Rabbit Polyclonal to Human TFPI_2
- Known as:
- Rabbit Polyclonal Human TFPI_2
- Catalog number:
- REF0012-100
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Agren
- Gene target:
- Rabbit Polyclonal Human TFPI_2
Ask about this productRelated genes to: Rabbit Polyclonal to Human TFPI_2
- Gene:
- TFPI2 NIH gene
- Name:
- tissue factor pathway inhibitor 2
- Previous symbol:
- -
- Synonyms:
- PP5, TFPI-2, REF1
- Chromosome:
- 7q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-14
- Date modifiied:
- 2016-10-05
Related products to: Rabbit Polyclonal to Human TFPI_2
Related articles to: Rabbit Polyclonal to Human TFPI_2
- The periosteum lies in a dynamic environment with a niche of periosteum-derived stem cells (PDSCs) for their reparative needs. Here, we report that epigenetic repression of tissue factor pathway inhibitor 2 (TFPI2) mediates the osteogenic potential of PDSCs and the ensuing fracture repair. - Source: PubMed
Publication date: 2025/01/25
Liu YangChen LuChang LiangWang Shuren - Tissue factor pathway inhibitor 2 (TFPI2) is known to regulate the proliferation of various cell types and tumor tissues; however, its role in the process of skin aging has not been elucidated. In this study, we identify TFPI2 as a potential antagonist of aging. Our findings indicate that TFPI2 expression is downregulated in aging skin tissues and senescent human dermal fibroblasts (HDFs), and that the depletion of TFPI2 accelerates the senescence of HDFs and the aging of skin. Mechanistically, RNA-seq analysis identifies that cell division cycle 6 (CDC6), a protein associated with the cell cycle, acts as a downstream target of TFPI2. Further liquid chromatography-mass spectrometry (LC-MS) analysis confirmed that TFPI2 interacts with p85β to activate the PI3K/Akt pathway. Subsequent experiments revealed that the activation of the PI3K/Akt pathway alleviates mitigates senescence in HDFs by promoting CDC6 expression and facilitating cell cycle progression. Collectively, these findings underscore the crucial role of the TFPI2/PI3K/Akt/CDC6 pathway in the process of skin aging, highlighting its potential in the development of anti-aging interventions. - Source: PubMed
Publication date: 2025/01/21
Wang FanYi CaitanZhong YunZhou LeiMeng XinMao RuiGuo YiXie HongfuZhang YiyaHuang YingxueLi Ji - Endothelial cell dysfunction has a critical role in the pathophysiology of atherosclerosis. This study aims to uncover pivotal genes and pathways linked to endothelial cell dysfunction in atherosclerosis, as well as to ascertain the assumed causal effects and potential mechanisms. - Source: PubMed
Publication date: 2025/01/10
Yang LuqunGuan XinCheng JiangweiNi LinYao HuijingGao YupingZhu KaiyiShi XiushanLi BingjieLin Yuanyuan - Bone metastasis and steroids are known to activate the coagulation system and induce osteoporosis, pathological bone fractures, and bone pain. Heparanase is a protein known to enhance the hemostatic system and to promote angiogenesis, metastasis, and inflammation. The objective of the present study was to evaluate the effects of steroids and malignancy on the coagulation factors and osteoblast activity in the bone tissue. The effects of dexacort and malignant medium were evaluated in osteoblasts derived from human bone marrow mesenchymal stem cells and human umbilical vein endothelial cells (HUVECs). The bones of mice treated with dexacort for 1 month were studied. Bone biopsies of ten patients with bone metastasis, ten with steroid-induced avascular necrosis (AVN), and ten with osteoarthritis were compared to ten controls. We found that dexacort and malignant medium significantly increased the heparanase levels in osteoblasts and HUVECs and decreased the levels of alkaline phosphatase (ALKP). Peptide 16AC, derived from heparanase, which interacts with tissue factor (TF), further increased the effect, while peptide 6, which inhibits interactions between heparanase and TF, reversed the effect in these cells. The bone microcirculation of mice treated with dexacort exhibited significantly higher levels of heparanase, TF, TF pathway inhibitor (TFPI), TFPI-2, thrombin, and syndecan-1, but reduced levels of osteocalcin and ALKP. The pathological human bone biopsies' microcirculation exhibited significantly dilated blood vessels and higher levels of heparanase, TF, TFPI, TFPI-2, and fibrin. In summary, steroids and malignancy increased the activation of the coagulation system in the bone microcirculation and reduced the osteoblast activity. Heparanase inhibitors should be further investigated to attenuate bone fractures and pain. - Source: PubMed
Publication date: 2024/11/26
Asayag KerenPeled EliAssalia MaiCrispel YonatanYanovich ChenCohen HaimKeren-Politansky AnatNadir Yona - Comprehensive protein profiling in intestinal tissues provides detailed information about the pathogenesis of colorectal cancer (CRC). This study quantified the expression levels of 92 oncology-related proteins in tumors, paired para-carcinoma tissues, and remote normal tissues from a cohort of 52 CRC patients utilizing the Olink technology. The proteomic profile of normal tissues closely resembled that of para-carcinoma tissues while distinctly differing from that of tumors. Among the 68 differentially expressed proteins (DEPs) identified between the tumor and normal tissues, WISP-1, ESM-1, and TFPI-2 showed the most pronounced alterations and exhibited relatively strong correlations. These markers also presented the highest AUC values for distinguishing between tissue types. Bioinformatic analysis of the DEPs revealed that the plasma membrane and the PI3K-AKT signaling pathway were among the most enriched GO terms and KEGG pathways. Furthermore, although TFPI-2 is typically recognized as a tumor suppressor, both Olink and enzyme linked immunosorbent assay (ELISA) analyses have demonstrated that its expression is significantly elevated in tumors compared with paired normal tissues. To the best of our knowledge, this is the first study to profile the proteome of intestinal tissue using the Olink technology. This work offers valuable insights into potential biomarkers and therapeutic targets for CRC, complementing the Olink profiling of circulating proteins. - Source: PubMed
Publication date: 2025/01/05
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