Smad2 ELISA Kit with Nuclear Extraction Kit
- Known as:
- Smad2 Enzyme-linked immunosorbent assay test Kit Nuclear Extraction Kit
- Catalog number:
- EK1601
- Product Quantity:
- Kit
- Category:
- Peptides
- Supplier:
- Panomics
- Gene target:
- Smad2 ELISA Kit with Nuclear Extraction
Related genes to: Smad2 ELISA Kit with Nuclear Extraction Kit
- Gene:
- SMAD2 NIH gene
- Name:
- SMAD family member 2
- Previous symbol:
- MADH2
- Synonyms:
- MADR2, JV18-1
- Chromosome:
- 18q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-15
- Date modifiied:
- 2016-10-05
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- Radiotherapy is one of the principal modalities for cancer treatment. However, its efficacy is often limited by a complex interplay of various factors, including high level antioxidant in tumor cells, efficient DNA damage repair capabilities, serious tumor tissue fibrosis and consequent hypoxia, etc. Hence, it represents a critical challenge for enhancing radiotherapy efficacy and reducing side effects to develop a radiosensitizer that can specifically work to the tumor while simultaneously incorporating multiple sensitization effects. Herein, a tumor in situ self-assembling gold nanorods (GNRs) system is developed to specifically form aggregates within tumor cells, resulting in a photothermal-enhanced radiotherapy via multilevel radiosensitization mechanisms. At the molecular level, the GNRs nanoagents suppress the transcription of radioresistance-associated genes under the control of the TGF-β signaling pathway by inhibiting TGF-β/Smad2/3 activation. Simultaneously, by downregulating key DNA repair proteins, the nanoagents compromise the ability of tumor cells to repair DNA damage induced by radiation. At the cellular level, the GNRs nanoagents induce cell cycle arrest at the G2/M phase, thereby sensitizing tumor cells to radiative energy. At the tissue level, under photothermal-enhanced ionizing radiation, the GNRs nanoagents reduce the activation of cancer-associated fibroblasts and facilitate the degradation of major extracellular matrix (ECM) components including collagen I and fibronectin. The remodeling of the ECM alleviates the hypoxic tumor microenvironment and, consequently, overcomes the associated radiotherapy resistance. This work reports a multifunctional radiosensitization platforms with systemic and multilevel synergistic mechanisms, providing an attractive paradigm for efficient cancer radiotherapy and facilitating combination therapy. STATEMENT OF SIGNIFICANCE: Radiotherapy is one of the principal modalities for cancer treatment, but its efficacy is often hindered by a protective "cell-microenvironment alliance." This network involves tumor antioxidant molecules, efficient DNA repair, a fibrotic and hypoxic tumor microenvironment (TME). Existing studies largely target tumor cells or the TME separately, neglecting their interaction and combined modulation. In this study, we developed a tumor in situ self-assembling gold nanorods system that employed a synergistic modulation strategy to simultaneously enhance the intrinsic radiosensitivity of tumor cells and modulate the radioresistant microenvironment, thereby achieving complementary mechanisms to improve radiotherapy efficacy. This system offers a comprehensive, clinically translatable strategy for a new generation of intelligent, multifunctional radiosensitization platforms. - Source: PubMed
Publication date: 2026/04/19
Liu LeHou XiaoxueChen JingGui HanLiu JinjianZhang TenglongXiao MengHuang FanLiu Jianfeng - This study demonstrates that lactate promotes M2-like macrophage polarization by activating the TGF-β/SNAIL signaling axis, thereby weakening CD8 T cell-mediated antitumor immunity and promoting breast cancer progression. In vitro experiments using bone marrow-derived macrophages (BMDMs) and THP-1 cells treated with 25 mM lactate revealed a marked increase in M2 markers (CD206, Arg-1, IL-10) and a reduction in M1 markers (iNOS, TNF-α, IL-12), confirmed by Western blotting and flow cytometry. RNA-Seq analysis identified TGF-β/SNAIL pathway activation, with increased TGFBR1/2 expression, Smad2/3 phosphorylation, and PI3K/AKT pathway enrichment. Functional studies revealed that lactate-polarized M2 macrophages impaired CD8 T cell cytotoxicity (reduced IFN-γ, GzmB, PRF1; elevated PD-1, Tim-3) and disrupted mitochondrial metabolism. In vivo validation using a breast cancer xenograft model showed that lactate treatment increased tumor growth and angiogenesis (VEGF/CD31), while TGF-β inhibition (SB431542) reversed these effects. Mechanistically, lactate-induced TGF-β/SNAIL signaling promoted EMT in cancer cells and created an immunosuppressive TME. These findings establish lactate as a critical metabolic regulator that coordinates macrophage polarization and T cell exhaustion through the TGF-β/SNAIL axis, highlighting this pathway as a promising therapeutic target for breast cancer immunotherapy. - Source: PubMed
