ArticleBiochemical and biophysical research communications2016
Galactose-1 phosphate uridylyltransferase (GalT) gene: A novel positive regulator of the PI3K/Akt signaling pathway in mouse fibroblasts.
Article in Biochemical and biophysical research communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Pathophysiology and targets for treatment in hereditary galactosemia: A systematic review of animal and cellular models.Journal of inherited metabolic disease · 2020Pooled it
- Reproductive potential in classical galactosemia: A case series based perspective.European journal of obstetrics & gynecology and reproductive biology: X · 2026Article
- Assessment of Long-Term Safety and Efficacy of Purple Sweet Potato Color (PSPC) and Myo-Inositol (MI) Treatment for Motor Related and Behavioral Phenotypes in a Mouse Model of Classic Galactosemia.Journal of inherited metabolic disease · 2025Article
- Epalrestat Alleviates Reactive Oxygen Species and Endoplasmic Reticulum Stress by Maintaining Glycosylation in IMS32 Schwann Cells Under Exposure to Galactosemic Conditions.International journal of molecular sciences · 2025Article
- Galactose-1-phosphate uridylyltransferase GalT promotes biofilm formation and enhances UV-B resistance of Bacillus thuringiensis.World journal of microbiology & biotechnology · 2024Article
- Whole-body galactose oxidation as a robust functional assay to assess the efficacy of gene-based therapies in a mouse model of Galactosemia.Molecular therapy. Methods & clinical development · 2024Article
- AAV9-basedMolecular genetics and metabolism reports · 2024Article
- Brain function in classic galactosemia, a galactosemia network (GalNet) members review.Frontiers in genetics · 2024Review
- The hypergonadotropic hypogonadism conundrum of classic galactosemia.Human reproduction update · 2023Article
- Early postnatal alterations in follicular stress response and survival in a mouse model of Classic Galactosemia.Journal of ovarian research · 2022Article
- Harnessing the Power of Purple Sweet Potato Color andInternational journal of molecular sciences · 2022Article
- Galactosemia: Biochemistry, Molecular Genetics, Newborn Screening, and Treatment.Biomolecules · 2022Review
- Pathophysiology and management of classic galactosemic primary ovarian insufficiency.Reproduction & fertility · 2021Review
- Current and Future Treatments for Classic Galactosemia.Journal of personalized medicine · 2021Review
- The yeast protein Ubx4p contributes to mitochondrial respiration and lithium-galactose-mediated activation of the unfolded protein response.The Journal of biological chemistry · 2020Article
- Salubrinal enhances eIF2α phosphorylation and improves fertility in a mouse model of Classic Galactosemia.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Fertility in classical galactosaemia, a study of N-glycan, hormonal and inflammatory gene interactions.Orphanet journal of rare diseases · 2018Article
- Biochemical changes and clinical outcomes in 34 patients with classic galactosemia.Journal of inherited metabolic disease · 2018Article
- Impaired fertility and motor function in a zebrafish model for classic galactosemia.Journal of inherited metabolic disease · 2018Article
- Assessment of ataxia phenotype in a new mouse model of galactose-1 phosphate uridylyltransferase (GALT) deficiency.Journal of inherited metabolic disease · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The vital importance of the Leloir pathway of galactose metabolism has been repeatedly demonstrated by various uni-/multicellular model organisms, as well human patients who have inherited deficiencies of the key GAL enzymes. Yet, other than the obvious links to the glycolytic pathway and glycan biosynthetic pathways, little is known about how this metabolic pathway interacts with the rest of the metabolic and signaling networks. In this study, we compared the growth and the expression levels of the key components of the PI3K/Akt growth signaling pathway in primary fibroblasts derived from normal and galactose-1 phosphate uridylyltransferase (GalT)-deficient mice, the latter exhibited a subfertility phenotype in adult females and growth restriction in both sexes. The growth potential and the protein levels of the pAkt(Thr308), pAkt(Ser473), pan-Akt, pPdk1, and Hsp90 proteins were significantly reduced by 62.5%, 60.3%, 66%, 66%, and 50%, respectively in the GalT-deficient cells. Reduced expression of phosphorylated Akt proteins in the mutant cells led to diminished phosphorylation of Gsk-3β (-74%). Protein expression of BiP and pPten were 276% and 176% higher respectively in cells with GalT-deficiency. Of the 24 genes interrogated using QIAGEN RT(2) Profiler PCR Custom Arrays, the mRNA abundance of Akt1, Pdpk1, Hsp90aa1 and Pi3kca genes were significantly reduced at least 2.03-, 1.37-, 2.45-, and 1.78-fold respectively in mutant fibroblasts. Both serum-fasted normal and GalT-deficient cells responded to Igf-1-induced activation of Akt phosphorylation at +15 min, but the mutant cells have lower phosphorylation levels. The steady-state protein abundance of Igf-1 receptor was also significantly reduced in mutant cells. Our results thus demonstrated that GalT deficiency can effect down-regulation of the PI3K/Akt growth signaling pathway in mouse fibroblasts through distinct mechanisms targeting both gene and protein expression levels.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.