Affinage

GPR161

G-protein coupled receptor 161 · UniProt Q8N6U8

Length
529 aa
Mass
58.6 kDa
Annotated
2026-06-10
40 papers in source corpus 24 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GPR161 is a constitutively active, ciliary GPCR that functions as the principal negative regulator of Hedgehog (Hh) signaling by coupling cAMP/PKA activity to formation of the Gli3 transcriptional repressor (PMID:23332756). Localized to primary cilia in a Tulp3/IFT-A-dependent manner, its constitutive Gαs coupling raises cAMP and drives Gli3 processing to its repressor form, suppressing basal Shh output during neural tube, limb, and skeletal development (PMID:23332756, PMID:29222391). A cryo-EM structure of active GPR161–Gs showed extracellular loop 2 occupying the orthosteric pocket and an extrahelical sterol adjacent to TM6/TM7 stabilizing the Gs-coupling conformation; sterol-binding mutations abolish cAMP signaling yet retain suppression of GLI2 ciliary accumulation, which instead depends on a C-terminal PKA-binding site (PMID:38326651). GPR161 acts as an A-kinase anchoring protein for type I PKA regulatory subunits through this cytoplasmic C-tail and is itself a PKA substrate, establishing a feedback loop tuning its ciliary residence (PMID:27357676, PMID:33531430). Upon Shh activation, ciliary Smoothened promotes GRK2-mediated phosphorylation of GPR161 and β-arrestin recruitment, which engages the BBSome–IFT machinery to drive clathrin-mediated removal of the receptor from cilia, relieving repression (PMID:27002170, PMID:40384633, PMID:31471295). Separation-of-function alleles establish that distinct ciliary and extraciliary GPR161 pools set tissue-specific Gli repressor thresholds governing neural tube patterning, neural tube closure, and limb/craniofacial morphogenesis (PMID:34346313, PMID:41417007). Loss of GPR161 derepresses Shh signaling and causes overproliferation phenotypes, defining it as a tumor suppressor in Shh-subtype medulloblastoma (PMID:29386106, PMID:30914320). Beyond Hedgehog, GPR161 functions as a mechanoresponsive ciliary receptor: fluid shear stress triggers GPR161-dependent cAMP/PKA signaling that drives osteogenic differentiation of mesenchymal stem cells via adenylyl cyclase 6 (PMID:33450431) and regulates saltatory neuronal migration via phosphorylation of the dynein regulator NDE1 through its mechanosensitive helix 8 (PMID:40737401). Truncating and rare patient variants link GPR161 to neural tube defects, cataracts, and spina bifida (PMID:18250320, PMID:30256984).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2008 Medium

    Before its signaling role was known, positional cloning of a spontaneous mouse mutant tied Gpr161 to a developmental disease phenotype and implicated its C-terminal tail in receptor trafficking.

    Evidence Positional cloning of the vacuolated lens mutant and endocytosis assay of a C-terminally truncated receptor

    PMID:18250320

    Open questions at the time
    • No signaling mechanism or pathway placement
    • Did not connect endocytosis defect to a downstream transduction cascade
  2. 2013 High

    Established the core mechanism: GPR161 is a ciliary, constitutively active GPCR that raises cAMP to drive Gli3 repressor formation and suppress Shh signaling, with Shh-triggered ciliary removal relieving repression.

    Evidence Mouse knockout, cAMP reporters, Gli3 processing westerns, and genetic epistasis with Tulp3/IFT-A in neural tube development

    PMID:23332756

    Open questions at the time
    • G protein coupling not directly demonstrated biochemically
    • Endogenous ligand not identified
    • Molecular machinery of ciliary export undefined
  3. 2014 Medium

    Identified a Hedgehog-independent role by placing GPR161 in a β-arrestin 2/IQGAP1 complex that activates mTOR and supports cancer cell proliferation.

    Evidence Co-IP of the GPR161–β-arrestin 2–IQGAP1 complex and shRNA knockdown in basal breast cancer cells

    PMID:24599592

    Open questions at the time
    • Single lab, Co-IP-based complex
    • Directness of IQGAP1/mTOR coupling not resolved
    • Relationship to ciliary cAMP role unclear
  4. 2015 Medium

    Extended the downstream cascade by linking GPR161 activity to retinoic acid and canonical Wnt regulation during neurulation.

