scholarly journals The regions within the N-terminus critical for human glucagon like peptide-1 receptor (hGLP-1R) cell Surface expression

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Aiysha Thompson ◽  
Venkateswarlu Kanamarlapudi
Keyword(s):  
Cell Surface ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
N Terminus ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals The PAR2 signal peptide prevents premature receptor cleavage and activation

2019 ◽  
Author(s):  
Belinda Liu ◽  
Grace Lee ◽  
Jiejun Wu ◽  
Janise Deming ◽  
Chester Kuei ◽  
...  
Keyword(s):  
Cell Surface ◽  
Signal Peptide ◽  
Synthetic Peptide ◽  
Surface Expression ◽  
Receptor Expression ◽  
Cell Surface Receptor ◽  
Cell Surface Expression ◽  
Peptide Ligand ◽  
Protease Activated Receptors ◽  
N Terminus

AbstractUnlike closely related GPCRs, protease-activated receptors (PAR1, PAR2, PAR3, and PAR4) have a predicted signal peptide at their N-terminus, which is encoded by a separate exon, suggesting that the signal peptides of PARs may serve an important and unique function, specific for PARs. In this report, we show that the PAR2 signal peptide, when fused to the N-terminus of IgG-Fc, effectively induced IgG-Fc secretion into culture medium, thus behaving like a classical signal peptide. The presence of PAR2 signal peptide has a strong effect on PAR2 cell surface expression, as deletion of the signal peptide (PAR2ΔSP) led to dramatic reduction of the cell surface expression and decreased responses to trypsin or the synthetic peptide ligand (SLIGKV). However, further deletion of the tethered ligand region (SLIGKV) at the N-terminus rescued the cell surface receptor expression and the response to the synthetic peptide ligand, suggesting that the signal peptide of PAR2 may be involved in preventing PAR2 from intracellular protease activation before reaching the cell surface. Supporting this hypothesis, an Arg36Ala mutation on PAR2ΔSP, which disabled the trypsin activation site, increased the receptor cell surface expression and the response to ligand stimulation. Similar effects were observed when PAR2ΔSP expressing cells were treated with protease inhibitors. Our findings indicated that these is a role of the PAR2 signal peptide in preventing the premature activation of PAR2 from intracellular protease cleavage before reaching the cells surface. The same mechanism may also apply to PAR1, PAR3, and PAR4.

scholarly journals Listeria monocytogenesTriggers the Cell Surface Expression of Gp96 Protein and Interacts with Its N Terminus to Support Cellular Infection

2012 ◽  
Vol 287 (51) ◽  
pp. 43083-43093 ◽  
Author(s):  
Mariana Martins ◽  
Rafael Custódio ◽  
Ana Camejo ◽  
Maria Teresa Almeida ◽  
Didier Cabanes ◽  
...  
Keyword(s):  
Cell Surface ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
N Terminus

scholarly journals Structural insights on melanocortin 5 receptor targeting to cell surface

2009 ◽  
Vol 15 (S3) ◽  
pp. 3-4 ◽  
Author(s):  
A. R. Rodrigues ◽  
H. Almeida ◽  
A. M. Gouveia
Keyword(s):  
Cell Membrane ◽  
Cell Surface ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Melanocortin Receptors ◽  
N Terminus ◽  
Available Information ◽  
G Protein Coupled ◽  
Structural Insights ◽  
Human Receptor

AbstractThe melanocortin 5 receptor (MC5R) is a G-protein coupled receptor (GPCR) with a typical seventransmembrane-domain structure. It is assumed that all GPCRs undergo several post-transcriptional modifications during synthesis and folding until finally target to the cell membrane. The available information about the specific domains responsible for the correct targeting of the melanocortin receptors to the cell surface is scarce. Regarding MC5R, it was shown that the first 20 aminoacids of the human receptor can be deleted without affecting the ligand binding affinity, but further deletions of the N terminus resulted in total loss of binding. These results were not directly correlated with the cell surface expression levels of the receptor. Thus, we aim to define the specific MC5R domains important to its correct trafficking and signaling, and preliminary results are here presented.

