Paper · 25753732

The orphan GPCR, Gpr161, regulates the retinoic acid and canonical Wnt pathways during neurulation.

Li BI and 7 others. Dev Biol, 2015. Cited by 28 papers, by iCite.

11 sourcespapers-2026-11-12-0.1.0

Cite this record

ConductScience Library. The orphan GPCR, Gpr161, regulates the retinoic acid and canonical Wnt pathways during neurulation. Papers, record 25753732. Release papers-2026-11-12-0.1.0, 12 Nov 2026. https://conductscience.org/library/papers/25753732

On this page

Paper

PubMed's record of the paper, with iCite's citation figures. No abstract is shown.

Title: The orphan GPCR, Gpr161, regulates the retinoic acid and canonical Wnt pathways during neurulation.; PubMed
Journal: Dev Biol; PubMed
Year: 2015; PubMed
Publication types: Journal Article, Research Support, Non-U.S. Gov't; PubMed
PubMed: https://pubmed.ncbi.nlm.nih.gov/25753732/; PubMed
DOI: https://doi.org/10.1016/j.ydbio.2015.02.007; PubMed
The journal: https://conductscience.org/library/journal-index/0372762; PubMed
Citations, by iCite: 28; iCite
Relative citation ratio, by iCite: 0.84; iCite
Revised in PubMed: 2025-02-13; PubMed

Authors8

The authors in the order PubMed's record lists them, with the ORCID iDs it states.

Order	Author	Forename
1	Li BI	Bo I
2	Matteson PG	Paul G
3	Ababon MF	Myka F
4	Nato AQ Jr	Alejandro Q
5	Lin Y	Yong
6	Nanda V	Vikas
7	Matise TC	Tara C
8	Millonig JH	James H

Source PubMed

Topics27

NLM's MeSH indexing of the paper, its major topics first.

MeSH term	Major
Gene Expression Regulation, Developmental	Major topic
Neurulation	Major topic
Receptors, G-Protein-Coupled	Major topic
Tretinoin	Major topic
Wnt Proteins	Major topic
Animals
Base Sequence
Cell Line
Genes, Reporter
Genetic Variation
Hedgehog Proteins
Homeodomain Proteins
In Situ Hybridization
Mice
Mice, Inbred C3H
Mice, Transgenic
Models, Genetic
Molecular Sequence Data
Mutation
Neural Tube Defects
Phenotype
Quantitative Trait Loci
RNA, Messenger
Signal Transduction
Time Factors
Wnt Signaling Pathway
Wnt3A Protein

Source PubMed

Grants0

Each grant PubMed's record writes, matched to the NIH project NIH's grant and paper links name for this paper, and each of those links the record does not write.

None in this release.

Trials0

The trials whose ClinicalTrials.gov record lists the paper, and the trial numbers the paper's PubMed record names.

None in this release.

Comments and corrections0

PubMed's comments and corrections, NLM's own indexing: retractions first, then expressions of concern, errata and updates, and comments last.

None in this release.

References0

The papers the reference list in PubMed's record names, those in our copy of PubMed, in the list's order.

None in this release.

Cited by20

The papers in our copy of PubMed whose reference list names this one, newest first. iCite, which reads more sources, counts 28 citations.