    Evidence Hypomorphic Gpr161vl allele with RA injection rescue and gene-expression analysis in mouse neural tube

    PMID:25753732

    Open questions at the time
    • Mechanism connecting GPR161 to RA/Wnt not molecular
    • Single lab pharmacological rescue
  5. 2016 High

    Resolved how GPR161 is removed from cilia: a two-step GRK2/β-arrestin recruitment followed by extraciliary clathrin-mediated endocytosis, promoted by ciliary Smoothened activity.

    Evidence Co-IP, dominant-negative and KO cells, live imaging, and clathrin inhibitors

    PMID:27002170

    Open questions at the time
    • BBSome/IFT linkage to export not yet defined
    • GRK2 phosphosites on GPR161 not mapped
  6. 2016 High

    Defined GPR161 as an AKAP that directly anchors type I PKA via its C-tail and is reciprocally phosphorylated by PKA, explaining how it compartmentalizes PKA activity at cilia.

    Evidence Phosphoproteomics, RI pull-down binding assays, mutagenesis, and zebrafish imaging

    PMID:27357676

    Open questions at the time
    • Structural basis of the RI interface not resolved
    • Functional separation of AKAP versus cAMP-generating roles not yet tested
  7. 2018 High

    Demonstrated tissue-specific, cilium-dependent Gli-repressor regulation by GPR161 in limb/skeletal morphogenesis and its tumor-suppressor function in Shh-medulloblastoma.

    Evidence Conditional KO mice in limb, craniofacial, neural stem cell, and granule progenitor lineages with epistasis to cilia mutants

    PMID:29222391 PMID:29386106

    Open questions at the time
    • Whether different tissues use distinct GPR161 effector pools unresolved
    • Quantitative link between cAMP levels and Gli thresholds not established
  8. 2019 Medium

    Defined the molecular export route by showing IFT-B subunit IFT38 bridges to the BBSome to drive Hh-induced GPR161 export, and extended disease relevance with dominant-negative spina bifida variants and cortical malformation phenotypes.

    Evidence Reciprocal IP and rescue with interaction-deficient IFT38; patient variant localization/reporter assays; conditional KO mice with proliferation and migration readouts

    PMID:30256984 PMID:30914320 PMID:31471295

    Open questions at the time
    • Order of β-arrestin versus BBSome engagement not fully resolved
    • Patient variant studies single-lab
    • Wnt dysregulation mechanism in variants unclear
  9. 2021 High

    Separated ciliary from extraciliary GPR161 functions and established a PKA-phosphorylation feedback loop tuning ciliary localization and Gαs coupling sensitivity, while extending function to mechanosensation in osteogenesis.

    Evidence CRISPR knock-in separation-of-function mice, BRET Gαs coupling and phospho-deficient mutants in zebrafish, and shear-stress/AC6 knockdown in MSCs

    PMID:33450431 PMID:33531430 PMID:34346313

    Open questions at the time
    • How extraciliary pool localizes and signals mechanistically undefined
    • Mechanotransduction sensor element not yet identified
  10. 2024 High

    Provided the structural mechanism: a cryo-EM active GPR161–Gs structure showing ELL2 in the orthosteric pocket and a sterol stabilizing Gs coupling, and dissociating cAMP signaling from a C-terminal PKA-binding site required for GLI2 suppression.

    Evidence Cryo-EM with sterol/PKA-site mutagenesis, cAMP assays, and GLI2 ciliary localization; FUZ identified as an interactor regulating ciliary localization via β-arrestin 2

    PMID:38326651 PMID:39369306

    Open questions at the time
    • Identity of any endogenous diffusible ligand unresolved
    • How sterol availability is regulated in vivo unknown
    • FUZ regulatory mechanism only partly defined
  11. 2025 Medium

    Mechanistically completed the export pathway (GRK2→β-arrestin→BBSome→IFT) and broadened GPR161's roles into neuronal migration mechanosensing, melanoma metabolism, and macrophage glycolytic reprogramming.

