Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

LHCGR and ALMS1 defects likely cooperate in the development of polycystic ovary syndrome indicated by double-mutant mice.

Journal of genetics and genomics = Yi chuan xue bao - 20 May 2021

Yu Li, Wang Lina, Tao Wufan, Zhang Wenxiang, Yang Shuanghao, Wang Jian, Fei Jia, Peng Rui, Wu Yiming, Zhen Xiumei, Shao Hong, Gu Weiyue, Li Rong, Wu Bai-Lin, Wang Hongyan

Abstract excerpt

Polycystic ovary syndrome (PCOS) is a heterogeneous disorder with evidence of polygenetic components, and obesity may be a risk factor for hyperandrogenism. Previous studies have shown that LHCGR is enriched in the ovary and LHCGR deficiency causes infertility without typical PCOS phenotypes. ALMS1 is implicated in obesity and hyperandrogenism, the common phenotypes among PCOS patients. Through whole-exome...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Biosynthetic Pathways
Share to Cell Cycle Proteins

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Exome Sequencing

Share to Immunohistochemistry

Share to Mice, Knockout

Share to Polycystic Ovary Syndrome

Share to Receptors, LH

Share to Steroids

Source

Identifiers

PMID: 34147365
DOI: 10.1016/j.jgg.2021.03.014

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

LHCGR and ALMS1 defects likely cooperate in the development of polycystic ovary syndrome indicated by double-mutant mice.PMID 34147365Read ↗

Genetics of the polycystic ovary syndrome.Semantic proximity Read ↗

Prenatal androgen exposure and transgenerational susceptibility to polycystic ovary syndrome.Semantic proximity Read ↗

High-throughput Sequencing to Identify Monogenic Etiologies in a Preselected Polycystic Ovary Syndrome CohortSemantic proximity Read ↗

Integrated Transcriptomic and Epigenetic Study of PCOS: Impact of Map3k1 and Map1lc3a Promoter Methylation on AutophagySemantic proximity Read ↗

Genetic Models for the Study of Luteinizing Hormone Receptor FunctionSemantic proximity Read ↗

Transcriptomic mapping of key reproductive and metabolic tissues and oocytes in mouse models of polycystic ovary syndromeSemantic proximity Read ↗

Infertility in Female Mice with a Gain-of-Function Mutation in the Luteinizing Hormone Receptor Is Due to Irregular Estrous Cyclicity, Anovulation, Hormonal Alterations, and Polycystic Ovaries.Semantic proximity Read ↗

Upregulated Ribosomal Pathway Impairs Follicle Development in a Polycystic Ovary Syndrome Mouse Model: Findings of Differential Gene Expression Analysis of OocytesSemantic proximity Read ↗

Novel mutations in LHCGR (luteinizing hormone/choriogonadotropin receptor): expanding the spectrum of mutations responsible for human empty follicle syndrome.Semantic proximity Read ↗

Exome Sequencing Reveals the POLR3H Gene as a Novel Cause of Primary Ovarian InsufficiencySemantic proximity Read ↗

Systems Genetics Reveals the Functional Context of PCOS Loci and Identifies Genetic and Molecular Mechanisms of Disease Heterogeneity.Semantic proximity Read ↗

Altered metabolic health during pregnancy in mice with lean polycystic ovary syndrome-like traits from high prenatal AMHSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.