Smad2 (Phospho_Thr220) Antibody
- Known as:
- Smad2 (Phospho_Thr220) Antibody
- Catalog number:
- E011323-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- Smad2 (Phospho_Thr220) Antibody
Related genes to: Smad2 (Phospho_Thr220) Antibody
- 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
Related products to: Smad2 (Phospho_Thr220) Antibody
Related articles to: Smad2 (Phospho_Thr220) Antibody
- Exosomes play pivotal roles in immunomodulation, tissue regeneration, and the treatment of diseases. However, their specific mechanisms of action remain unclear. Therefore, this study aimed to elucidate the therapeutic mechanisms of human umbilical cord mesenchymal stem cell-derived exosomes (hUC-MSC-exosomes) in androgenic alopecia (AGA). We established a modified AGA mouse model and found that hUC-MSC-Exosomes could be taken up by dermal papilla cells (DPCs), promoted the transition of hair follicles from telogen to anagen, ameliorated hair follicle miniaturization, and enhanced hair regeneration and thickening. - Source: PubMed
Publication date: 2026/06/26
Chen QimeiWang XueerZhang YaruiLiang FengtingZhang HaoGuo ChenhuiHuang MianboYang JingjingWang XuanMiao YongZhang LinZhang Min - Salvia miltiorrhiza Bunge (SM), a traditional medicinal herb, demonstrates potential in treating pulmonary fibrosis (PF). Although preclinical studies suggest anti-fibrotic properties, its mechanisms remain unclear. This study elucidates the efficacy and molecular pathways of SM in pulmonary fibrosis. - Source: PubMed
Publication date: 2026/06/26
Xing ZhangNaifan DuanYan XueFeng ChenZiyi ZhouJiacheng LinWei Zhang - To investigate the protective effects of Rupr. polysaccharides (PAP), alkaloids, and flavonoids in alleviating diabetic kidney disease (DKD) and to elucidate the role of the PI3K/AKT/GSK-3β/Nrf2 signaling pathway. Active components were extracted and quantified. In vitro, high-glucose (HG)-induced human kidney-2 (HK-2) cells were used to screen the optimal fraction via CCK-8, reactive oxygen species (ROS), TdT-mediated dUTP Nick-End Labeling (TUNEL), and Western Blot (WB) assays. In vivo, a DKD rat model was established using 2% Streptozotocin (STZ) and a high-fat with high-sugar diet. Rats were treated with PAP and LY294002. Renal damage and signaling pathway proteins were evaluated using histological staining and WB. Among the tested components, PAP conferred the most pronounced cytoprotection against HG-induced injury in HK-2 cells. PAP significantly reduced glomerular damage, collagen deposition, and glycogen accumulation in the kidneys of DKD rats. Mechanistically, PAP activated the PI3K/AKT/GSK-3β/Nrf2 pathway, upregulating HO-1 and NQO1, while inhibiting the TGF-β1/Smad2 pathway and Bcl-2/Bax-mediated apoptosis. These protective effects were significantly attenuated by LY294002. Among the tested fractions under the present experimental conditions, PAP exhibited the most pronounced protective activity. These protective effects were partially mediated through the PI3K/AKT/GSK-3β/Nrf2 pathway, which enhanced antioxidant capacity while reducing fibrosis and apoptosis. - Source: PubMed
Publication date: 2026/06/22
Mei MeiSun HuaweiZhang KaiZhang FengSun ShiqingYu EnbinZhang Yu - Chronic kidney disease (CKD) remains a leading cause of premature mortality and global disease burden, yet the molecular mechanisms underlying its progression are still incompletely understood. Accumulating evidence highlights circadian disruption as an underappreciated driver of CKD that warrants systematic re-examination. The kidney harbors an autonomous circadian oscillator, principally regulated by the CLOCK:BMAL1 transcription factor complex, which coordinates glomerular filtration, tubular electrolyte handling, blood pressure rhythmicity, inflammatory tone, and cellular repair. In CKD, retained uremic toxins, sustained oxidative stress, and persistent NF-κB activation collectively suppress this clock machinery, generating a self-reinforcing cycle of renal injury and circadian dysregulation. CKD is also accompanied by progressive attenuation of nocturnal melatonin secretion, weakening a central hormonal cue for peripheral clock entrainment and cytoprotection. Melatonin acts both as a chronobiotic and as a pleiotropic cytoprotective molecule. Through MT1/MT2 receptors, the nuclear receptor RORα, and receptor-independent antioxidant pathways, it may enhance Nrf2/HO-1 signaling, restrain NF-κB and NLRP3 inflammasome activity, suppress TGF-β1/Smad2/3-mediated fibrogenesis, preserve mitochondrial integrity, and engage SIRT1-linked clock regulation. Current clinical studies suggest that nightly melatonin supplementation can improve sleep quality and selected oxidative or circadian surrogate endpoints in hemodialysis patients; however, whether melatonin slows CKD progression or preserves renal function remains unproven. This review synthesizes the molecular interface between circadian dysregulation and CKD progression and articulates a rationale for adequately powered clinical trials evaluating melatonin as a candidate chronotherapeutic adjunct rather than an established renoprotective therapy. - Source: PubMed
Publication date: 2026/06/18
Lu Kuo-ChengLu Chien-LinHou Yi-ChouHuang Yen-SungChang Yu-TienZheng Cai-MeiWu Chia-Chao - Sponge spicules have emerged as promising biomaterial scaffolds due to their biocompatibility and unique structural properties; however, achieving stable and bioactive functionalization remains a key challenge. The tripeptide GHK is known to promote collagen synthesis and wound repair, yet its therapeutic efficacy is often limited by rapid diffusion and instability. Here, we report ALTUM, a thiol-functionalized sponge spicule composite in which GHK is covalently conjugated via disulfide linkage to enable controlled and redox-responsive peptide delivery. ALTUM exhibited sustained GHK retention under physiological and storage conditions, while exposure to reduced glutathione (GSH) selectively accelerated peptide release through disulfide bond cleavage. This dual release behavior-long-term stability combined with reduction-triggered activation-distinguishes ALTUM from conventional delivery systems. The composite also demonstrated structural stability under thermal, cyclic, and photostability conditions. In an artificial human skin model, ALTUM enhanced dermal penetration of GHK and significantly increased collagen deposition in the dermal layer, demonstrating its capacity to promote collagen production within deeper skin tissue, compared to simple spicule-peptide mixtures. ALTUM was fabricated at an optimized spicule-to-peptide ratio of 3% (/), preserving the needle-shaped spicule morphology after surface modification. In vitro, ALTUM exhibited a sustained release profile, with GHK release markedly accelerated in the presence of 10 mM glutathione (GSH) compared with non-reductive conditions, reaching approximately 60% cumulative release over 35 days. In the bioprinted artificial human skin model, ALTUM delivered 9.72 ng/cm of GHK, more than five-fold higher than the physical mixture of spicules and free GHK (1.9 ng/cm), and significantly increased type I collagen expression in human dermal fibroblasts. Mechanistically, ALTUM-mediated delivery was associated with increased TGF-β expression and engagement of the SMAD signaling pathway, as indicated by increased phosphorylation of SMAD2/3, consistent with involvement of the TGF-β-SMAD axis in the observed collagen induction. Collectively, these findings establish ALTUM as a structurally stable, redox-responsive dermal delivery platform that enhances collagen synthesis and skin regeneration. - Source: PubMed
Publication date: 2026/06/21
Hong Won-KyuHuang Patrick Po-HanDuncan DianeMarco RochaChoi Ho-SungJo Young-Wook