Ask about this productRelated genes to: GPR161 Blocking Peptide
- Gene:
- GPR161 NIH gene
- Name:
- G protein-coupled receptor 161
- Previous symbol:
- -
- Synonyms:
- RE2
- Chromosome:
- 1q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-01
- Date modifiied:
- 2016-10-05
Related products to: GPR161 Blocking Peptide
Related articles to: GPR161 Blocking Peptide
- Bardet-Biedl syndrome is a pleiotropic ciliopathy marked by retinal degeneration, obesity, polydactyly, renal and reproductive anomalies, and cognitive impairment. BBS1, the most frequently mutated gene in Bardet-Biedl syndrome, encodes a key component of the BBSome complex, which is essential for ciliary membrane trafficking. Although BBS1 is known to be essential for proper BBSome function, the effects of disease-associated BBS1 variants on its activity remain incompletely understood. - Source: PubMed
Publication date: 2026/06/19
Maskova KristynaHajsmanova HanaBykova SofiiaSmite SindijaPrasai AvishekRozbesky DanielHuranova Martina - Hedgehog (HH) signaling in vertebrates is dependent on the primary cilium, an organelle that scaffolds signal transduction. HH signals induce ciliary enrichment of Smoothened (SMO) and ciliary departure of the G protein-coupled receptor (GPCR) GPR161 to trigger GLI activation of the HH transcriptional program. Recently, SMO has been shown to inhibit protein kinase A (PKA). To test the hypothesis that SMO inhibits PKA at cilia to activate the HH signal transduction pathway, we developed a ciliary PKA reporter. Ciliary PKA activity was graded during zebrafish development. Activation of the HH signal transduction pathway by either Sonic hedgehog (SHH) or SMO agonist (SAG) inhibited ciliary PKA activity. Blocking SMO phosphorylation by GRK2/3 prevented ciliary SMO from inhibiting ciliary PKA activity. The SMO C-terminal PKA pseudosubstrate site was critical for SMO-mediated inhibition of ciliary PKA activity. A ciliary GPCR, SSTR3, activated ciliary PKA and induced HH transcriptional responses in NIH-3T3 cells via a different mechanism: activation of Gαi/o. A different ciliary GPCR, GPR161, possesses an A-Kinase Anchoring Protein (AKAP), which we found was critical for the ciliary localization of the catalytic subunit of PKA (PKA-C) to promote ciliary PKA activity. We propose that HH signal transduction is inhibited by GPR161-mediated ciliary enrichment of PKA-C, and activated by GRK2/3-phosphorylated SMO inhibition of ciliary PKA activity. - Source: PubMed
Publication date: 2026/06/10
Nguyen Thi DKonjikusic Mia JDel Castillo Lorenzo MIrannejad RoshanakReiter Jeremy F - Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS), are severe respiratory disorders characterized by a dysregulated and excessive inflammatory response within the pulmonary system. Recent studies have underscored the pivotal role of macrophage activation in driving inflammatory processes, with glycolytic reprogramming emerging as a critical regulator of macrophage function. In this study, we observed significantly elevated expression levels of G protein-coupled receptor 161 (GPR161) in peripheral circulating monocytes from patients with ARDS, with GPR161 expression positively correlating with disease severity. Utilizing genetically engineered mouse models, including global and macrophage-specific conditional knockout mice, we demonstrated that GPR161 deficiency attenuated pulmonary inflammatory damage in lipopolysaccharide-induced and sepsis-associated ALI mice. In vitro experiments further elucidated the essential role of GPR161 in macrophage activation and glycolytic reprogramming. Mechanistic investigations, integrating RNA sequencing with co-immunoprecipitation and surface plasmon resonance assays, identified complement component 5a receptor 1 (C5aR1) as a downstream target of GPR161 and showed that GPR161 promotes glycolytic reprogramming in macrophages by suppressing C5aR1 expression. Collectively, these findings demonstrate that GPR161 enhances macrophage activation and glycolytic reprogramming in ALI/ARDS through a C5aR1-dependent mechanism. These results establish macrophage GPR161 as a promising therapeutic target for the treatment of ALI/ARDS. - Source: PubMed
Publication date: 2026/05/25
Li Yu-HuanYang XueChen YingWang MiaoShu HanWan KeSun Dan-TongYao NingYang Ying-LiZhao FeiHan Bo-BoYao ChaoSong BiaoBao JingSun Geng-YunLi JunLi Xiao-Feng - Neural stem/progenitor cells (NPCs) have primary cilia, which are critical organelles for Sonic hedgehog signaling. However, little is known about the components of primary cilia in NPCs and whether manipulating signaling in the cilia is sufficient to alter dorsal/ventral regional identity. Using a human telencephalic organoid model, we perform comprehensive proteomic profiling of NPC cilia and find enrichment in GTPase signaling. Deletion of the ciliary GTPase ARL13B reduces ciliary localization of GPR161, an orphan G protein-coupled receptor 161 that negatively regulates Sonic hedgehog, resulting in ventralization of NPCs. GPR161 deletion also induces ventralization. To investigate whether manipulation of ciliary signaling is sufficient to restore dorsal identity in this context, we optogenetically elevate ciliary cAMP, rescuing dorsal fate in GPR161 KO organoids. Furthermore, chemogenetic induction of GPR161 removal from cilia is sufficient to increase ventral NPCs. These data indicate that ciliary signaling functions as a critical switch regulating dorsal/ventral fate decisions. - Source: PubMed
Publication date: 2026/05/22
Shimada Issei SGoto AkariHashimoto YutakaInoue HajimeSugawara TakutoDoura TomohiroFujita TsubasaIwata ToshiakiShimmoto RikoTakase HiroshiItoh MasayukiKiyonaka ShigekiKato Yoichi - Lung cancer is rare before age 45, and its inherited genetic basis remains poorly defined. - Source: PubMed
Publication date: 2026/04/15
Selvan Myvizhi EsaiRothberg Bonnie Elyssa GouldPatel Abhijit ASang JianHorowitz AmirChristiani David CKlein Robert JGümüş Zeynep H