OTF2 Blocking Peptide
- Known as:
- OTF2 Blocking Peptide
- Catalog number:
- 33r-10812
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- OTF2 Blocking Peptide
Related genes to: OTF2 Blocking Peptide
- Gene:
- POU2F2 NIH gene
- Name:
- POU class 2 homeobox 2
- Previous symbol:
- OTF2
- Synonyms:
- OCT2
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-03-08
- Date modifiied:
- 2017-07-07
Related products to: OTF2 Blocking Peptide
Related articles to: OTF2 Blocking Peptide
- Although PD-1 blockade shows strong antitumor efficacy and is being considered for chronic infections including (), its influence on early lymphocyte responses to remains poorly understood. In this study, we characterized the transcriptional and developmental states of pulmonary B and T cells in mice lacking PD-1 after 7 days post- infection. We found that loss of PD-1 disturbed pulmonary lymphocyte homeostasis, characterized by abnormal regulatory T cell (Tregs) expansion, early exhaustion-like differentiation of cytotoxic T cells, and impaired maturation of memory B cells. These alterations are associated with changes in key transcriptional regulators, including reduced activity of factors promoting effector differentiation (e.g., , in T cells; , in B cells) and upregulation of regulators driving regulatory or suppressive phenotypes (e.g., in Tregs). Additionally, PD-1 deficiency rewired B-T cell communication with diminished antigen presentation and co-stimulation while amplifying proinflammatory signals. These insights provide a transcriptional blueprint for PD-1-mediated immune balance, with implications for host-directed therapies in .IMPORTANCEWhile PD-1 inhibition can boost protective T cell responses, it has also been linked to increased TB susceptibility. Our study reveals that PD-1 plays a previously unrecognized role in shaping the earliest immune responses to . In mice lacking PD-1, lung lymphocytes failed to develop in a balanced manner: regulatory T cells expanded excessively, cytotoxic T cells showed signs of early exhaustion, and memory B cell maturation was delayed. These changes disrupted the normal communication between B and T cells, weakening adaptive immunity while amplifying inflammation. By defining PD-1 as a critical organizer of early lymphocyte fate, our findings highlight the risks of indiscriminate PD-1 blockade in infectious contexts and point toward more precise strategies for host-directed TB therapies and vaccine design. - Source: PubMed
Publication date: 2026/07/24
Yang BingWang HaoqiZhang SiqiCai JinruCao GangMa XuanDai Jinxia - Kidney renal clear cell carcinoma (KIRC) features an immunosuppressive tumor microenvironment (TME). We investigated the role of transcription factor POU2F2 in KIRC oncogenesis and macrophage polarization. Single-cell and spatial transcriptomics showed that POU2F2 is upregulated in KIRC and associated with metastasis and poor prognosis. POU2F2 knockdown inhibited KIRC cell proliferation, migration, and invasion in vitro. POU2F2 expression correlated with macrophage infiltration and JAK-STAT signaling. Co-culture assays showed that POU2F2 silencing reduced macrophage recruitment and shifted M2 polarization toward an anti-tumor M1 phenotype. Overall, POU2F2 acts as an oncogenic driver and prognostic biomarker in KIRC, promoting an immunosuppressive TME and representing a potential therapeutic target. - Source: PubMed
Publication date: 2026/07/08
Tang GonglinLiu FeiSun MingzeLiu ChenyueWu JitaoZhao Hongwei - Immune-mediated killing triggers dynamic transcriptional adaptations in tumor cells that can reciprocally regulate the cytolytic process. Unraveling such feedback mechanisms is crucial for advancing cancer immunotherapy. Here, we identified tissue factor pathway inhibitor 2 (TFPI2) as a central node in natural killer (NK)-glioblastoma cross talk. Using transcriptomic and functional approaches, we demonstrated that NK cell attack induces TFPI2 expression in glioblastoma cells via IL1β- and TNFα-driven activation of NFκB signaling. TFPI2 not only restrains tumor proliferation by suppressing the POU2F2-CCND1 axis but also enhances NK cytotoxicity through two complementary mechanisms: It supports optimal ICAM1 expression to promote NK-tumor adhesion, and it selectively represses the immune checkpoint molecule SIGLEC15, restoring NK cell effector function. In vivo, loss of TFPI2 accelerates glioblastoma progression and abrogates the efficacy of adoptive NK cell therapy in a context-dependent manner; the functionality is likely restricted to tumors retaining the capacity for TFPI2 induction upon inflammatory stimuli. Our findings identified the TFPI2-ICAM1 and TFPI2-SIGLEC15 axes as conditional regulators of immune-tumor adhesion and checkpoint control, supporting TFPI2 as a candidate therapeutic target for a subset of glioblastomas amenable to inflammatory reprogramming. - Source: PubMed
Publication date: 2026/06/18
Zheng DongpengLi FengqiZhang ZhuangDong YunyiZhang XuebinLi XuerenYang JingyuePeng ShouchunChen BudongSun ShupengLiu ZichuanMu Xin - Preeclampsia (PE) is a major pregnancy complication that poses risks to both the mother and the fetus. Oxidative stress (OS) plays a crucial role in its pathogenesis. This study aims to explore the diagnostic value of oxidative stress-related genes for PE. - Source: PubMed
Ye WenhuaYin Haiyan - The overall survival rate of acute myeloid leukemia (AML) remains less than 30%. Metabolic reprogramming of leukemia cells, such as the Warburg effect, enables them to adapt to the microenvironment and thereby develop. Elucidating the landscape of lactate regulation in AML helps clarify the pathogenesis from the perspective of metabolic reprogramming and identify possibilities for optimizing current treatment modalities. - Source: PubMed
Publication date: 2026/03/23
Guo ZhiboZhang WenleiGao ZengliangLi QiGuo DanYue LijuanLiu YutongNi XiaotingFan ShengjinHai Xin