Insulin-like growth factor 2 (IGF2) belongs to the member of the insulin-like growth factors family, which plays key roles in animal growth, differentiation and proliferation, as well as reproduction and the regulation of ovarian follicle development. However, little is known about the goose gene. In this study, a 1879bp fragment that covered the complete coding region (CDS) of goose cDNA was identified for the first time. The cDNA consists of an open reading frame of 574 nucleotides with the capacity to encode a prepro-IGF-II protein of 187 amino acids, which comprises a signal peptide (24 residues), IGF-II peptide (67 residues), and C-terminal peptide (96 residues), and is closely related to that of chicken. qPCR indicates that the goose mRNA is differentially expressed in all examined tissues of fertilized eggs (28 days) and laying Zhedong White geese (270 days). Two novel single nucleotide polymorphisms (SNPs) were detected in exon 1 (G63A, Chr2: G26541617A) and intron 1 (G38A, Chr2: G26541479A) regions, and the synonymous mutation G63A showed a significant association with egg numbers (E180d) of Sanhua goose population (<0.05). All the information derived from this study could be valuable and facilitate further studies on the functions of goose gene.
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http://dx.doi.org/10.1080/10495398.2021.2015603 | DOI Listing |
Adv Sci (Weinh)
January 2025
Key Laboratory of Drug Quality Control and Pharmacovigilance (Ministry of Education), State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, P. R. China.
Patients with ulcerative colitis (UC) have a higher risk of developing colorectal cancer (CRC), however, the metabolic shifts during the UC-to-CRC transition remain elusive. In this study, an AOM-DSS-induced three-stage colitis-associated colorectal cancer (CAC) model is constructed and targeted metabolomics analysis and pathway enrichment are performed, uncovering the metabolic changes in this transition. Spatial metabolic trajectories in the "normal-to-normal adjacent tissue (NAT)-to-tumor" transition, and temporal metabolic trajectories in the "colitis-to-dysplasia-to-carcinoma" transition are identified through K-means clustering of 74 spatially and 77 temporally differential metabolites, respectively.
View Article and Find Full Text PDFQuant Imaging Med Surg
January 2025
Department of Radiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Background: Pediatric growth hormone deficiency (GHD) is a disease resulting from the impaired growth hormone-insulin-like growth factor-1 (GH-IGF-1) axis, but the effects of GHD on children's behavior and brain microstructural structure alterations have not yet been fully clarified. We aimed to investigate the quantitative profiles of gray matter and white matter in pediatric GHD using synthetic magnetic resonance imaging (MRI).
Methods: The data of 50 children with GHD and 50 typically developing (TD) children were prospectively collected.
Nucl Med Commun
January 2025
Department of Nuclear Medicine, First Hospital of Shanxi Medical University.
Objectives: To investigate the effects of selenium on functional and histopathological changes and mRNA expression levels of insulin-like growth factors 1 and 2 (IGF-1 and -2) and aquaporins 4 and 5 (AQP-4 and -5) in 131I-induced damaged rat parotid glands.
Methods: Rats were divided into three groups: iodotherapy-with-selenium, iodotherapy-only, and control. Rats in the iodotherapy-with-selenium group were intragastrically administered 131I on the first day and selenomethionine through drinking water.
Breast Cancer Res
January 2025
Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC, 27157, USA.
Obesity is a modifiable risk factor for breast cancer. Yet, how obesity contributes to cancer initiation is not fully understood. The goal of this study was to determine if the body mass index (BMI) and metabolic hallmarks of obesity are related to DNA damage in normal breast tissue.
View Article and Find Full Text PDFRev Endocr Metab Disord
January 2025
Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Illinois at Chicago, Chicago, IL, USA.
This review focuses on our current understanding of how growth hormone releasing hormone (GHRH): 1) stimulates GH release and synthesis from pituitary growth hormone (GH)-producing cells (somatotropes), 2) drives somatotrope proliferation, 3) is negatively regulated by somatostatin (SST), GH and IGF1, 4) is altered throughout lifespan and in response to metabolic challenges, and 5) analogues can be used clinically to treat conditions of GH excess or deficiency. Although a large body of early work provides an underpinning for our current understanding of GHRH, this review specifically highlights more recent work that was made possible by state-of-the-art analytical tools, receptor-specific agonists and antagonists, high-resolution in vivo and ex vivo imaging and the development of tissue (cell) -specific ablation mouse models, to paint a more detailed picture of the regulation and actions of GHRH.
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