Ask about this productRelated genes to: VIPR1 antibody
- Gene:
- VIPR1 NIH gene
- Name:
- vasoactive intestinal peptide receptor 1
- Previous symbol:
- -
- Synonyms:
- VPAC1, RDC1, HVR1, VPAC1R
- Chromosome:
- 3p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-13
- Date modifiied:
- 2016-10-05
Related products to: VIPR1 antibody
Related articles to: VIPR1 antibody
- Intestinal homeostasis and regeneration rely on intestinal stem cells (ISCs). Li et al. identified neuronal vasoactive intestinal peptide (VIP) as a brake on ISCs through VIPR1 to limit regeneration. In Nature Immunology, Jakob et al. and Pirzgalska et al. further showed that VIP-VIPR1 signaling restrains secretory lineage expansion and balances immune responses.. - Source: PubMed
Anastasio CamillaPeduto Lucie - Intestinal stem cells (ISCs) drive epithelial renewal and regeneration, yet how neural cues shape ISC behavior remains unclear. Here, we identify a neuronal checkpoint that directly restrains ISC regenerative output during injury. We show that vasoactive intestinal peptide (VIP)-producing enteric neurons directly signal to ISCs through the epithelial receptor VIP receptor 1 (VIPR1). In steady state, VIP-VIPR1 signaling restrains ISC hyperproliferation by engaging an extracellular signal-regulated kinase (ERK)-Notum-Wnt/β-catenin inhibitory axis. During colitis, VIPergic neurons expand within the ulcerated regions and amplify this pathway, thereby suppressing ISC-driven regeneration and exacerbating epithelial injury. Selective deletion of Vipr1 in the epithelium or in ISCs releases this neuronal brake, restores early regenerative activity, and markedly alleviates colitis. The ISC-suppressive function of VIP-VIPR1 signaling is conserved in human intestinal models. Together, these findings define VIPR1 as an ISC-intrinsic neuronal checkpoint that restricts ISC-driven epithelial regeneration and highlight epithelial VIPR1 blockade as a potential strategy to enhance mucosal regeneration in colitis. - Source: PubMed
Publication date: 2026/02/23
Li ChaoliangWang HaohaoZhang PanruiYang JianboYe ChaoWei XiaoweiZhou YuchenYang ZhentaoCao DanZhang KaiguangZhou RongbinZhu ShuPan Wen - Many G-protein-coupled receptors (GPCRs) use endocytosis to promote gene transcription by prolonging signaling through the Gs-coupled cAMP/cAMP-dependent PKA cascade. However, not all GPCRs efficiently internalize after agonist-induced activation, and, among those that do, considerable differences have been observed in the ability of different GPCRs to stimulate endosomal cAMP production in different cell types. We asked if endocytosis distinguishes the signaling profiles of GPCRs that are naturally coexpressed in the same cells, focusing on three Gs-coupled GPCRs endogenous to human embryonic kidney-derived (293) cells: the vasoactive intestinal peptide receptor-1 (VIPR1/VPAC1) and β2-adrenergic receptor (βAR/ADRB2), which both rapidly internalize after activation, and the adenosine-2B receptor (AR/ADORA2B) which we show here does not. For VIPR1, endocytosis significantly prolongs both the global cAMP elevation and cytoplasmic PKA activity increase. For β2AR, endocytosis has little effect on the global cAMP elevation but, nonetheless, it significantly prolongs the cytoplasmic PKA activity increase. AR differs still further, with endocytosis having little effect on signal duration measured at either intermediate step. We then show that further downstream steps in the cascade, nuclear PKA activation and transcriptional induction, are significantly endocytosis dependent when stimulated through VIPR1 and β2AR but endocytosis independent through AR. We conclude that endocytosis indeed distinguishes the signaling profiles of endogenously coexpressed GPCRs. We propose that quantitative differences in GPCR internalization and activation in endosomes program in cells a GPCR-selective, spatiotemporal "cAMP code" that is spatially "decoded" by proximity to local cytoplasmic PKA stores and then temporally interpreted by the nucleus. - Source: PubMed
Publication date: 2026/02/05
Blythe Emily EFagan Rita Rvon Zastrow Mark - Two studies in Nature Immunology by Jakob, Sterczyk et al. and Pirzgalska et al. show that neuron-derived vasoactive intestinal peptide (VIP) regulates intestinal epithelial differentiation and orchestrates immune responses. Through its receptor VIPR1, VIP restrains secretory lineage expansion, balances type 1 and type 2 immunity, and establishes a neuro-epithelial circuit preserving gut barrier integrity. - Source: PubMed
Publication date: 2026/01/20
Al Nabhani ZiadThevin ValentinMorelli Luisa - Polycystic ovary syndrome (PCOS) is a common endocrine disorders in women of reproductive age with limited targeted therapies. This study aimed to identify and prioritize potential druggable genes for PCOS through a purely computational, multi-omics approach. - Source: PubMed
Publication date: 2025/12/12
Xu DanJia DanFang XiaohuiChen WansuLiu YingSong QingxiaSong Xiudao