TIMP 2
- Known as:
- TIMP 2
- Catalog number:
- 30112002
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- BioTeZ
- Gene target:
- TIMP 2
Related genes to: TIMP 2
- Gene:
- TIMP1 NIH gene
- Name:
- TIMP metallopeptidase inhibitor 1
- Previous symbol:
- TIMP, CLGI
- Synonyms:
- EPO
- Chromosome:
- Xp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2017-07-26
Related products to: TIMP 2
102D1 TIMP-13A4 TIMP-2Anserine tissue inhibitors of metalloproteinase 3,TIMP-3ELISA KitAnserine anti - tissue inhibitors of metalloproteinase 3,TIMP-3ELISA KitAnti- TIMP-2 AntibodyAnti-Human TIMP-1Anti-Human TIMP-1Anti-Human TIMP-1Anti-human TIMP-1 (MAB), Source: Monoclonal Murine, MABAnti-human TIMP-1, bt, Source: Polyclonal bt. Rabbit, PABAnti-human TIMP-1, bt, Source: Polyclonal bt. Rabbit, PABAnti-human TIMP-1, bt, Source: Polyclonal bt. Rabbit, PABAnti-human TIMP-1, Source: Polyclonal Rabbit, PABAnti-human TIMP-1, Source: Polyclonal Rabbit, PABAnti-human TIMP-1, Source: Polyclonal Rabbit, PAB Related articles to: TIMP 2
- Congestive splenomegaly (SM)secondary to portal hypertension refers to pathologicalsplenic enlargementcaused byelevatedportal venous pressure; however, the molecular mechanisms underlying splenic fibrosis remain incompletely understood. - Source: PubMed
Publication date: 2026/09/28
Bo ZhaoLi JingtongZhang HongliangLu JiaqiZhong YuxuChu HaiboXu YongboLiu Tao - Diabetic Foot Ulcer (DFU), a severe chronic diabetes complication with low healing and high recurrence rates, is a major global health challenge. Overexpression of matrix metalloproteinase-9 (MMP-9) and the consequent MMP-9/TIMP1 (tissue inhibitor of metalloproteinase 1) imbalance delays healing by degrading the extracellular matrix, impairing granulation tissue formation, and exacerbating inflammation. Conventional therapies do not dynamically respond to fluctuating protease levels in chronic wounds. This study introduces an MMP-9-responsive protein release system (M9RR), where the therapeutic protein (i.e., TIMP1) is linked to a membrane-anchoring domain at its C-terminus via an MMP-9-cleavable peptide, thereby exposing the fusion protein to the extracellular side of cell membranes. The system enables targeted release of TIMP1 in high-MMP-9 microenvironments, thereby neutralizing excessive MMP-9 activity. In vitro, M9RR demonstrates MMP-9 specificity, broad mammalian cell applicability, and protection of HaCaT keratinocytes and BJ fibroblasts from MMP-9-induced damage. In db/db diabetic mice, the MMP-9-responsive TIMP1 release system (TIMP1) significantly improves wound contraction, granulation tissue formation, epithelial regeneration, and collagen remodeling. Additionally, a cryomicroneedle (CryoMNs)-based co-delivery system for basic fibroblast growth factor (bFGF) and TIMP1 shows effective diabetic wound healing. This modular M9RR system offers a precise, adaptive therapeutic strategy for DFU and holds promise for other MMP-related diseases. - Source: PubMed
Publication date: 2026/09/27
Zhang YuanDeng JianiCheung Man YeeFu TingtingQi XufengCai DongqingSun JianminLu GangShi PengChan Wai-YeeLi XuZhao Hui - Platelets are key components of the tumor microenvironment that contribute to colorectal cancer (CRC) progression. However, effective platelet-related prognostic tools for CRC risk stratification and prognostic assessment are lacking. Therefore, we aimed to develop a platelet-related prognostic model to improve risk stratification and prognostic evaluation. A tumor-cell-expressed platelet-related transcriptional signature, termed platelet-related risk score (PLRS), was established using LASSO and Cox regression based on TCGA-COADREAD, GSE39582 and GSE183635. After strict screening for intact survival information, 573, 531 and 85 tumor samples were retained correspondingly. Patients were stratified into high- and low-PLRS groups according to the median cutoff value of PLRS derived from the training cohort. A single-cell dataset GSE178341 was utilized for single-cell transcriptomic validation. All analyses were performed in R. Wilcoxon test, Kaplan-Meier method, log-rank test, multivariate Cox regression and ROC curves were applied with two-sided < 0.05. qRT-PCR was conducted for hub gene validation. The PLRS model involved six prognostic genes (, , , , , and ). The high- and low-PLRS groups showed significant differences in disease stage and survival in TCGA datasets, which was