    Evidence β-arrestin/IFT27/BBSome KO cells and activation-mimetic mutants; helix-8 mutagenesis with phospho-NDE1; STAT3–GPR161–TXNIP ChIP/knockdown; macrophage-specific KO with Co-IP/SPR for C5aR1

    PMID:40384633 PMID:40737401 PMID:41834581 PMID:42185764

    Open questions at the time
    • Non-Hedgehog effector mechanisms are single-lab
    • Whether these roles share the ciliary cAMP module is unclear
    • Directness of some interactions (C5aR1, NDE1) needs orthogonal confirmation

Open questions

Synthesis pass · forward-looking unresolved questions
  • The endogenous activating ligand of GPR161 and the unifying molecular basis linking its ciliary cAMP/AKAP function to its diverse non-Hedgehog roles remain undefined.
  • No deorphanized endogenous agonist established
  • Mechanism switching between mechanosensation and constitutive signaling unknown
  • Therapeutic targetability untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 3 GO:0140299 molecular sensor activity 2 GO:0060090 molecular adaptor activity 1
Localization
GO:0005929 cilium 4 GO:0005886 plasma membrane 2
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-9609507 Protein localization 3 R-HSA-162582 Signal Transduction 2
Partners
ARRB1ARRB2C5AR1FKBP8FUZGRK2IFT38IQGAP1
Complex memberships
BBSome (functional engagement for ciliary export)

