Gpra:the Ligand Of The Gpra Is The Neuropeptide
The receptor coupled to G-protein linked with susceptibility to lasthme (G protein-coupled
receptor for asthma susceptibility: GPRA) is a protein found in many l apithalium Dorgan. GPRA is a protein belonging to the family of receptors coupled to G-protein (GPCR). This family is divided into 4 classes (A, B, C and F / S), based on the sequences shared between the receptors . GPRA is a Class A because it has a residue of 14 amino acids characteristic of this class of receptors .
Since the vasopressin receptor has the highest rate licensing (27) with GPRA , some rank it in the subfamily of receptors, such as vasopressin (vasopressin receptor-like receptors) . This protein has two major isoforms: lisoforme A (GPRA-A) and B lisoforme (GPRA-B). They have sizes of 371 and 377 amino acids. These two isoforms each have seven transmembrane domains which are also characteristic of all protein-coupled receptors G .
In addition, there are 5 other isoforms have been identified. The smallest of the attendees is lisoforme C, which is a protein of 94 amino acids. Then, the size of GPRA-D is 158 amino acids, that of GPRA-E is 136 amino acids and that of the GPRA-F is 305 amino acids. There is also the GPRA-Bcourte which has 366 amino acids. It may be noted quil is a deletion of 11 amino acids between the long and short of GPRA-B .
This protein comes from chromosome 7 in lhumain and, more specifically, p14-p15 loci . It is encoded by single gene encoding this segment of chromosome, cest to say the gene GPRA154. The different isoforms of GPRA produced by this gene are the result of dune d apissage lARNm difference. In fact, for the GPRA-A and GPRA-B, cest unusual spray different exons encoding the carboxy-terminal intracellular ends that create the difference between the two forms . In the case of truncated forms, GPRA-C has only three exons, while the GPRA-D has a deletion of lexon 3. For its part, the GPRA-E does not have lexon 4. In the latter two cases these deletions have resulted visiting dun early stop codon. For the GPRA-F is missing exons 3 and 4, but the remaining exons of GPRA-A remain .
In the cell, there are only the GPRA-A and GPRA-B long that successfully is integrated in the cytoplasmic membrane to become receivers. The other isoforms remain in the cytoplasm and does latteindront ever. It should be noted that the presence of truncated isoforms naffecte not translocation of the GPRA-A and GPRA-B .
GPRA is expressed in many tissues. Indeed, it is expressed in all epithelial cells that are connected in some way, to lasthme and allergies. It is therefore found in the bronchi, the gastrointestinal tract (esophagus, stomach, small intestine and colon) and in the skin. It is also observed in epithelial cells of the submucosa of the spleen, kidney, prostate and breast. Some glandular epithelia such as salivary glands, also contain the GPRA. Smooth muscle cells of the bronchi and arteries also contain . Regulated expression of the GPRA is very high in the brain.
First offers, the ligand of the GPRA-A is the neuropeptide S (NPS). The latter is a fragment of 20 amino acids from the C-terminal dun dun precursor polypeptide. This neuropeptide is found in most places where the GPRA is expressed . The binding of NPS GPRA lAMPcyclique induces an increase of calcium and the interior of the cell . In fact, when the NPS binds to the GPRA, the alpha subunit of the G protein will break off and go and settle on an adenylate cyclase . The latter will transform LATP cAMP which will, subsequently activate protein kinases. Receptors of the endoplasmic reticulum ion will, during this process, activated, causing the release of calcium in the cytoplasm. Some studies also suggest that the CDK GPRA might be autocrine or paracrine .
The specific mechanism of action of the GPRA is not yet known. However, after several experiments, it was possible leffet TO FOLLOW regulated expression of GPRA-A on cell growth. Indeed, cells containing this isoform are growing more slowly than the cells do not express it. For cons, the term of the GPRA-B ninfluence not cell growth and the precise role of this isoform is not yet determined.
Lasthme is a chronic inflammation of the airways characterized by bronchoconstriction, mucus creation well as linflammation of bronchial lapithaclium. It usually manifests itself by dyspnea, wheezing, coughing, and lessoufflement. This disease is often associated with allergies. However, the precise cause is not known because lasthme is the result of several factors combined environmental and acquired . This respiratory disease affects people of all ages, but it appears mainly during lEnfance. Lasthme affects 100 to 150 million people worldwide and is responsible for 18,000 deaths per year .
At dune crisis, there is a constriction of smooth muscle as well as linflammation the surface of the bronchi that cause a narrowing of the airways . Lair goes so easily, which explains the doppression sensation in the chest and wheezing heard lexpiration. Moreover, people with asthma studied revealed that several genes are implicated in this disease, including LADAME-33, PHF11, DPP10 and HLA-G. There are obviously also GPRA154 gene that was discovered recently .
This gene is associated with lasthme and a high rate DIGE in the blood. It is found mainly in the Finnish population and Quebec . This gene of 133 kb contains seven different haplotypes, whose alleles are modified by single nucleotide polymorphisms dun (single nucleotide polymorphism (SNP)). Lasthme laugmentation DIGE and serum are associated with four of these haplotypes . In one study conducted on the subject, it was possible oIdentify one of these SNPs that alter the primary structure of the gene by substituting lisoleucine for an asparagine at position 107 of the protein . Furthermore, aberrant expression of lARNmessager and GPRA was observed in bronchial epithelial cells of asthmatics .
by: Laura Steinfield
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