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
- - Source: PubMed
Publication date: 2026/09/21
Tian ZhenfengTan YingLin XingyiSu MingxinPan LeleLin LijunOu GuangshengChen Yinting - Albuminuria reflects renal and cardiovascular damage in type 2 diabetes (T2D), but its association is not fully understood. We evaluated the association of macroalbuminuria with cardiac structure and function. - Source: PubMed
Publication date: 2026/09/21
Olloquiegui Xabier IrazustaAndueza Saioa EcheverriaIzco Marina PascualSalinas Gonzalo Luis AlonsoLorente Loreto FernándezAlbéniz Susana RavassaSolis-Barquero Sergio MAramendía-Vidaurreta VerónicaMora-Gutiérrez José MaríaOrbe JosuneFernández-Seara Maria AGarcía-Fernández Nuria - Metabolic dysfunction-associated steatohepatitis (MASH), a progressive form of metabolic dysfunction-associated steatotic liver disease, is characterized by hepatocellular injury, chronic inflammation, and fibrosis, yet effective antifibrotic therapies remain limited. The urotensin II (UII)/urotensin II receptor (UTR) system has been implicated in injury and tissue remodeling in several chronic liver conditions, but its role in MASH remains unclear. We examined KR-36996, an orally active UTR antagonist, in a methionine- and choline-deficient (MCD) diet-induced mouse model of fibrosing steatohepatitis. Male C57BL/6 mice were fed the MCD diet for 4 weeks and treated orally with KR-36996 at 30 mg/kg/day. Liver injury, steatosis, inflammation, fibrosis, hepatic UII/UTR expression, and MAPK signaling were assessed by serum biochemistry, histology, immunohistochemistry, RT-qPCR, and Western blotting. KR-36996 reduced serum alanine aminotransferase and aspartate aminotransferase levels and attenuated hepatic inflammation, with fewer inflammatory foci, reduced F4/80-positive macrophage accumulation, and lower Il1b, Ccl2, and Tnf expression. It also decreased collagen deposition, α-smooth muscle actin immunoreactivity, and the fibrogenic markers Col1a1 and Timp1. MCD feeding increased hepatic UII and UTR protein levels and enhanced JNK phosphorylation; KR-36996 reduced JNK phosphorylation, whereas ERK and p38 phosphorylation remained unchanged. These findings indicate that UTR antagonism primarily attenuates inflammatory and fibrogenic responses, whereas evidence for an antisteatotic effect was limited in this model, and support further evaluation of the UII/UTR axis as a potential therapeutic target for the inflammatory and fibrotic components of steatohepatitis. - Source: PubMed
Publication date: 2026/09/17
Han Ye SolLee Seung HyeongLee Seo YoungLee Kyeong EunOh Kwang-SeokLee Byung HoLee Jeong Hyun - MGAT5-mediated N-glycosylation plays a central role in tumor progression and metastasis by affecting proteins involved in tumor cell behavior. One relevant target is Tissue inhibitor of metalloproteases 1 (TIMP1), which, beyond its classical role as a metalloproteinase inhibitor, promotes oncogenic signaling through interactions with CD63 and β1-integrins. Emerging evidence suggests that aberrant TIMP1 N-glycosylation may regulate these diverse functions. Here, we investigated the role of MGAT5 in melanoma cell behavior and how MGAT5-mediated aberrant N-glycosylation influences TIMP1 function, including its activity as a signaling molecule and as an inhibitor of metalloproteinases. We performed Mgat5 knockout using CRISPR/Cas9 in metastatic melanoma cells to understand the role of MGAT5 in cell proliferation, migration, invasion, and tumor growth. Through site-directed mutagenesis, we generated melanoma cells expressing aglycosylated TIMP1 and evaluated the effect of N-glycosylation on TIMP1 function, including its role as a signaling molecule, by co-immunoprecipitation and anoikis resistance assays, and as an inhibitor of metalloproteinases, by zymography. We demonstrated that Mgat5 knockout reduced metastatic melanoma cell proliferation, migration, invasion, and tumor growth, TIMP1 is a target of MGAT5 in metastatic melanoma cells, and aberrant glycosylation of TIMP1 favors its interaction with CD63/β1-integrins and cell survival while decreasing its ability to inhibit metalloproteases (MMPs). Therefore, MGAT5 plays a pro-tumor role in metastatic melanoma cells and the aberrant glycoform of TIMP1 directs its function as a signaling molecule, orchestrating the pleiotropic functions of TIMP1. - Source: PubMed
Publication date: 2026/09/17
Justo Beatriz LaísLengert André van HelvoortHan Sang WonJasiulionis Miriam Galvonas - Acute full‑thickness skin wounds represent a significant clinical challenge due to tissue loss, risk of bacterial contamination, and the need for rapid and effective regeneration. Injectable thermosensitive hydrogels incorporating antibacterial nanomaterials represent a promising strategy for advanced wound care. In this study, a multifunctional hydrogel composed of Graphene oxide (GO), branched polyethyleneimine (BPEI), and silver nanoparticles (AgNPs) dispersed in Pluronic F127 was developed and evaluated for wound healing applications. The GO-BPEI-AgNP nanocomposite was synthesized via amidation and microwave-assisted methods and characterized using DLS, UV-vis, FTIR, XRD, and SEM-EDX analyses. Biocompatibility was assessed in HaCaT keratinocytes using the Alamar Blue assay, while scratch assays and antibacterial activity against. In vivo wound healing efficacy and histopathological changes were evaluated in a rat full-thickness skin wound model, together with qRT-PCR analysis of wound-healing-related genes. The hydrogel exhibited favorable injectability, nanoscale morphology, and high biocompatibility (IC: 246.7 µg/mL). It significantly enhanced keratinocyte migration and demonstrated antibacterial activity. In vivo findings revealed accelerated wound closure, enhanced epidermal regeneration, and modulation of PDGFA, VEGFC, COL1A1, TIMP1, and MMP9 expression. Collectively, the GO‑BPEI‑AgNP hydrogel shows strong potential as an injectable antibacterial biomaterial for acute full‑thickness wound repair, with potential relevance to infection‑associated wound environments. - Source: PubMed
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