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2013 GPR161 localizes to primary cilia in a Tulp3/IFT-A-dependent manner. Constitutive GPR161 activity increases cAMP levels and promotes processing of Gli3 to its repressor form, thereby repressing Shh signaling. Shh pathway activation directs GPR161 internalization from cilia, preventing its activity. Thus GPR161 couples PKA activation to Shh pathway repression during neural tube development. Mouse knockout/loss-of-function, cAMP reporter assays, immunofluorescence localization in primary cilia, Gli3 processing western blot, genetic epistasis with Tulp3/IFT-A mutants Cell High 23332756
2016 Removal of GPR161 from primary cilia upon Shh pathway activation is a two-step process: (1) β-arrestin recruitment to the signaling-competent receptor facilitated by GPCR kinase Grk2, promoted by ciliary Smoothened activation; (2) clathrin-mediated endocytosis outside the ciliary compartment. Smoothened activity in cilia increases GPR161–β-arrestin binding to promote GPR161 removal both at rest and upon Shh stimulation. Co-immunoprecipitation, dominant-negative and knockout cell lines, live-cell imaging, pharmacological inhibitors of clathrin-mediated endocytosis, overexpression of Smoothened mutants The Journal of cell biology High 27002170
2016 GPR161 functions as an A-kinase anchoring protein (AKAP) for type I PKA regulatory subunits (RI), binding directly via a hydrophobic interaction interface in its cytoplasmic C-terminal tail. The GPR161–RI binary complex promotes GPR161 compartmentalization at the plasma membrane and recruits PKA RI to primary cilia in zebrafish. GPR161 is itself a substrate of PKA phosphorylation, and mutation of the PKA phosphorylation site affects its ciliary localization. Phosphoproteomics, cell-based protein-protein interaction reporters, direct binding assays (RI pull-down), site-directed mutagenesis, zebrafish in vivo imaging Proceedings of the National Academy of Sciences of the United States of America High 27357676
2014 GPR161 forms a signaling complex with β-arrestin 2 and IQGAP1 (a regulator of mTORC1 and E-cadherin). GPR161 overexpression activates mTOR signaling and decreases IQGAP1 phosphorylation. Knockdown of GPR161 impairs proliferation of basal breast cancer cell lines. Co-immunoprecipitation (GPR161–β-arrestin 2–IQGAP1 complex), shRNA knockdown, overexpression in mammary epithelial cells, 3D culture, western blot for mTOR pathway Proceedings of the National Academy of Sciences of the United States of America Medium 24599592
2008 A deletion/frameshift mutation in Gpr161 truncates its C-terminal tail, causing reduced receptor-mediated endocytosis and leading to neural tube defects and cataracts in the vacuolated lens mouse mutant. Positional cloning, characterization of endocytosis by functional assay of C-terminally truncated receptor Proceedings of the National Academy of Sciences of the United States of America Medium 18250320
2018 Gpr161 promotes Gli transcriptional repressor formation over activator formation in limb/skeletal morphogenesis in a primary cilium-dependent manner. Limb-specific deletion causes prematurely expanded Shh signaling and polysyndactyly; endochondral bone formation defects result from accumulation of proliferating periarticular-like chondrocytes and lack of Ihh signaling. All defects are suppressed in the absence of cilia. Conditional knockout mice (limb-specific, craniofacial mesenchyme-specific), genetic epistasis with cilia mutants, histology, in situ hybridization for Shh/Ihh targets Development (Cambridge, England) High 29222391
2018 Gpr161 acts as a tumor suppressor in Shh-subtype medulloblastoma by restricting Gli3-mediated repression. Deletion in neural stem cells or granule cell (GC) progenitors increases downstream Shh pathway activity and GC progenitor proliferation in a cilium-dependent manner. Conditional knockout mice (neural stem cell- and GC progenitor-specific), immunofluorescence, pathway target gene expression, Gli3 repressor analysis Cell reports High 29386106
2019 The IFT-B complex subunit IFT38 interacts with BBSome subunits BBS1, BBS2, and BBS9. This IFT-B–BBSome interaction is required for GPR161 export from cilia upon Hedgehog signaling stimulation; cells expressing an IFT38 mutant lacking this interaction show significant accumulation of GPR161 within cilia. Visible immunoprecipitation assay, IFT38-knockout cell lines expressing wild-type or interaction-deficient IFT38 mutant, immunofluorescence for ciliary GPR161 accumulation Biology open High 31471295