PMID	Title	Journal	Year	In Papers	Source
41,417,007	GPR161-GLI3 repressor signaling at cilia directs apical constriction and cell fate during cranial neural tube closure.	Development	2025	https://conductscience.org/library/papers/41417007	PubMed
41,390,872	Identifying the biomarkers associated with G protein-coupled receptors of parkinson's disease.	Sci Rep	2025	https://conductscience.org/library/papers/41390872	PubMed
40,456,828	ELTD1 inhibits differentiation of hemogenic endothelium progenitors from human embryonic stem cells through the HPIP-Wnt pathway.	Exp Mol Med	2025	https://conductscience.org/library/papers/40456828	PubMed
38,326,651	GPR161 structure uncovers the redundant role of sterol-regulated ciliary cAMP signaling in the Hedgehog pathway.	Nat Struct Mol Biol	2024	https://conductscience.org/library/papers/38326651	PubMed
37,885,410	Pax3 lineage-specific deletion of Gpr161 is associated with spinal neural tube and craniofacial malformations during embryonic development.	Dis Model Mech	2023	https://conductscience.org/library/papers/37885410	PubMed
34,887,903	Wnt1 Lineage Specific Deletion of Gpr161 Results in Embryonic Midbrain Malformation and Failure of Craniofacial Skeletal Development.	Front Genet	2021	https://conductscience.org/library/papers/34887903	PubMed
34,769,531	Role of the Purinergic P2Y2 Receptor in Pulmonary Hypertension.	Int J Environ Res Public Health	2021	https://conductscience.org/library/papers/34769531	PubMed
34,346,313	Ciliary and extraciliary Gpr161 pools repress hedgehog signaling in a tissue-specific manner.	Elife	2021	https://conductscience.org/library/papers/34346313	PubMed
32,030,357	Genome-wide CRISPR screening identifies new regulators of glycoprotein secretion.	Wellcome Open Res	2019	https://conductscience.org/library/papers/32030357	PubMed
31,693,581	The search for genetic determinants of human neural tube defects.	Curr Opin Pediatr	2019	https://conductscience.org/library/papers/31693581	PubMed

1 to 10 of 20

See all 20 cited by

Genes0

The genes the Gene search release ties to the paper: Swiss-Prot's references first, then PubTator's text mining.

None in this release.

Drugs0

The drugs whose trials, in the Pipelines release, list the paper.

None in this release.

Data0

The data bank entries PubMed's record names. Trial numbers are under Trials.

None in this release.

Data dates

The date of each source this release read.

PubMed: 2026-11-06; PubMed
iCite: 2026-11-05; iCite
PMC's ID file: 2026-11-05; PMC's ID file
NIH RePORTER's grant and paper links: 2026-11-01; NIH RePORTER's grant and paper links
Trials: 2026-11-12
Gene search: 2026-11-11
Pipelines: 2026-09-18

Sources 11

ChEMBL, through Open TargetsCC BY-SA 3.0
ClinicalTrials.govNo license stated
HGNCCC0
iCiteCC BY 4.0
NCBI GenePublic domain (US government)
NIH RePORTER's grant and paper linksPublic domain
Open TargetsCC0 1.0
PMC's ID filePublic domain (US government)
PubMedNLM's terms
PubTator 3Public domain
UniProtCC BY 4.0

Each source's terms

ChEMBL, through Open TargetsCC BY-SA 3.0, for the parts from ChEMBL. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
ClinicalTrials.govnone stated
HGNCCC0: https://www.genenames.org/about/license/
iCiteCC BY 4.0
NCBI GeneNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
NIH RePORTER's grant and paper linksPublic domain (NIH RePORTER)
Open TargetsCC0 1.0. Open Targets asks that users cite its latest paper: Buniello et al. 2025, Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery, Nucleic Acids Research 53(D1):D1467, PMID 39657122. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
PMC's ID fileNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
PubMedNLM's terms
PubTator 3Public domain
UniProtCC BY 4.0. UniProt's licence file: "All databases and documents in the UniProt FTP directory may be copied and redistributed freely, without advance permission, provided that this copyright statement is reproduced with each copy." UniProt asks that users cite its latest paper: The UniProt Consortium, UniProt: the Universal Protein Knowledgebase in 2025, Nucleic Acids Research 53:D609-D617, https://doi.org/10.1093/nar/gkae1010. Read on 9 Nov 2026 at https://www.uniprot.org/help/license

ClinicalTrials.gov's data carry an international copyright outside the United States: https://clinicaltrials.gov/about-site/terms-conditions.

For software

Read this paper from software.

The record and each of its lists are JSON, twenty rows a page. No key.

GET https://conductscience.org/api/papers/v1/25753732

GET https://conductscience.org/api/papers/v1/25753732/authors

API reference For AI assistants