Purinergic Receptor P2x, Ligand-Gated Ion Channel, 3 Proteine (P2RX3)

Human Purinergic Receptor P2x, Ligand-Gated Ion Channel, 3 (P2RX3) Interaktionspartner

1. Druggable negative allosteric site of P2X3 receptors.

2. conclude that the inter-subunit salt bridge between E112 and R198 of the head and dorsal fin domains, respectively, serves to control the mobility of these domains during agonist-activation of the hP2X3R

3. P2X3 expressions in endometriosis endometrium and endometriotic lesions were significantly higher as compared with control endometrium, and positively correlated with pain.

4. P2X3 receptor expression was up-regulated in neurons from patients with temporal lobe epilepsy.

5. X-ray crystal structures of the human P2X3 receptor in apo (zeige C9orf3 Proteine)/resting, agonist-bound/open-pore, agonist-bound/closed-pore/desensitized and antagonist-bound/closed states

6. there is a relationship between the elevated expression of P2X3 receptor and P2X7 receptor (zeige P2RX7 Proteine) in peripheral blood leukocytes and high serum epinephrine and norepinephrine levels in hyperthyroidism patients.

7. Data show that monoclonal antibodies directed against human P2X3 (12D4) potentiated the slow inactivating current mediated by the heteromeric purinergic receptor (zeige P2RX1 Proteine) hP2X2/3 channel.

8. Data indicate P2X3 purinergic receptors as potential new targets for hepatocellular carcinoma (HCC (zeige FAM126A Proteine)) therapy.

9. Results demonstrate that the stoichiometry of the heterotrimeric hP2X2/3 receptor is not fixed, but determined by the relative availability of P2X2 (zeige P2RX2 Proteine) and P2X3 subunits

10. Urothelial P2X3 receptors decreased significantly in responders after Lipotoxin instillation, but not after BoNT-A injection.

Mouse (Murine) Purinergic Receptor P2x, Ligand-Gated Ion Channel, 3 (P2RX3) Interaktionspartner

1. This study demonstrated that the P2X3-immunoreactive nerve endings in the rat tracheal mucosa have unique morphological characteristics, and these endings may be rapidly adapting receptors and/or irritant receptors that are activated by mucosal irritant stimuli.

2. Data suggest that the negative inhibition of P2X3R activity by the BNP/NPR-A (zeige NPR1 Proteine) pathway results in a decreased P2X3R-mediated excitability of trigeminal neurons in wildetype cultures. In familial hemiplegic migraine type-1 model cultures, however, lack of efficient P2X3Rs downregulation contributes to the neuronal hyperexcitability phenotype.

3. P2X3 receptors on mouse trigeminal ganglion neurons are subjected to contrasting modulation by inhibitory brain natriuretic peptide (zeige BNP Proteine) and facilitatory calcitonin gene-related peptide (zeige CALCA Proteine) that both operate via complex intracellular signaling.

4. mouse trigeminal neurons endogenous BNP acts on NPR-A (zeige NPR1 Proteine) receptors to determine constitutive depression of P2X3 receptor function. Tonic inhibition of P2X3 receptor activity by BNP/NPR-A (zeige NPR1 Proteine)/PKG (zeige PRKG1 Proteine) pathways occurs via two distinct mechanisms: P2X3 serine phosphorylation and receptor redistribution to non-raft membrane compartments

5. This study observed maltodextrin and fat preference deficits in "taste-blind" P2X2 (zeige P2RX2 Proteine)/P2X3 knockout mice.

6. a slow modulatory action by BNP on TRPV1 (zeige TRPV1 Proteine) and P2X3 receptors outlining the role of this peptide as a negative regulator of trigeminal sensory neuron excitability to nociceptive stimuli

7. P2X(3)R overexpression may underlie ectopic mechanical allodynia in the whisker pad skin

8. genetic manipulation of TRPV1 (zeige TRPV1 Proteine) and P2X3 leads to reduction in colorectal mechanosensation peripherally and compensatory changes and/or disinhibition of other channels centrally.

9. up-regulation of P2X3 receptors probably is already maximal and is apparently contributed by basal CGRP (zeige CALCA Proteine) and BDNF (zeige BDNF Proteine) levels

10. Structure and function of P2RX3 is reviewed, and its role in treatment of pain is discussed. [Review Article]