2019 Novel rare GPR161 variants found in spina bifida patients mislocalize to primary cilia, dysregulate both Shh and Wnt signaling, and inhibit cell proliferation in vitro, acting in a dominant-negative manner. Sanger sequencing of patient cohort, immunofluorescence for ciliary localization of variant proteins, Shh/Wnt pathway reporter assays, cell proliferation assay Human molecular genetics Medium 30256984
2019 Gpr161 deletion in mouse neuroepithelial cells/radial glia leads to Shh pathway derepression, radial glial overproliferation, ventriculomegaly, polymicrogyria, and disrupted neuronal migration, with periventricular nodular heterotopia. Conditional knockout mice (neuroepithelial/radial glia-specific), in toto imaging, BrdU/EdU proliferation assays, immunofluorescence for progenitor markers Developmental biology Medium 30914320
2021 A ciliary-localization-defective but cAMP-signaling-competent knock-in variant (Gpr161mut1) revealed that ciliary and extraciliary GPR161 pools establish tissue-specific Gli repressor thresholds. Ciliary GPR161 is required for Gli2 activator-dependent suppression in the ventral-most neural tube progenitors, while extraciliary GPR161 prevents ventralization; limb and midface morphogenesis depend on Gli repressor thresholds set by ciliary GPR161. CRISPR/Cas9 knock-in mice, immunofluorescence, pathway target gene expression, genetic epistasis eLife High 34346313
2021 PKA feedback-mediated phosphorylation of Gpr161 fine-tunes ciliary localization and PKA activity. PKA phosphorylation-deficient Gpr161 forms directly couple to Gαs and display increased sensitivity to Shh, causing excess high-level Hh target gene expression in zebrafish. Loss of Gpr161 in zebrafish leads to constitutive activation of medium and low, but not maximal, levels of Hh target gene expression. Zebrafish gpr161 morphants/mutants, BRET Gαs coupling assay, phosphorylation-deficient mutant analysis, in situ hybridization for Hh targets Development (Cambridge, England) Medium 33531430
2021 Gpr161 is a mechanoresponsive GPCR at the primary cilium of mesenchymal stem cells (MSCs). Fluid shear stress activates Gpr161-mediated cAMP signaling, which requires IFT88/cilia and adenylyl cyclase 6 (AC6), to drive osteogenic differentiation. Hh signaling downstream of this axis is required for loading-induced osteogenesis. Gpr161 siRNA knockdown, fluid shear stress application, cAMP measurement, IFT88 knockdown, AC6 inhibition, osteogenic differentiation assays Bone Medium 33450431
2024 Cryo-EM structure of active human GPR161 bound to heterotrimeric Gs revealed: (1) extracellular loop 2 occupies the canonical GPCR orthosteric ligand pocket; (2) a sterol binds adjacent to transmembrane helices 6 and 7, stabilizing the Gs-coupling conformation — mutations preventing sterol binding suppress cAMP signaling but retain GPR161's ability to suppress GLI2 accumulation in cilia; (3) a PKA-binding site in the GPR161 C-terminus is critical for suppressing GLI2 ciliary accumulation. Cryo-EM structure determination, site-directed mutagenesis of sterol-binding and PKA-binding sites, cAMP reporter assays, immunofluorescence for GLI2 ciliary localization Nature structural & molecular biology High 38326651
2025 β-arrestin (ARRB1/ARRB2) is required for GPR161 export from cilia. GRK2 phosphorylates GPR161, enabling β-arrestin recruitment in its activated conformation, which then interacts with the BBSome to connect GPR161 to the IFT machinery for export. Activation-mimetic β-arrestin mutants cause constitutive GPR161 export. ARRB1/ARRB2 double knockout impairs GPR161 export. β-arrestin double KO cell lines, IFT27 and BBSome-subunit KO cells, overexpression of activation-mimetic β-arrestin mutants, Co-IP of β-arrestin with BBSome, immunofluorescence for ciliary GPR161 Journal of cell science High 40384633
2024 Fuz is genetically epistatic to Gpr161 in Shh signaling during mouse neural tube development. FUZ protein biochemically interacts with GPR161, and Fuz regulates GPR161-mediated ciliary localization via β-arrestin 2. Genetic epistasis in double-mutant mice, co-immunoprecipitation of FUZ and GPR161, β-arrestin 2 interaction assay, ciliary localization immunofluorescence Development (Cambridge, England) Medium 39369306