The N Terminus of the Human α1D-Adrenergic Receptor Prevents Cell Surface Expression

2004 ◽  
Vol 309 (1) ◽  
pp. 388-397 ◽  
Author(s):  
Chris Hague ◽  
Zhongjian Chen ◽  
Andre S. Pupo ◽  
Nancy A. Schulte ◽  
Myron L. Toews ◽  
...  
Keyword(s):  
Cell Surface ◽  
Adrenergic Receptor ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
N Terminus

Persistent HIV Transcription Induces Sialyl-Lewis-X Glyco-Antigen Cell-Surface Expression

2020 ◽  
Author(s):  
Florent Colomb ◽  
Leila B. Giron ◽  
Leticia Kuri Cervantes ◽  
Tongcui Ma ◽  
Samson Adeniji ◽  
...  
Keyword(s):  
Cell Surface ◽  
Surface Expression ◽  
Sialyl Lewis X ◽  
Cell Surface Expression ◽  
Lewis X ◽  
Hiv Transcription ◽  
Sialyl Lewis

Influence of β-D-mannuronic acid, as a new member of non-steroidal anti-inflammatory drugs family, on expression pattern of chemokines and their receptors in rheumatoid arthritis

2019 ◽  
Vol 16 ◽  
Author(s):  
Mona Aslani ◽  
Arman Ahmadzadeh ◽  
Zahra Aghazadeh ◽  
Majid Zaki-Dizaji ◽  
Laleh Sharifi ◽  
...  
Keyword(s):  
Cell Surface ◽  
Mrna Expression ◽  
Surface Expression ◽  
Phase Iii ◽  
Cell Surface Expression ◽  
Optimum Dose ◽  
High Dose ◽  
Mannuronic Acid ◽  
Anti Inflammatory ◽  
High Doses

Background: : Based on the encouraging results of phase III clinical trial of β-D-mannuronic acid (M2000) (as a new anti-inflammatory drug) in patients with RA, in this study, we aimed to evaluate the effects of this drug on the expression of chemokines and their receptors in PBMCs of RA patients. Methods:: PBMCs of RA patients and healthy controls were separated and the patients' cells were treated with low, moderate and high doses (5, 25 and 50 μg/mL) of M2000 and optimum dose (1 μg/mL) of diclofenac, as a control in RPMI-1640 medium. Real-time PCR was used for evaluating the mRNA expression of CXCR3, CXCR4, CCR2, CCR5 and CCL2/MCP-1. Cell surface expression of CCR2 was investigated using flow cytometry. Results:: CCR5 mRNA expression reduced significantly, after treatment of the patients' cells with all three doses of M2000 and optimum dose of diclofenac. CXCR3 mRNA expression down-regulated significantly followed by treatment of these cells with moderate and high doses of M2000 and optimum dose of diclofenac. CXCR4 mRNA expression declined significantly after treatment of these cells with moderate and high doses of M2000. CCL2 mRNA expression significantly reduced only followed by treatment of these cells with high dose of M2000, whereas, mRNA and cell surface expressions of CCR2 diminished significantly followed by treatment of these cells with high dose of M2000 and optimum dose of diclofenac. Conclusion:: According to our results, M2000 through the down-regulation of chemokines and their receptors may restrict the infiltration of immune cells into the synovium.

The immunogenicity of VP7, a rotavirus antigen resident in the endoplasmic reticulum, is enhanced by cell surface expression.

1990 ◽  
Vol 64 (10) ◽  
pp. 4776-4783 ◽  
Author(s):  
M E Andrew ◽  
D B Boyle ◽  
P L Whitfeld ◽  
L J Lockett ◽  
I D Anthony ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Surface ◽  
Surface Expression ◽  
Cell Surface Expression
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