confirmed in the GEO dataset (GSE39582). The multivariate analysis established the PLRS as an independent prognostic factor. Single-cell analyses revealed distinct transcriptional trajectories, immune microenvironments, and communication patterns between the PLRS groups. Stromal, immune, and ESTIMATE scores positively correlated with PLRS, whereas tumor purity was inversely correlated. Exploratory drug sensitivity analysis using GDSC and CCLE cell line datasets suggested potential associations between PLRS and multiple therapeutic agents, warranting validation in clinical cohorts. qRT-PCR in RKO cells compared with the CCD-18Co fibroblast control partially confirmed the expression trends of four PLRS genes (, , , and ), whereas showed no significant difference and was not tested due to primer-design failure. Validation in normal colonic epithelial cells is warranted. The PLRS model demonstrated statistically significant prognostic value and may serve as a complementary tool for CRC risk stratification, providing a basis for further investigation into platelet-related transcriptional programs. - Source: PubMed
Publication date: 2026/09/18
Xie YunLi JunYan ZuweiZhang Wenguang - : While live-cell therapies face significant translational hurdles, cell-free secretomes derived from fetal progenitor cells offer a unique, scalable approach natively programmed for scarless tissue repair. : This GLP-compliant study evaluated the therapeutic efficacy spectrum of an off-the-shelf, clinical-grade, intratracheal lyophilized FE002-Lu lung fibroblast conditioned medium (LFCM) across five controlled Wistar rat models of induced lung injury: bleomycin (5 mg/kg), asbestos (100 µg/rat), hyperoxia (100% oxygen exposure), silica (30 mg/rat), and lipopolysaccharide (LPS, 4 mg/kg). Following lung injury induction and symptom onset, symptomatic rats were randomized to receive intratracheal LFCM (low, mid, or high dose) or a vehicle control every 4 days for 28 days. : The intervention demonstrated an exceptional safety profile, maintaining 100% survival with no severe procedural toxicity across all cohorts. Across all study arms, LFCM effectively attenuated pulmonary inflammation, reducing pro-inflammatory markers (IL-1β, IL-6, TNF-α, and CINC-1) in bronchoalveolar lavage fluid. Concurrently, high LFCM doses consistently elevated the anti-inflammatory cytokine IL-10. Within the lung tissue, mid- and high doses significantly reduced key pro-fibrotic drivers, including TGF-β1, TIMP-1, WISP-1, and hydroxyproline. Treatments consistently decreased α-SMA expression and pro-fibrotic gene mRNA levels, mitigating pulmonary myofibroblast activation. This correlated with reduced Ashcroft scores and collagen deposition, thereby preserving lung architecture. Notably, the FE002-Lu LFCM treatment exerted a biphasic regulation of extracellular matrix turnover: it elevated Cathepsin-D and MMP-12 in the bleomycin arm to actively clear newly deposited fibrotic debris, while reducing these markers in the hyperoxia and LPS arms to prevent acute collateral degradation of the native lung matrix. In both particulate models (asbestos and silica), the LFCM mid-dose established an optimal therapeutic threshold, avoiding the localized secretome saturation and pro-fibrotic exacerbation occasionally observed at higher doses. : Lyophilized FE002-Lu LFCM acts as a potent, pleiotropic biologic that effectively resolves acute pulmonary inflammation and arrests progressive fibrotic remodeling across multiple distinct in vivo models. By overcoming the cold-chain and delivery limitations inherent to pulmonary live-cell therapies, this stable, cell-free secretome represents a highly scalable, "off-the-shelf" candidate poised for non-invasive, aerosolized clinical translation. - Source: PubMed
Publication date: 2026/08/24
Applegate Lee AnnPorcello AlexandreLaurent Alexis E - Synovial fluid biomarkers reflect the intra-articular response to an anterior cruciate ligament (ACL) rupture and may provide insight into biological processes associated with posttraumatic joint degeneration. While increasing age has been associated with inferior clinical outcomes after ACL reconstruction, age-dependent differences in biomarker expression and their relationship to longer term outcomes remain unclear. - Source: PubMed
Publication date: 2026/09/24
Ehlers MalloryKurtz Jessica LMontgomery Samuel RKaplan Daniel JStrauss Eric J