR5 in Suppressing Microglial Neurotoxicity

2008 ◽  
Vol 28 (46) ◽  
pp. 11980-11988 ◽  
Author(s):  
K. Gamo ◽  
S. Kiryu-Seo ◽  
H. Konishi ◽  
S. Aoki ◽  
K. Matsushima ◽  
...  
Keyword(s):  
G Protein ◽  
Chemokine Receptor ◽  
G Protein Coupled Receptor ◽  
Chemokine Receptor Ccr5 ◽  
G Protein Coupled ◽  
Receptor Ccr5

A cell-based time-resolved fluorescence assay for selection of antibody reagents for G protein-coupled receptor immunohistochemistry

2004 ◽  
Vol 291 (1-2) ◽  
pp. 123-135 ◽  
Author(s):  
Jui-Lan Su ◽  
Jim Fornwald ◽  
Philip Rivers ◽  
Susan Goldsworthy ◽  
Noeleen A. Looney ◽  
...  
Keyword(s):  
G Protein ◽  
Fluorescence Assay ◽  
Time Resolved Fluorescence ◽  
G Protein Coupled Receptor ◽  
Time Resolved ◽  
A Cell ◽  
G Protein Coupled ◽  
Selection Of

scholarly journals The G protein coupled receptor CCR5 in cancer

2020 ◽  
pp. 29-47 ◽  
Author(s):  
Chandan Upadhyaya ◽  
Xuanmao Jiao ◽  
Anthony Ashton ◽  
Kishan Patel ◽  
Andrew V. Kossenkov ◽  
...  
Keyword(s):  
G Protein ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled ◽  
Receptor Ccr5

scholarly journals DNA Display Selection of Peptide Ligands for a Full-Length Human G Protein-Coupled Receptor on CHO-K1 Cells

PLoS ONE ◽  
2012 ◽  
Vol 7 (1) ◽  
pp. e30084 ◽  
Author(s):  
Nobuhide Doi ◽  
Natsuko Yamakawa ◽  
Hideaki Matsumoto ◽  
Yasutsugu Yamamoto ◽  
Tetsuya Nagano ◽  
...  
Keyword(s):  
G Protein ◽  
Peptide Ligands ◽  
Full Length ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled ◽  
Selection Of

Cell membrane hybrid bilayers containing the G-protein-coupled receptor CCR5

2002 ◽  
Vol 307 (1) ◽  
pp. 117-130 ◽  
Author(s):  
N Madhusudhana Rao ◽  
Vitali Silin ◽  
Kevin D Ridge ◽  
John T Woodward ◽  
Anne L Plant
Keyword(s):  
Cell Membrane ◽  
G Protein ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled ◽  
Hybrid Bilayers ◽  
Receptor Ccr5

scholarly journals An Update on Glioblastoma Biology, Genetics, and Current Therapies: Novel Inhibitors of the G Protein-Coupled Receptor CCR5

2021 ◽  
Vol 22 (9) ◽  
pp. 4464
Author(s):  
Tamara Lah Turnšek ◽  
Xuanmao Jiao ◽  
Metka Novak ◽  
Sriharsha Jammula ◽  
Gina Cicero ◽  
...  
Keyword(s):  
Stem Cells ◽  
G Protein ◽  
Stromal Cells ◽  
Single Cells ◽  
Therapy Response ◽  
G Protein Coupled Receptor ◽  
Glioblastoma Stem Cells ◽  
Current Therapies ◽  
G Protein Coupled ◽  
Receptor Ccr5

The mechanisms governing therapeutic resistance of the most aggressive and lethal primary brain tumor in adults, glioblastoma, have increasingly focused on tumor stem cells. These cells, protected by the periarteriolar hypoxic GSC niche, contribute to the poor efficacy of standard of care treatment of glioblastoma. Integrated proteogenomic and metabolomic analyses of glioblastoma tissues and single cells have revealed insights into the complex heterogeneity of glioblastoma and stromal cells, comprising its tumor microenvironment (TME). An additional factor, which isdriving poor therapy response is the distinct genetic drivers in each patient’s tumor, providing the rationale for a more individualized or personalized approach to treatment. We recently reported that the G protein-coupled receptor CCR5, which contributes to stem cell expansion in other cancers, is overexpressed in glioblastoma cells. Overexpression of the CCR5 ligand CCL5 (RANTES) in glioblastoma completes a potential autocrine activation loop to promote tumor proliferation and invasion. CCL5 was not expressed in glioblastoma stem cells, suggesting a need for paracrine activation of CCR5 signaling by the stromal cells. TME-associated immune cells, such as resident microglia, infiltrating macrophages, T cells, and mesenchymal stem cells, possibly release CCR5 ligands, providing heterologous signaling between stromal and glioblastoma stem cells. Herein, we review current therapies for glioblastoma, the role of CCR5 in other cancers, and the potential role for CCR5 inhibitors in the treatment of glioblastoma.

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