Zhu PeilingTian ZhishengWang YingLiao HaiyingMi Zehui - Cartilage tissue engineering requires biomaterials that can effectively maintain the tissue-specific functions of chondrocytes to enable the restoration of cartilage structure and function. Decellularised extracellular matrix (dECM)-derived hydrogels serve as tissue-specific biomaterials capable of preserving native biochemical cues and maintaining physiological chondrocyte phenotype in three-dimensional culture. However, their sol-gel transition relies heavily on collagen fibrillogenesis, a slow and poorly controllable process that limits mechanical tunability and suffers from inter-batch variability. Therefore, further efforts are required to functionalise cartilage dECM to achieve reproducible and controllable physicochemical properties. Here, we present a light-activated cartilage dECM hydrogel system based on ruthenium/sodium persulfate (Ru/SPS)-mediated dityrosine crosslinking, enabling rapid hydrogel formation under visible light irradiation while providing tunable mechanical properties and improved biological functionality. Comparison of the decellularisation protocols indicated that Triton X-100 combined with ammonium hydroxide efficiently eliminated residual DNA while preserving a substantial proportion of the native cartilage proteome. Pepsin-solubilised cartilage dECM hydrogels formed via dityrosine-based photo-crosslinking exhibited rapid gelation behaviour and superior mechanical characteristics compared to conventional thermally gelled dECM. The photo-crosslinked dECM hydrogels were cytocompatible, supported human bone marrow-derived mesenchymal stem cells (hBMSCs), and favoured cartilage-specific phenotypes, as demonstrated by chondrogenic genes upregulation, including COL2A1 and ACAN, compared with gelatin methacrylate (GelMA) hydrogels. Importantly, this photo-crosslinking strategy overcomes the incompatibility between oxygen-sensitive redox-based photochemistry and hypoxic culture conditions, enabling the incorporation of oxygen-scavenging microcapsules to establish low-oxygen microenvironments. Under hypoxia, the cartilage dECM hydrogels promoted a more articular-like phenotype in hBMSC-derived chondrocytes, with transcriptomic features associated with TGF-β/SMAD2/3 and IGF-1/2-IGF-1R signalling. Collectively, these findings establish photo-crosslinked cartilage dECM hydrogels as a biomaterial platform with tunable mechanical properties and favourable biological functionality for cartilage tissue bioengineering and biomimetic in vitro cartilage models. - Source: PubMed
Publication date: 2026/04/20
Li LinOng Louis Jun YeLim Khoon SKaluthara Liyanage Chamikara DushmanthaQu YunkunWen JingyiWilliams CaitlinMolley Thomas GBarrero Roberto AWakale ShitalCrawford RossKilian KristopherToh Yi-ChinPrasadam Indira - Glioblastoma (GBM), a rare, highly aggressive and chemoresistant brain cancer, exhibits profound metabolic plasticity that relies, in part, on aberrant transforming growth factor-β (TGF-β) signaling. Such plasticity was recently associated with TGF-β-regulated apoptosis and autophagy. Here, we questioned whether TGF-β-regulated apoptotic/autophagic phenotypes are recapitulated in a preclinical in vitro 3D spheroid culture model of human U87 GBM-derived cells, and how metabolic alterations affect such phenotypes. - Source: PubMed
Publication date: 2026/03/30
Payet-Desruisseaux MaellisZgheib AlainDanalache Bogdan AlexandruDesjarlais MichelAnnabi Borhane - Platelet-rich plasma (PRP) has been found effective in wound healing, yet the underlying mechanisms in the healing of diabetic wounds remain unclear. In this study, we focus on investigating the role of PRP in enhancing the wound healing in a diabetic mouse model, specially through the modulation of the PI3K/AKT signaling pathway and its effect on collagen production and angiogenesis in the wounds of diabetic mouse model. In our in vitro experiments, we observed that PRP, in a concentration-dependent manner, significantly stimulated the proliferation, migration, and collagen synthesis in human dermal fibroblasts. Concurrently, PRP activated the PI3K/AKT and TGF-β/SMAD2 signaling pathways. In vivo, utilizing a diabetic mouse model of wound healing, PRP treatment significantly enhanced wound healing by accelerating wound closure, improving collagen deposition and organization, and promoting angiogenesis, as evidenced by increased expression of CD31 and VEGF. Importantly, the application of the PI3K inhibitor LY294002 effectively inhibited the observed effects of PRP. Additionally, the activation of the TGF-β/SMAD2 signaling pathway induced by PRP was also suppressed when PI3K was inhibited, suggesting that the PI3K/AKT pathway functions upstream to regulate TGF-β/SMAD2 signaling. These findings elucidate the role of PRP in facilitating diabetic wound healing through the activation of the PI3K/AKT pathway, which subsequently cross-regulates TGF-β/SMAD2 signaling, thereby enhancing cellular functions vital for tissue regeneration. Our results contribute valuable mechanistic insights into the therapeutic potential of PRP in addressing impaired wound healing in diabetic patients. - Source: PubMed
Liu HongyanHuang WenzhenJiang ShutingYan BeizhanKong CunquanZhu WeiyanXie QiCui Cuiyun