SLC2A4 Peptide
- Known as:
- SLC2A4 Peptide
- Catalog number:
- 42-800P
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- SLC2A4 Peptide
Related genes to: SLC2A4 Peptide
- Gene:
- SLC2A4 NIH gene
- Name:
- solute carrier family 2 member 4
- Previous symbol:
- GLUT4
- Synonyms:
- -
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-03-06
- Date modifiied:
- 2016-10-05
Related products to: SLC2A4 Peptide
Related articles to: SLC2A4 Peptide
- Skeletal muscle satellite cells are indispensable for muscle growth and regeneration, and their myogenic differentiation is precisely controlled by transcription factors. As a core member of the TEAD family, participates in various biological processes, yet its function and regulatory mechanism in porcine skeletal muscle satellite cells (PSCs) remain largely unknown. High-purity PSCs were isolated and identified from 7-day-old Large White piglets. Combined approaches of siRNA-mediated knockdown, RT-qPCR, Western blotting, immunofluorescence, EdU assays, and transcriptome sequencing were applied to explore the role of during myogenic differentiation. expression was gradually upregulated during PSC differentiation and positively correlated with myogenic marker genes. Knockdown of did not affect PSC proliferation but significantly suppressed myogenic differentiation, as indicated by reduced expression of myogenic genes and blocked myotube formation. Transcriptomic analysis demonstrated that DEGs were highly enriched in metabolic pathways, particularly the AMPK signaling pathway. knockdown led to excessive upregulation of and prominent induction of . Collectively, these results indicate that promotes myogenic differentiation in PSCs, likely by maintaining metabolic homeostasis. This study provides the first characterization of in porcine skeletal muscle satellite cells and demonstrates that it promotes myogenic differentiation. - Source: PubMed
Publication date: 2026/05/18
Zhou HuanhuanZeng JiayiZhang XiaoyuZeng XinqiXu KeChen Hongbo - AMPK signaling and GLUT4 trafficking are key regulators of cellular glucose handling; however, the effects of biogenic silver nanoparticles (AgNPs) in preadipocyte models remain underexplored. This study characterizes Syzygium caryophyllatum-mediated SC-AgNPs (21.78 nm TEM, λ 449 nm) in 3T3-L1 preadipocytes. The identical batch, verified stable by UV-vis and visual inspection, was tested across viability (MTT), ROS (DCFDA), mitochondrial function (TMRE), apoptosis (Annexin V/PI), and AMPK/GLUT4 regulation (endpoint RT-PCR, Western blot) using vehicle controls. SC-AgNPs showed high biocompatibility (IC 605.8 μg/mL, > 95% viability at 5-50 μg/mL) with modest changes in cellular responses, including controlled ROS elevation (1.3-fold) and mitochondrial hyperpolarization (2.21-fold), while apoptosis was observed at IC (91.7%). At sub-toxic working concentrations, GLUT4 mRNA/protein increased 1.55-/1.6-fold (GAPDH/β-actin normalized), while total AMPK expression decreased (0.2- to 0.7-fold), indicating that the underlying regulatory mechanism remains unclear and requires further investigation. These findings provide preliminary evidence of GLUT4 modulation in 3T3-L1 preadipocytes under non-cytotoxic conditions. However, due to the use of undifferentiated cells and the absence of functional assays, these results should be interpreted cautiously and require validation in differentiated and insulin-resistant adipocyte models. - Source: PubMed
Bhavi Santosh MallikarjunYarajarla Ramesh Babu - Pelvic floor dysfunction (PFD) is a common disease in women that seriously affects physical and psychological health. Menopause-associated estrogen reduction is one of the risk factors. However, the role and mechanism of estrogen in PFD remains unclear. In this study, we observed atrophy of both fast and slow muscle fibers in the pelvic floor muscle (PFM) of ovariectomized rats, accompanied by decreased expression of estrogen receptor α (ERα). Estrogen deficiency severely impaired the proliferation, differentiation, and mitochondrial function of C2C12 myoblasts and increased apoptosis, which could be rescued by ERα agonist. Mechanistically, estrogen deficiency led to the downregulation of ERα, which in turn suppressed the expression of glucose transporter 4 (GLUT4) and its trafficking regulator Rac family small GTPase 1 (RAC1). This disruption abolished the critical co-localization of GLUT4 with RAC1, resulting in defective glucose uptake, mitochondrial dysfunction, and ultimately impaired myoblast proliferation and differentiation. Both ERα activation and GLUT4 overexpression rescued these defects. Thus, our study delineates a novel ERα/GLUT4 pathway that mediates PFM atrophy under estrogen deficiency conditions, providing a potential therapeutic target for PFD. - Source: PubMed
