GDF5, human recombinant
- Known as:
- GDF5, H. sapiens Rec.
- Catalog number:
- bp-024
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- GDF5 human recombinant
Related genes to: GDF5, human recombinant
- Gene:
- GDF5 NIH gene
- Name:
- growth differentiation factor 5
- Previous symbol:
- -
- Synonyms:
- CDMP1, BMP14
- Chromosome:
- 20q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-05
- Date modifiied:
- 2016-10-05
Related products to: GDF5, human recombinant
Related articles to: GDF5, human recombinant
- Bone regeneration assisted by synthetic bone substitutes largely depends on the integration of the vascular, neural, and lymphatic systems in the bone. Bone marrow mesenchymal stem cells (BMSCs) are the key cells for this process. However, their role in regulating the integration has not been fully characterized. - Source: PubMed
Publication date: 2026/06/15
Zhang NanLuo YuwenLuo PengCao JiaruiCheng YuningKang MengyaoMao JianpingNie Jing-JunChen Da-Fu - Synovial joints are complex organs composed of specialized tissues whose coordinated formation is essential for proper joint function. The cellular composition and regulatory programs governing late synovial joint development are less well characterized as compared to earlier stages of joint development. Here, we generated single-cell transcriptomic data of Growth differentiation factor 5 (Gdf5)-lineage cells from the embryonic mouse knee joint at embryonic day 17.5 and integrated these data with those from earlier developmental stages to infer transcriptional state progression across joint development. We identified nine distinct Gdf5-lineage populations corresponding to major joint tissues, including articular chondrocytes, superficial lining cells, ligament-tenogenic progenitors, synovial fibroblasts, and progenitor populations, and we validated their localization within the embryonic joint. We found a meniscus-associated progenitor state characterized by low expression of canonical chondrocyte markers and high expression of pleiotrophin (Ptn), distinguishing it from conventional articular chondrocytes. In addition, we found that Col22a1 and tetraspanin 15 (Tspan15) mark a transcriptionally and spatially distinct superficial lining cell population. To identify potential regulatory mechanisms underlying articular chondrocyte development, we reconstructed dynamic gene regulatory networks along the progenitor-to-chondrocyte trajectory, revealing a transition from a common regulatory state to cell type-specific regulatory program at later stages. In summary, our study provides data that improves our understanding of the developmental transcriptional programs that contribute to the major tissues of the synovial joint. - Source: PubMed
Publication date: 2026/06/04
Yea Ji-HyeBian QinCheng Yu-HaoSu Emily YTan YuqiKim Dong WonWang HongYoo SooyeonBlackshaw SethCahan Patrick - The diamond concept, originally articulated for bone fracture healing, defines five essential and interdependent elements for successful repair: growth factors, an osteoconductive scaffold, mesenchymal progenitor cells, an optimal mechanical environment, and adequate vascularisation. Tendons and ligaments are dense, hypovascular collagenous tissues with limited intrinsic regenerative capacity. When injured, they heal by biomechanically inferior fibrotic scarring rather than by regeneration. No unifying biological framework currently exists to guide the development of biological augmentation strategies for soft tissue repair. - Source: PubMed
Publication date: 2026/05/19
Maffulli NicolaGiannoudis Peter - Laryngotracheal fibrosis is a rare but severe complication of prolonged intubation, leading to airway narrowing, respiratory distress, dysphonia, and, in advanced cases, life-threatening airway obstruction. Current treatments are primarily surgical, while pharmacologic approaches such as mitomycin C, corticosteroids, or 5-fluorouracil show inconsistent efficacy and potential toxicity. Thus, there remains a critical need for safe and effective antifibrotic therapies. Transforming growth factor-beta (TGF-β) is a key mediator of fibrosis, promoting fibroblast activation, migration, and expression of profibrotic markers such as alpha-smooth muscle actin (α-SMA). - Source: PubMed
Publication date: 2026/05/09
Toth EnikoSzabo KittiVegh Attila GergelyZvara AgnesPuskas Laszlo GBach AdamMigh EdeHorvath PeterTiszlavicz LaszloRovo LaszloKeller-Pinter Aniko - Intervertebral disc degeneration is associated with loss of nucleus pulposus (NP) cell phenotype and extracellular matrix, both processes linked to changes in cytoskeletal contractility and cell shape. Here, we tested whether microenvironment-specific modulation of RhoA signaling can restore NP-like morphology and gene expression in NP cells cultured in 2D and in 3D alginate. In 2D monolayer culture, where cells are spread and mechanically activated, pharmacologic inhibition of RhoA with CT04 reduced RhoA activity, decreased actomyosin contractility gene expression, and shifted morphology toward a smaller, more circular phenotype. Bulk RNA sequencing showed that CT04 treatment increased expression of NP phenotypic and matrix-related genes including , , , and while decreasing expression of catabolic and fibroblast-associated genes including and , consistent with enrichment of extracellular matrix pathways. In contrast, RhoA activation with CN03 in 2D culture increased actin and phosphorylated myosin light chain intensity but produced limited phenotypic improvement. In 3D alginate, which minimizes integrin-mediated adhesion, baseline actomyosin markers were reduced relative to 2D culture. In alginate, RhoA activation with CN03 increased the amount of actin, phosphorylated myosin light chain, and actomyosin gene expression, yet also promoted a more compact, circular morphology and increased NP markers, including and with repeated dosing. Across culture conditions, increased cell roundness was consistently associated with increased expression, indicating strong coupling between cytoskeletal state, morphology, and NP matrix programs. Together, these findings demonstrate that RhoA pathway perturbation can promote NP phenotypic gene expression in both 2D and 3D culture, but the direction of optimal modulation depends on the microenvironment, supporting RhoA signaling as a context-dependent therapeutic target for disc regeneration. - Source: PubMed
Publication date: 2026/04/07
Bond GabriellaKim Min Kyu MLisiewski LaurenJacobsen TimothyChahine Nadeen