Ask about this productRelated genes to: TIMP2 antibody
- Gene:
- TIMP2 NIH gene
- Name:
- TIMP metallopeptidase inhibitor 2
- Previous symbol:
- -
- Synonyms:
- CSC-21K
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-18
- Date modifiied:
- 2016-10-05
Related products to: TIMP2 antibody
Related articles to: TIMP2 antibody
- Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation and aberrant immune responses. Puerarin (PUE), a natural isoflavone from , exhibits multiple pharmacological activities, but its role in psoriasis remains unclear. The M5-induced HaCaT cell model was used to evaluate the effects of PUE on proliferation, apoptosis, and inflammation. Cell viability, proliferation, and apoptosis were assessed by CCK-8, EdU, and flow cytometry, while cytokine levels were measured by ELISA. TIMP2 and endoplasmic reticulum (ER) stress-related proteins were detected by RT-qPCR and Western blot. A TIMP2 overexpression assay was performed to verify the mechanism. PUE showed no cytotoxicity in HaCaT cells, but significantly inhibited M5-induced proliferation and inflammatory cytokine release while promoting apoptosis. Mechanistically, PUE reduced the expression of TIMP2 and ERS-related proteins, and TIMP2 overexpression partially reversed these effects. PUE alleviates proliferation and inflammation of keratinocytes in association with downregulation of TIMP2 and inhibition of ER stress-related markers, suggesting that the TIMP2-ERS axis may be implicated as a potential therapeutic target in psoriasis. - Source: PubMed
Publication date: 2026/05/09
Wang QingXia Jie - Contrast-induced acute kidney injury (CI-AKI) remains a concern in patients with ST-elevation myocardial infarction (STEMI) undergoing emergent percutaneous coronary intervention (PCI), but creatinine-based CI-AKI definitions incompletely capture longer-term renal trajectories. Early tubular stress biomarkers such as tissue inhibitor of metalloproteinases-2 (TIMP-2) may provide incremental risk information beyond conventional functional markers. - Source: PubMed
Publication date: 2026/05/06
Mugazov MirasSaparov EldarVassilyev DmitriyOgizbayeva AlinaVassilyeva NatalyaOmertayeva Dinara - Bone pathologies, such as osteoporosis, are characterized by excessive activity of osteoclasts (OCs)-bone-resorbing cells. As a therapeutic strategy to modulate this activity, we designed a chimera molecule that simultaneously inhibits two key regulators of OC function, matrix metalloproteinase 9 (MMP9) and CD44. The novel fusion molecule, designated C9-PEX, where C9 is a variant of tissue inhibitor of matrix metalloproteinase 2 (N-TIMP2) and PEX is the hemopexin domain in MMP9, exhibits strong binding affinity for CD44 and effectively inhibits the activity of the MMP9 catalytic domain, with an apparent low-picomolar K under our fluorogenic assay conditions. In addition, cell-binding assays showed enhanced binding of C9-PEX vs. comparative control proteins, C9 and Ala-C9-PEX. In murine bone marrow-derived OC cultures, gelatin zymography showed that C9-PEX significantly inhibited OC-secreted MMP9, whereas OC differentiation and bone-slice resorption assays showed reduced OC differentiation and reduced OC-mediated bone resorption without detectable toxic effects on cell proliferation and survival. At matched nominal concentrations, C9-PEX consistently outperformed the comparative control proteins and a 1:1 C9 +PEX mixture, supporting a functional advantage of simultaneous target engagement within a single fusion format. Although binding-site/valency-equivalent dosing, formal combination quantification, and normalization of resorption area to OC number on bone slices were not applied in the present study, these findings support C9-PEX as a promising multi-specific inhibitor of OC-mediated resorption in a murine in vitro system. Future studies using human OCs and in vivo models will be required to define the translational efficacy of C9-PEX and the exposure levels required for therapeutic activity. - Source: PubMed
Publication date: 2026/05/05
Pasternak DanOhayon ShaniLevaot NoamPapo Niv - The Six1 (SIX homeobox 1) gene is pivotal in renal and pulmonary development and differentiation. Its dysregulation is implicated in oncogenesis and tumor progression via enhancing cell proliferation and delaying senescence. However, whether or how it functions in the natural aging have not been investigated. To answer this question, we generated Six1 gene knockout mice using CRISPR-Cas9 technology. All Six1 biallelic knockout mice died at birth since the underdeveloped lungs. In Six1 mice, the developmental deficiencies in kidneys with vacuolar degeneration and epithelial disruption in renal tubules, as well as hematopoietic interstitial infiltration and lungs with interstitial condensation and alveolar hypoplasia were observed. These developmental deficiencies persist with age and age-dependent phenotypes become more pronounced in Six1 mice compared to the wild-type, with upregulation of senescence markers (p16, p53) and senescence-associated secreted factors (e.g., TNF-α, TIMP-2), increased α-SMA expression and collagen deposition, as well as susceptibility to pulmonary fibrosis. Transcriptomic sequencing coupled with bioinformatics analysis indicated that genes with altered expression in Six1 mouse lungs showed enrichment in pathways associated with senescence, including the NF-κB and TNF signaling pathways. These transcriptional patterns were also associated with gene sets involved in mitochondrial metabolic processes. Collectively, these findings suggest that Six1 haploinsufficiency is associated with transcriptional signatures linked to aging-related pathways under physiological conditions in mice, providing potential clues for future studies exploring mechanisms of aging. - Source: PubMed
Publication date: 2026/05/06
Guo TianxuLiu HanMa JunjunYan HuanyuChen YanglinZhao LihuaGuo XiyunLv LiminWang YixiCheng LinxinYang GuangZhang YuYu JinboWang XiDuo ShuguangLi XiheLi Rongfeng - Pediatric acute kidney injury (AKI) often presents insidiously and progresses rapidly. Traditional diagnostic criteria based on serum creatinine and urine output are markedly delayed and insufficient to capture injury patterns across different etiologies. This paper aims to summarize recent advances in pediatric AKI biomarker research since the release of the ADQI 23 (2020) consensus. Focusing on three major clinical scenarios-cardiac surgery, sepsis, and nephrotoxic drugs-it reviews early biomarker evidence and explores their potential applications in risk stratification. At the mechanistic level, this paper outlines key pathological pathways in pediatric AKI progression: oxygenation-perfusion imbalance after cardiac surgery, endothelium-immune dysregulation driven by sepsis, and tubular-mitochondrial injury associated with nephrotoxic exposure. In CS-AKI, uNGAL shows the earliest elevation within hours after cardiopulmonary bypass, followed by sequential changes in IL-18, L-FABP, and KIM-1. [TIMP-2] × [IGFBP7] and exosomal miRNA aid in identifying high-risk or severe AKI. In SA-AKI, suPAR and glycocalyx/endothelial injury markers (e.g., syndecan-1, Angpt-2/sTM/Tie-2), combined with urinary DKK3 and complement Ba, can be used for early risk stratification and predicting poor outcomes. In NT-AKI, uNGAL has high negative predictive value for excluding severe AKI, while uKIM-1, uCysC, uOPN, and multi-biomarker combinations can indicate subclinical tubular injury earlier after drug exposure. Overall, single biomarkers struggle to cover AKI heterogeneity. Future efforts should integrate functional dynamic assessments (e.g., FST, RRI), scenario-based multi-biomarker combinations, and AI dynamic models to propose evidence-based, scenario-stratified identification pathways. These will serve as structured references for prospective studies and clinical workflow optimization. - Source: PubMed
Publication date: 2026/05/06
Jin WenqinYe QingCheng Dongqing