TFPI-2 IHC Antibody
- Known as:
- TFPI-2 Immunohistochemistry Antibody
- Catalog number:
- IW-PA1248
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- IHC
- Gene target:
- TFPI-2 IHC Antibody
Related genes to: TFPI-2 IHC Antibody
- 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: TFPI-2 IHC Antibody
Related articles to: TFPI-2 IHC Antibody
- Combinations of anti-PD-1/PD-L1 immunotherapy (IO) and anti-VEGF tyrosine kinase inhibitor (TKI) are recommended as first-line therapy for metastatic renal cell carcinoma (RCC). We aimed to evaluate the predictive value of tissue factor pathway inhibitor 2 (TFPI2) for IO + TKI response. - Source: PubMed
Publication date: 2026/05/22
Wang JiajunDu LingzhiWang YingWang HangZhu YanjunXu Xianglai - Glioma stem cells (GSCs) are a small subset of self-renewing, plastic, and multipotent neoplastic cells in glioblastoma (GBM) that sit at the apex of a cellular differentiation hierarchy. Elucidating pathways that enhance GSC properties and determine their cell-specific interactions within the immunosuppressive GBM microenvironment are critical for developing effective therapeutic approaches. The CLOCK-BMAL1 complex, which is well known for its activity as a circadian rhythm-regulating transcription factor, plays a critical role in maintaining GSC stemness, and the gene encoding CLOCK was found to be amplified in about 5% of GBM cases. Here, Zhou et al. have uncovered a "symbiotic exclusivity" relationship between CLOCK-BMAL1 and TFPI2, which is also amplified in a small proportion of GBM cases. This relationship forms a HIF-1α/NF-κB P65-mediated positive feedback loop that boosts the proliferative and tumor-enhancing capacities of GSC and immunosuppressive microglia. This self-amplifying regulatory circuit represents an opportunity for intervention to inhibit GBM growth. - Source: PubMed
Publication date: 2026/05/15
Basakis PetrosShih Ling-KaiLi JiaboBrat Daniel J - Breast cancer (BC) incidence continues to rise, and recurrence and metastasis remain major contributors to mortality. The epithelial-mesenchymal transition (EMT), associated with the acquisition of invasive functions by epithelial cells, also promotes resistance to anticancer therapies. Here, an EMT-based prognostic model was developed to enhance BC outcome prediction. - Source: PubMed
Publication date: 2026/03/15
Wu ZizhengZheng JieMen ShuaiSui ShuangruiYan WeitaoLiu YinfengHan Meng - Trophoblast dysfunction and abnormal cell death are associated with unexplained spontaneous miscarriage (USM), while the underlying mechanisms remain unclear. This research aims to elucidate the pathogenic functions of the RNA-binding protein KH-type splicing regulatory protein (KHSRP) in USM. - Source: PubMed
Publication date: 2026/03/31
Jin GehuiHuang JinyuanWang XiaoyeFan MengjieWu WenxueSun YueLiu XueTian Chan - Glioblastoma (GBM) is a highly aggressive brain tumor characterized by extensive crosstalk between glioblastoma stem cells (GSCs) and immunosuppressive microglia, with our previous work identifying CLOCK and TFPI2 as key regulators of this interaction. Here, we uncover a 'symbiotic exclusivity' pattern between CLOCK and TFPI2, showing that, despite mutually exclusive amplifications, they sustain symbiotic regulatory interactions in GBM. The CLOCK-BMAL1 complex transcriptionally upregulates TFPI2, while TFPI2-driven hypoxia inducible factor 1 α (HIF-1α) signaling activates nuclear factor k B (NF-kB) P65 to upregulate the CLOCK-BMAL1 complex, creating a positive feedback loop to promote stemness, immunosuppression, and tumor progression. Disrupting the CLOCK-TFPI2 interplay through dual inhibition of their downstream effectors reduces GSC stemness and immunosuppressive microglia, activates antitumor immunity, and synergizes with anti-PD1 therapy to achieve complete tumor regression in 50%-62.5% of tumor-bearing mice. This study uncovers a promising therapeutic strategy for a broader subset of patients with GBM with high expression of either CLOCK or TFPI2, and provides a framework for identifying 'symbiotic exclusivity' genes in cancer. - Source: PubMed
Publication date: 2026/03/17
Zhou FeiPang LizhiLiu YangKhan FatimaChen Peiwen