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Hai-Qing Zhang

Publications and source records attributed to Hai-Qing Zhang.

2 recordsLinked to original sources
PubMed2026

Description of Sulfitobacter gelatinilyticus sp. nov. and Sulfitobacter weihaiensis sp. nov., isolated from marine sediment.

Two Gram-stain-negative, yellowish-white, facultative anaerobic and rod-shaped bacterial strains, designated F26169LT and F26204T, were isolated from coastal sediment of Jingzi Port, Weihai. Based on phenotypic, physiological, biochemical, chemotaxonomic and phylogenomic analyses, the two strains were affiliated with the genus Sulfitobacter. They showed obvious differences in phenotypic, chemotaxonomic and genomic characteristics compared with closely related taxa in this genus, and the ANI, AAI and dDDH values between them and related species were all lower than the standard thresholds for bacterial species delineation. Genomic analysis revealed the presence of genes encoding a complete sulfur oxidation (SOX) pathway and dimethylsulfoniopropionate (DMSP) lyases in both strains. Accordingly, strains F26169LT and F26204T are proposed as two novel species of the genus Sulfitobacter, for which the names Sulfitobacter gelatinilyticus sp. nov. and Sulfitobacter weihaiensis sp. nov., are proposed, respectively. The type strains are F26169LT (= KCTC 92635 T = MCCC 1H01356T) and F26204T (= KCTC 92634 T = MCCC 1H01357T).

Geologic Sediments↗
PubMed2026

GPR3 in neuro-metabolic-immune-reproductive nexus - a potential therapeutic target for Multi-System diseases.

BACKGROUND: GPR3(G-protein-coupled receptor 3), an orphan G-protein-coupled receptor (GPCR) with constitutive Gs activity, is expressed in the brain, liver, ovary, and other tissues, regulating cell proliferation, differentiation, and apoptosis across the nervous, reproductive, immune, and metabolic systems. This review synthesizes evidence on its integrated signaling and physiological functions to address the lack of a comprehensive multisystem pathophysiology overview. METHODS: A systematic literature search was conducted on PubMed and Web of Science, using keywords such as "GPR3", "GPCR", "neurodegeneration", "metabolism", "immune", "reproduction", "agonist", "inhibitor", and "therapeutic target". This search identified GPR3's roles in neurodegenerative diseases, immune inflammation, reproduction, and energy metabolism. The analysis focused on signaling pathways, ligand regulation, and therapeutic potential. RESULTS: The research indicates that GPR3 is involved in neuronal survival, synaptic plasticity, and microglial activity via the cAMP/PKA, PI3K/Akt, and β - arrestin pathways. It promotes amyloid - β formation in Alzheimer's disease (AD), yet provides neuroprotection in Parkinson's disease (PD) models. It may contribute to anxiety/depression - like states, maintain oocyte meiotic arrest in the ovary, and activate thermogenic genes in adipose tissue. GPR3 modulates immune responses. Using oleic acid (OA) and diphenyleneiodonium (DPI) as activators, and AF64394 and cannabidiol (CBD) as antagonists, it shows potential in disease models. CONCLUSION: GPR3 acts as a central molecular hub integrating neural, metabolic, immune, and reproductive signaling, highlighting its potential as a therapeutic target for chronic multisystem disorders. However, its dual roles in certain pathologies and translation challenges necessitate further research.

Humans↗