scholarly journals FMRFamide-like peptides encoded on the flp-18 precursor gene activate two isoforms of the orphan Caenorhabditis elegans G-protein-coupled receptor Y58G8A.4 heterologously expressed in mammalian cells

Biopolymers ◽  
2007 ◽  
Vol 90 (3) ◽  
pp. 339-348 ◽  
Author(s):  
Teresa M. Kubiak ◽  
Martha J. Larsen ◽  
Jerry W. Bowman ◽  
Timothy G. Geary ◽  
David E. Lowery

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Brandon Norman ◽  
Lauren DeLong ◽  
Myra Dickey ◽  
Mollie Jewell ◽  
Patti T. Erickson ◽  
...  


Aging Cell ◽  
2020 ◽  
Vol 19 (6) ◽  
Author(s):  
Anubhuti Dixit ◽  
Anjali Sandhu ◽  
Souvik Modi ◽  
Meghana Shashikanth ◽  
Sandhya P. Koushika ◽  
...  


2019 ◽  
Vol 87 (4) ◽  
Author(s):  
Alexandra Anderson ◽  
Yee Lian Chew ◽  
William Schafer ◽  
Rachel McMullan

ABSTRACT G protein-coupled receptors contribute to host defense across the animal kingdom, transducing many signals involved in both vertebrate and invertebrate immune responses. While it has become well established that the nematode worm Caenorhabditis elegans triggers innate immune responses following infection with numerous bacterial, fungal, and viral pathogens, the mechanisms by which C. elegans recognizes these pathogens have remained somewhat more elusive. C. elegans G protein-coupled receptors have been implicated in recognizing pathogen-associated damage and activating downstream host immune responses. Here we identify and characterize a novel G protein-coupled receptor required to regulate the C. elegans response to infection with Microbacterium nematophilum. We show that this receptor, which we designate pathogen clearance-defective receptor 1 (PCDR-1), is required for efficient pathogen clearance following infection. PCDR-1 acts upstream of multiple G proteins, including the C. elegans Gαq ortholog, EGL-30, in rectal epithelial cells to promote pathogen clearance via a novel mechanism.



2021 ◽  
Author(s):  
Hannes Schihada ◽  
Rawan Shekhani ◽  
Gunnar Schulte

AbstractHeterotrimeric G proteins constitute the primary transducers of G protein-coupled receptor (GPCR) signaling. Besides mediating ligand-induced GPCR activation, G proteins transduce basal levels of activity in various physiological and pathophysiological settings evoked by constitutively active, native GPCRs or disease-related receptor mutants. Several generations of optical biosensors were developed and optimized to monitor GPCR ligand-induced G protein activation, however, quantitative approaches to detect constitutively active GPCRs are not available. Here, we designed and validated a set of eight bioluminescence-resonance-energy-transfer (BRET)-based G protein sensors, covering all four major families of G proteins, and established a protocol to identify constitutive GPCR/G protein signaling in living cells. These sensors rely on the encoding of all three G protein subunits on a single plasmid, enabling their cellular expression at desired relative levels and resulting in reduced signal variability in mammalian cells. Based on this sensor platform, we further present here an experimental protocol to quantify constitutive signaling of native and mutated GPCRs through these heterotrimeric transducers. This approach will aid in the characterization of constitutively active GPCRs and the exploration of their role in health and disease.One Sentence SummaryThis Resource article describes the validation of a biophysical approach to directly assess the constitutive signaling activity of G protein-coupled receptors through heterotrimeric G proteins in living cells using optical biosensors.



1998 ◽  
Vol 187 (5) ◽  
pp. 801-806 ◽  
Author(s):  
Elizabeth Geras-Raaka ◽  
Leandros Arvanitakis ◽  
Carlos Bais ◽  
Ethel Cesarman ◽  
Enrique A. Mesri ◽  
...  

Kaposi's sarcoma–associated herpesvirus (KSHV)/human herpesvirus 8, which is consistently present in tissues of patients with Kaposi's sarcoma and primary effusion lymphomas, contains a gene that encodes a G protein–coupled receptor (KSHV-GPCR). We recently showed that KSHV-GPCR exhibits constitutive signaling via activation of phosphoinositide-specific phospholipase C and stimulates cell proliferation and transformation. In this study, we determined whether normal cellular mechanisms could inhibit constitutive signaling by KSHV-GPCR and thereby KSHV-GPCR–stimulated proliferation. We show that coexpression of GPCR-specific kinases (GRKs) and activation of protein kinase C inhibit constitutive signaling by KSHV-GPCR in COS-1 monkey kidney cells and in mouse NIH 3T3 cells. Moreover, GRK-5 but not GRK-2 inhibits KSHV-GPCR–stimulated proliferation of rodent fibroblasts. These data provide evidence that cell regulatory pathways of receptor desensitization may be therapeutic targets in human diseases involving constitutively active receptors.







2020 ◽  
Vol 26 (1) ◽  
pp. 187-197
Author(s):  
Stacy A. Henry ◽  
Selina Crivello ◽  
Tina M. Nguyen ◽  
Magdalena Cybulska ◽  
Ngoc S. Hoang ◽  
...  


2007 ◽  
Vol 47 (1) ◽  
pp. 271-280 ◽  
Author(s):  
Nigel J. Pyne ◽  
Catherine M. Waters ◽  
Jaclyn S. Long ◽  
Noreen A. Moughal ◽  
Gabor Tigyi ◽  
...  


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