Rat TFPI ELISA
- Known as:
- Rat TFPI Enzyme-linked immunosorbent assay test
- Catalog number:
- kt-30014
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Rat TFPI ELISA
Related genes to: Rat TFPI ELISA
- Gene:
- TFPI NIH gene
- Name:
- tissue factor pathway inhibitor
- Previous symbol:
- LACI
- Synonyms:
- EPI, TFI, TFPI1
- Chromosome:
- 2q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-03
- Date modifiied:
- 2016-10-05
- 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: Rat TFPI ELISA
Related articles to: Rat TFPI ELISA
- Tissue factor pathway inhibitor (TFPI) is a serine protease inhibitor existing in two isoforms, TFPI-1 and TFPI-2. Peptides derived from the TFPI C-terminus exhibit potent antimicrobial activity. In this study, a TFPI-1 homolog from Sebastes schlegelii (SsTFPI-1) was identified, and its sequence characteristics, immune response profile, and the antimicrobial activity of its C-terminal peptide TS20 were systematically characterized. The open reading frame of SsTFPI-1 is 867 bp in length, encoding 288 amino acids that comprise a signal peptide, three Kunitz domains, and a low-complexity region. SsTFPI-1 was ubiquitously expressed across all examined tissues, with the highest expression in blood, and its transcript levels were significantly upregulated in the spleen or head kidney following stimulation with Listonella anguillarum, Edwardsiella piscicida, or poly(I:C). Subcellular localization revealed that SsTFPI-1 predominantly localizes in the cytoplasm of EPC cells, and its C-terminus undergoes endogenous cleavage. Antimicrobial assays demonstrated that TS20 exerts pronounced antibacterial activity against Micrococcus luteus with favorable thermal stability. Mechanistically, TS20 disrupts the bacterial cell membrane, enters the cells, binds to DNA, and progressively degrades it. Furthermore, TS20 significantly inhibits SVCV infection in EPC cells by targeting both viral particles and host cells, thereby reducing viral adhesion and entry, while simultaneously downregulating the expression of type I interferon (IFN-I) related genes. In vivo experiments confirmed that TS20 significantly reduced viral loads of SVCV and RBIV-C1 in common carp and turbot, respectively. Collectively, these findings elucidate the immunological role of SsTFPI-1 in S. schlegelii and underscore the potential of TS20 as a promising antimicrobial agent. - Source: PubMed
Publication date: 2026/08/12
Zhu Zhi-ShuChen Zi-YueWang Guang-HuaJing HaoYang KaiSun NuoDu Yi-LinWang Zi-QiZhang Min - Colorectal cancer (CRC) is a major global malignancy, with ferroptosis emerging as a key regulator of its progression. Although TFPI-2, a kunitz-type serine protease inhibitor, was reported to have important clinical implications for CRC diagnosis and prognosis, few studies have investigated its functional role in CRC cells, and its involvement in ferroptosis remains unknown. TFPI-2 expression in CRC and adjacent normal tissues was detected by IHC, RT-qPCR, and Western blot. Plasmid transfection was used to silence or overexpress TFPI-2 in CRC cells, followed by functional assays including CCK-8 assays, EdU staining, Transwell assays, and EMT marker detection. In vivo tumor growth was evaluated using a xenograft model. Ferroptosis was assessed by measuring ROS, Fe²⁺ levels, MDA, GSH, and expression of key regulators (GPX4, TFR1, FSP1). Mechanistic insights from analyses of p65 and IκBα were obtained through RT-qPCR, Western blot and immunofluorescence. To investigate the involvement of the NF-κB signaling pathway, HCT116 cells were treated with the NF-κB inhibitor Bay 11-7082. CRC tissues exhibited decreased TFPI-2 expression. Overexpressing TFPI-2 suppressed CRC cell proliferation, invasion, and EMT, whereas TFPI-2 knockdown exacerbated these malignant phenotypes. These findings were further validated in xenograft models, where TFPI-2 exerted tumor-suppressive effects. Mechanistically, TFPI-2 knockdown inhibited ferroptosis by promoting NF-κB pathway activity. This study reveals that TFPI-2 suppresses CRC progression by inducing ferroptosis through NF-κB signaling, providing new insights for future CRC therapy. - Source: PubMed
Shi XiaojingZhang JingLu JianQiXu Zheng - - Source: PubMed
Publication date: 2025/09/17
Wang GuangliHuang WenheLi WeiChen ShaoyingChen WeibinZhou YanchunPeng PeiGu Wei - Bone and bone-marrow (BM) have the same blood supply and thus may be considered as one organ. We previously demonstrated that the microcirculation hemostatic balance that includes heparanase, tissue factor (TF), TF pathway inhibitor (TFPI) and TFPI-2 are organ dependent. The present study aim was to investigate the effect of BM microcirculation blood on osteoblasts and human umbilical vein endothelial cells (HUVECs) compared with peripheral-blood (PB). Fourteen patients were recruited. BM blood was drawn from the pelvis and PB from the arm of each patient. Mesenchymal stem cells (MSCs) from the bone pellet were differentiated to osteoblasts. Cells were evaluated by ELISA, chromogenic assays and immunostaining. We found that levels of heparanase, TF, TFPI, and TFPI-2 were reduced in osteoblasts compared with MSCs (p < 0.05). Level of heparanase was lower in BM plasma compared with PB (p < 0.05). BM plasma attenuated heparanase procoagulant activity and level and increased proliferation in osteoblasts and HUVECs compared to PB plasma or the control. BM plasma increased HUVECs tube-formation compared with PB and control. Peptide 16AC, derived from heparanase that interacts with TF, enhanced, while peptide 6, that inhibits the interaction of heparanase-TF-complex, decreased heparanase level, procoagulant activity, and proliferation in osteoblast and HUVECs. In conclusion, osteoblasts acquire an attenuated hemostatic characteristic during differentiation. The microcirculation blood of the bone supports low hemostatic parameters in osteoblasts and enhances proliferation of cells and angiogenesis. The present data support the growing notion that the local microcirculation within a tissue or organ uniquely affects local hemostasis and angiogenesis. - Source: PubMed
Publication date: 2025/04/21
Asayag KerenPeled EliCrispel YonatanYanovich ChenCohen HaimKeren-Politansky AnatNadir Yona - - Source: PubMed
Konduri Santhi DRao Chilukuri NChandrasekar NirmalaTasiou AnastasiaMohanam SanjeevaKin YoshiakiLakka Sajani SDinh DzungOlivero William CGujrati MeenaFoster Donald CKisiel WalterRao Jasti S