DPP4
- Known as:
- DPP4
- Catalog number:
- 80040
- Product Quantity:
- 10 µg
- Category:
- -
- Supplier:
- BPS Bioscience
- Gene target:
- DPP4
Ask about this productRelated genes to: DPP4
- Gene:
- DPP4 NIH gene
- Name:
- dipeptidyl peptidase 4
- Previous symbol:
- CD26, ADCP2
- Synonyms:
- DPPIV
- Chromosome:
- 2q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-03-05
- Date modifiied:
- 2016-02-05
Related products to: DPP4
Related articles to: DPP4
- A receptive endometrium is essential for successful embryo implantation, yet its dynamic cellular and molecular features remain poorly understood due to limitations in current in vitro models. We aimed to establish a 3D co-culture endometrial model mimicking physiological conditions, characterizing its response to varied culture conditions using receptivity-associated gene expression profiling. Epithelial Ishikawa or RL95-2 cells were layered above stromal St-T1b cells separated by Matrigel and cultured in different media (growth factor-reduced, serum-containing standard, cytokine-supplemented and EGF-supplemented) or exposed to hormonal stimuli (E2, P4, cAMP) over a 10-day differentiation period. Our model effectively recapitulates the layered structure of the endometrium, as confirmed by scanning electron microscopy and immunofluorescence. Transcriptional analysis of fertility-associated markers revealed media- and cell line-dependent alterations of key receptivity markers; In standard media gene expression alterations occurred for HEY1 in both, but for HEY2 solely in the Ishikawa model and EDNRB only in the RL95-2 model, in cytokine-supplemented media for LIF and TAGLN in both models, while HPSE only in RL95-2 models and DPP4 and HEY1 only in Ishikawa models. Notably, the long-term hormonal treatment triggered a transcriptomic signature, especially in the RL95-2 model that closely correlates to the clinically determined one at the window of implantation (WOI). We conclude that our in vitro model reflects the phenotypic and transcriptional dynamics of the in vivo endometrium and responds distinctly to external stimuli. It serves as a robust platform to study endometrial receptivity mechanisms and holds potential for future applications in infertility and implantation research. - Source: PubMed
Publication date: 2026/09/23
Kyriakopoulou KonstantinaHeukamp Mariam AFranchi MarcoObermeyer UllaFuchs EvelinEspinoza-Sanchez NancyHellmold JohannaHanker LarsGötte MartinEl-Shorafa Heba M - Sitagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor commonly used to treat diabetes, has been linked to improved wound healing in diabetic patients. However, its direct effects on skin repair are not well understood and its underlying mechanisms remain unclear. This study investigated the concentration dependent effects of sitagliptin on HaCaT keratinocytes and primary fibroblasts in vitro and explored the molecular pathways involved. Sitagliptin enhanced keratinocyte migration at 150 μg/mL, without affecting proliferation, while no significant effects were observed on fibroblast proliferation and migration, indicating a cell-type specific response. Sitagliptin treatment induced morphological changes in HaCaT keratinocytes, including elongated actin filaments and increased cell surface area, consistent with cytoskeletal changes that support motility. Proteomic analysis revealed keratin remodeling (Keratin5 (KRT5), Keratin 16 (KRT16), Keratin 17 (KRT17) upregulation and Keratin6A (KRT6A) downregulation), increased Enkurin domain-containing protein 1 (ENKD1), Family with sequence similarity 83 member H (FAM83H) and epidermal growth factor receptor (EGFR), and reduced β-catenin (CTNNB1), suggesting cytoskeletal reorganization and reduced intercellular adhesion associated with enhanced keratinocyte migration. Targeted RT-qPCR validation confirmed these transcriptional changes and identified integrin β1 (ITGB1) as an induced network hub in the associated protein-protein interaction network. Overall, sitagliptin enhances keratinocyte migration in association with changes in cytoskeletal and cell-adhesion-related proteins, although a direct causal relationship between these molecular changes and enhanced migration remains to be established. These findings provide preliminary evidence that, beyond glycemic control, sitagliptin may have therapeutic potential for wound healing applications to accelerate skin repair and tissue regeneration. - Source: PubMed
Publication date: 2026/09/22
Sutnut PiyatidaNamviriyachote NantapornMuangman PornpromRoytrakul SittirukViravaidya-Pasuwat Kwanchanok - Selective elimination of senescent hepatocytes by DPP4-CAR-NK cells could rescue liver fibrosis; therefore improving liver function and metabolic homeostasis in CCl-induced liver fibrotic and naturally aged mice. - Source: PubMed
Publication date: 2026/07/01
Hua RuiXu KangPeng HuanLiu KundaLong NanZeng ChenyeWang YidaGuo YannanWang Zhao - Cannabis sativa, a medicinal plant rich in cannabinoids, terpenoids, and flavonoids, has been shown to have various pharmacological activities. This study investigated the antidiabetic potential of C. sativa inflorescence extracts using in vitro and computational models. Dried C. sativa inflorescences were extracted sequentially with hexane, dichloromethane, and methanol, before their metabolites were identified by GC-MS. The extracts were tested for α-amylase and α-glucosidase inhibition, glucose uptake activity, and antioxidant effects using DPPH and nitric oxide (NO) inhibition assays. Thirty-six metabolites were further docked against diabetes-related proteins. Among the extracts, the hexane extract showed the strongest bioactivity with notable α-amylase inhibition (IC: 727 µg/mL), DPPH free radical scavenging (IC: 478.62 µg/mL), and nitric oxide inhibition activity (IC: 356.51 µg/mL). Docking analyses revealed strong binding affinities for 8-hydroxy-delta-9-THC, cannabivarin, and 9-tetrahydrocannabinol with DPP-4, PTP1B, and other target proteins. These findings highlight the potential of C. sativa inflorescences as a source of antidiabetic agents, warranting further in vivo and clinical validation. - Source: PubMed
Chinheya Rosa MNgoungoure Viviane L NAli IbeabuchiOlofinsan KolawoleJim TseboTankeu FrancineMatsabisa Motlalepula G - - Source: PubMed
Publication date: 2026/09/19
Odic PierreNardi OlivierFoucault-Fruchard Laura