| General information | Literature | Expression | Regulation | Mutation | Interaction |
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Basic Information |
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|---|---|
Gene ID | 7434 |
Name | VIPR2 |
Synonymous | C16DUPq36.3|DUP7q36.3|PACAP-R-3|PACAP-R3|VIP-R-2|VPAC2|VPAC2R|VPCAP2R;vasoactive intestinal peptide receptor 2;VIPR2;vasoactive intestinal peptide receptor 2 |
Definition | PACAP type III receptor|VIP and PACAP receptor 2|helodermin-preferring VIP receptor|pituitary adenylate cyclase-activating polypeptide type III receptor|vasoactive intestinal polypeptide receptor 2 |
Position | 7q36.3 |
Gene type | protein-coding |
Source | Count: VIPR2; 7434 |
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Sentence |
Abstract |
| "Pulmonary vascular remodeling and inflammation often coexist in clinical and experimentally induced pulmonary arterial hypertension (PAH). In some instances, the pulmonary hypertension may be the primary, or at least the initial, problem, while inflammatory or autoimmune responses appear to initiate or dominate the picture in other cases. Based on studies in a model of PAH resulting from targeted deletion of the neuropeptide vasoactive intestinal peptide (VIP) gene, we propose that, at least in this experimental model, but possibly also in other situations, both vascular remodeling and inflammation may be mediated by one and the same mechanism: uncontrolled activation of calcineurin-NFAT (nuclear factor of activated T cells) signaling. If this hypothesis is validated, VIP would emerge as an endogenous modulator of pulmonary vascular remodeling and inflammation, through its suppression of NFAT activation." | Pulmonary vascular remodeling and inflammation often coexist in clinical and experimentally induced pulmonary arterial hypertension (PAH). In some instances, the pulmonary hypertension may be the primary, or at least the initial, problem, while inflammatory or autoimmune responses appear to initiate or dominate the picture in other cases. Based on studies in a model of PAH resulting from targeted deletion of the neuropeptide vasoactive intestinal peptide (VIP) gene, we propose that, at least in this experimental model, but possibly also in other situations, both vascular remodeling and inflammation may be mediated by one and the same mechanism: uncontrolled activation of calcineurin-NFAT (nuclear factor of activated T cells) signaling. If this hypothesis is validated, VIP would emerge as an endogenous modulator of pulmonary vascular remodeling and inflammation, through its suppression of NFAT activation. |
| "Pulmonary vascular remodeling and inflammation often coexist in clinical and experimentally induced pulmonary arterial hypertension (PAH). In some instances, the pulmonary hypertension may be the primary, or at least the initial, problem, while inflammatory or autoimmune responses appear to initiate or dominate the picture in other cases. Based on studies in a model of PAH resulting from targeted deletion of the neuropeptide vasoactive intestinal peptide (VIP) gene, we propose that, at least in this experimental model, but possibly also in other situations, both vascular remodeling and inflammation may be mediated by one and the same mechanism: uncontrolled activation of calcineurin-NFAT (nuclear factor of activated T cells) signaling. If this hypothesis is validated, VIP would emerge as an endogenous modulator of pulmonary vascular remodeling and inflammation, through its suppression of NFAT activation." | Pulmonary vascular remodeling and inflammation often coexist in clinical and experimentally induced pulmonary arterial hypertension (PAH). In some instances, the pulmonary hypertension may be the primary, or at least the initial, problem, while inflammatory or autoimmune responses appear to initiate or dominate the picture in other cases. Based on studies in a model of PAH resulting from targeted deletion of the neuropeptide vasoactive intestinal peptide (VIP) gene, we propose that, at least in this experimental model, but possibly also in other situations, both vascular remodeling and inflammation may be mediated by one and the same mechanism: uncontrolled activation of calcineurin-NFAT (nuclear factor of activated T cells) signaling. If this hypothesis is validated, VIP would emerge as an endogenous modulator of pulmonary vascular remodeling and inflammation, through its suppression of NFAT activation. |