Publication date: 2026/05/14
Huang XiaoyuZhou MengqiWang YingChen MaoXiao YaLi LingyunZhu FangyiChen LiyingTian XiaoyuWu ShimanLi BingshuHong Li - Aerobic exercise improves systemic insulin sensitivity by modulating muscle glucose metabolism. The CHRONO/BMAL1 pathway constitutes a core component of the endogenous molecular clock and participates in glucose metabolic regulation; however, whether it mediates exercise-induced metabolic benefits under high-fat diet (HFD) conditions remains unclear. We therefore investigated the role of this pathway in conferring protective effects of aerobic exercise against HFD-induced glucose metabolic dysfunction in skeletal muscle, by subjecting wild-type (WT) and inducible muscle-specific Chrono overexpression (Chrono IMOE) mice to an HFD with or without 12-week exercise. Unlike in WT mice, exercise failed to ameliorate adipose mass, dyslipidemia, and insulin resistance in HFD-fed Chrono IMOE mice. Mechanistically, in skeletal muscle of Chrono IMOE mice, Chrono overexpression suppressed exercise-induced reductions in CHRONO expression and CHRONO-BMAL1 binding, as well as the increase in BMAL1 levels. Consequently, despite elevated p-TBC1D1 and GLUT4 expression, exercise failed to promote GLUT4 sarcolemmal colocalization or upregulate gene expression of key enzymes for glycolysis and glycogen metabolism in skeletal muscle of Chrono IMOE mice. These findings demonstrate that preventing CHRONO‑BMAL1 dissociation via muscle-specific Chrono overexpression abrogates exercise-induced GLUT4 membrane trafficking, transcriptional activation of glycolytic/glycogen metabolic genes, and systemic insulin sensitivity improvements in HFD-fed mice, establishing CHRONO‑BMAL1 dissociation as a required step for these exercise adaptations. - Source: PubMed
Publication date: 2026/05/14
Xu LeiJia JieYan LuWang YangwenjieMiao ShudanZhang Ying - High-fat diets (HFDs) are a key contributor to obesity and promote oxidative stress and inflammation, which are associated with muscle atrophy and insulin resistance (IR). Passiflora edulis exhibits anti-obesity, antioxidant, and anti-inflammatory effects. The study aimed to investigate the potential benefit of P. edulis f. flavicarpa (PF) extract in preventing obesity-associated muscle atrophy and IR. The PF extract effectively inhibited cholesterol micelle solubility with an IC of 3431 µg/mL and decreased fat accumulation in 3T3-L1 adipocytes. Furthermore, this study investigated a model of HFD-induced IR and muscle atrophy in rats. Thirty-five male Sprague-Dawley (SD) rats were induced with obesity by HFD and were administered 250 and 500 mg/kg/day of PF extract. Rats fed with an HFD were associated with fat accumulation and oxidative stress, which promoted inflammation, muscle damage, muscle atrophy, and IR in obese rats. However, administration of PF extract effectively mitigated these effects. The PF extract decreased fat accumulation in white adipose tissues and gastrocnemius (GAS) muscle by inhibiting fat absorption and synthesis, particularly Cd36 and Hmgcr. The PF extract also notably reduced oxidative stress-induced muscle inflammation and damage via elevating nuclear factor erythroid 2-related factor 2 (Nrf2) and reducing nuclear factor kappa B (NF-κB) expressions. Additionally, PF extract was found to mechanistically prevent muscle atrophy by inhibiting Fbxo32, Trim63, and B-cell lymphoma 2 (BCL2)-associated X (Bax) expressions, while enhancing Bcl2 expression. We also found that PF extract mitigated muscle IR by upregulation of the insulin receptor substrate-1/phosphatidylinositol-3 kinase/protein kinase B (IRS-1/PI3K/AKT) pathway and Slc2a4 expression. The findings indicate that PF extract can prevent skeletal muscle loss and IR in obesity by modulating oxidative stress, inflammation, and activating IRS-1/PI3K/AKT signaling pathway. - Source: PubMed
Chobsuay NraratChonpathompikunlert PennapaSrivilai JukkarinMalakul WachirawadeeLimpeanchob NanteetipAimjongjun SathidTunsophon Sakara