2025 GPR161 acts as a mechanoreceptor at the primary cilium driving saltatory neuronal migration. Fluid shear stress induces GPR161-dependent cAMP/PKA signaling, leading to phosphorylation of NDE1 (a dynein complex regulator) and microtubule reorganization to regulate the rhythmicity of neuronal migration. The mechanosensitive helix 8 of GPR161 is essential for this function. Ex vivo neuronal migration model, microfluidic shear stress assays, GPR161 knockout/knockdown, helix-8 mutagenesis, phospho-NDE1 western blot, immunofluorescence for microtubule organization Science advances Medium 40737401
2025 GPR161 promotes melanoma proliferation and metabolic activity through a STAT3–GPR161–TXNIP regulatory axis: STAT3 binds the GPR161 promoter and transcriptionally activates GPR161; GPR161 in turn negatively regulates TXNIP expression, reducing glycolytic capacity and proliferation when GPR161 is depleted. Promoter analysis, chromatin immunoprecipitation-qPCR for STAT3 binding, siRNA/shRNA knockdown, TXNIP overexpression/knockdown, glycolytic capacity assays Journal of microbiology and biotechnology Medium 41834581
2026 GPR161 promotes glycolytic reprogramming in macrophages during acute lung injury through suppression of complement component 5a receptor 1 (C5aR1). Co-immunoprecipitation and surface plasmon resonance identified C5aR1 as a downstream target/interactor of GPR161; macrophage-specific GPR161 knockout attenuates pulmonary inflammatory damage. Global and macrophage-specific conditional KO mice, RNA sequencing, co-immunoprecipitation, surface plasmon resonance, glycolytic capacity assays Cellular & molecular biology letters Medium 42185764
2025 FKBP8 was identified as a novel interacting protein of GPR161 (and FUZ), validated by affinity purification-mass spectrometry; GPR161 interactome is enriched for proteins associated with proteasomal catabolic processes, trafficking, receptor complex, and ER-Golgi transport. Affinity-based LC-MS/MS immunoprecipitation, STRING network analysis, co-IP validation of FKBP8 bioRxivpreprint Low 41000683
2025 Tumors arising from Gαs pathway inactivation are independent of GPR161 (and of canonical Smoothened), establishing an SMO-independent oncogenic Hedgehog signaling model that bypasses GPR161's negative regulatory role. Genetic epistasis in mouse BCC-like tumor models (Gαs pathway inactivation combined with GPR161 deletion), histology, bulk and single-cell RNA sequencing bioRxivpreprint Medium bio_10.1101_2025.02.21.639530
2024 ARL13B maintains GPR161 ciliary localization; ARL13B KO reduces ciliary GPR161 and increases Shh signaling. GPR161 deletion in human iPSC-derived brain organoids decreases Gli3 repressor formation and increases Shh signaling, causing ventralization of dorsal cortical progenitors. Pharmacological or optogenetic elevation of ciliary cAMP rescues Gli3 repressor formation and dorsal neural stem cell identity in GPR161 KO organoids. CRISPR KO in human iPSC-derived brain organoids, immunofluorescence for GPR161 and Gli3 repressor, cAMP pharmacology, optogenetic cAMP elevation bioRxivpreprint Medium bio_10.1101_2024.07.18.604098
2025 GPR161-driven GLI3 repressor (GLI3R) signaling at the primary cilium controls apical constriction and cell fate during cranial neural tube closure. A functional non-ciliary Gpr161 knock-in implicated ciliary GPR161 localization in initiation and maintenance of cranial closure. GLI3R expression (but not GLI2 loss) rescued exencephaly in Gpr161 KO mice, and GLI3R restricted forebrain ventral floor plate expansion and mediated apical constriction in lateral midbrain neural folds. Gpr161 mutant allelic series including non-ciliary knock-in, genetic epistasis with Gli2 KO and Gli3R expression, in toto imaging of cell behavior, immunofluorescence Development (Cambridge, England) High 41417007
2015 Gpr161 regulates the retinoic acid (RA) and canonical Wnt pathways during neurulation, downstream of Gpr161 activity. RA injection restores canonical Wnt marker expression and rescues Gpr161 hypomorphic neural tube defects, placing RA upstream of Wnt as part of the Gpr161 downstream cascade. Hypomorphic Gpr161vl allele, modifier QTL mapping, QRT-PCR, in situ hybridization, IHC, intraperitoneal RA injection rescue experiment Developmental biology Medium 25753732

Source papers

Stage 0 corpus · 40 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 The ciliary G-protein-coupled receptor Gpr161 negatively regulates the Sonic hedgehog pathway via cAMP signaling. Cell 409 23332756
2016 Smoothened determines β-arrestin-mediated removal of the G protein-coupled receptor Gpr161 from the primary cilium. The Journal of cell biology 119 27002170
2016 Gpr161 anchoring of PKA consolidates GPCR and cAMP signaling. Proceedings of the National Academy of Sciences of the United States of America 94 27357676
2014 G-protein-coupled receptor GPR161 is overexpressed in breast cancer and is a promoter of cell proliferation and invasion. Proceedings of the National Academy of Sciences of the United States of America 67 24599592
2008 The orphan G protein-coupled receptor, Gpr161, encodes the vacuolated lens locus and controls neurulation and lens development. Proceedings of the National Academy of Sciences of the United States of America 61 18250320
2019 Germline GPR161 Mutations Predispose to Pediatric Medulloblastoma. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 56 31609649
2015 Whole-exome sequencing identifies homozygous GPR161 mutation in a family with pituitary stalk interruption syndrome. The Journal of clinical endocrinology and metabolism 55 25322266
2018 The G protein-coupled receptor Gpr161 regulates forelimb formation, limb patterning and skeletal morphogenesis in a primary cilium-dependent manner. Development (Cambridge, England) 54 29222391
2018 Basal Suppression of the Sonic Hedgehog Pathway by the G-Protein-Coupled Receptor Gpr161 Restricts Medulloblastoma Pathogenesis. Cell reports 48 29386106
2019 Requirement of IFT-B-BBSome complex interaction in export of GPR161 from cilia. Biology open 42 31471295
2020 Hedgehog and Gpr161: Regulating cAMP Signaling in the Primary Cilium. Cells 36 31947770
2020 Enterotoxigenic Escherichia coli infection promotes enteric defensin expression via FOXO6-METTL3-m6A-GPR161 signalling axis. RNA biology 31 32914682
2019 Dominant negative GPR161 rare variants are risk factors of human spina bifida. Human molecular genetics 30 30256984
2019 Derepression of sonic hedgehog signaling upon Gpr161 deletion unravels forebrain and ventricular abnormalities. Developmental biology 30 30914320
2024 GPR161 structure uncovers the redundant role of sterol-regulated ciliary cAMP signaling in the Hedgehog pathway. Nature structural & molecular biology 29 38326651
2021 Ciliary and extraciliary Gpr161 pools repress hedgehog signaling in a tissue-specific manner. eLife 28 34346313
2015 The orphan GPCR, Gpr161, regulates the retinoic acid and canonical Wnt pathways during neurulation. Developmental biology 28 25753732
2021 Primary cilium-mediated MSC mechanotransduction is dependent on Gpr161 regulation of hedgehog signalling. Bone 24 33450431
2021 Feedback control of the Gpr161-Gαs-PKA axis contributes to basal Hedgehog repression in zebrafish. Development (Cambridge, England) 15 33531430
2021 Wnt1 Lineage Specific Deletion of Gpr161 Results in Embryonic Midbrain Malformation and Failure of Craniofacial Skeletal Development. Frontiers in genetics 14 34887903
2024 In vivo and in vitro anti-inflammation of Rhapontici Radix extract on mastitis via TMEM59 and GPR161. Journal of ethnopharmacology 12 38942158
2023 Primary cilia, A-kinase anchoring proteins and constitutive activity at the orphan G protein-coupled receptor GPR161: A tale about a tail. British journal of pharmacology 10 36772847
2009 Mucosal or systemic administration of rE2 glycoprotein antigen loaded PLGA microspheres. International journal of pharmaceutics 8 19429284
2023 Pax3 lineage-specific deletion of Gpr161 is associated with spinal neural tube and craniofacial malformations during embryonic development. Disease models & mechanisms 7 37885410
2022 Development of Highly Sensitive Sandwich ELISA for the Early-Phase Diagnosis of Chikungunya Virus Utilizing rE2-E1 Protein. Infection and drug resistance 5 35924014
2017 Suspension culture process for H9N2 avian influenza virus (strain Re-2). Archives of virology 5 28685290
2018 Selective Cleavage of C-O Bonds in Lignin Catalyzed by Rhenium(VII) Oxide (Re2 O7 ). ChemPlusChem 4 31950656
2015 Synthesis and X-ray crystal structure of the dirhenium complex Re2(i-C3H7COO)4Cl2 and its interactions with the DNA purine nucleobases. Journal of inorganic biochemistry 3 26315264
2025 β-Arrestin mediates the export of ciliary GPR161 but not Smoothened together with the BBSome and intraflagellar transport machinery. Journal of cell science 2 40384633
2025 GPR161 mechanosensitivity at the primary cilium drives neuronal saltatory migration. Science advances 2 40737401
2024 Linkage between Fuz and Gpr161 genes regulates sonic hedgehog signaling during mouse neural tube development. Development (Cambridge, England) 2 39369306
2023 GPR161 structure uncovers the redundant role of sterol-regulated ciliary cAMP signaling in the Hedgehog pathway. bioRxiv : the preprint server for biology 2 37292845
2019 Identification and spatiotemporal expression of gpr161 genes in zebrafish. Gene 2 31884103
2025 GPR161-GLI3 repressor signaling at cilia directs apical constriction and cell fate during cranial neural tube closure. Development (Cambridge, England) 1 41417007
2024 The novel linkage between Fuz and Gpr161 genes regulates sonic hedgehog signaling during mouse embryonic development. bioRxiv : the preprint server for biology 1 38260275
2026 Oncogenic GPR161 Drives Melanoma Proliferation and Metabolic Activity through TXNIP Inhibition. Journal of microbiology and biotechnology 0 41834581
2026 Expression Analysis of the orphan receptors GPR161, GPR132, GPR20, and GPR139 in patients with cervicitis and low-grade, and high-grade squamous intraepithelial lesions. Genetics and molecular biology 0 41915403
2026 GPR161 contributes to macrophage glycolytic reprogramming via targeting C5aR1 in acute lung injury. Cellular & molecular biology letters 0 42185764
2025 Identification of novel interacting proteins of FUZ and GPR161. bioRxiv : the preprint server for biology 0 41000683
2023 Pax3 lineage-specific deletion of Gpr161 is associated with spinal neural tube and craniofacial malformations during embryonic development. bioRxiv : the preprint server for biology 0 37461574

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