Cynomolgus 4-1BB / TNFRSF9 Protein
- Known as:
- Cynomolgus 4-1BB / TNFRSF9 Protein
- Catalog number:
- 41B-C52H4
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Cynomolgus 4-1BB / TNFRSF9 Protein
Ask about this productRelated genes to: Cynomolgus 4-1BB / TNFRSF9 Protein
- Gene:
- TNFRSF9 NIH gene
- Name:
- TNF receptor superfamily member 9
- Previous symbol:
- ILA
- Synonyms:
- CD137, 4-1BB
- Chromosome:
- 1p36.23
- Locus Type:
- gene with protein product
- Date approved:
- 1996-06-12
- Date modifiied:
- 2016-10-05
Related products to: Cynomolgus 4-1BB / TNFRSF9 Protein
Related articles to: Cynomolgus 4-1BB / TNFRSF9 Protein
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Publication date: 2026/07/09
Xu Shao-JunChen ChaoYe Ming-QiangHuang JinTu Jia-HuaShen Yan-MingLuo Yun-FanSun Zhao-MinChen JieLin Ji-HongGuan JunHuang Han-XingChen Shu Chen - Nasopharyngeal carcinoma (NPC), highly prevalent in southern China, often leads to treatment failure in advanced stages due to recurrence or metastasis. While METTL14 plays a crucial role in cancer, its regulation of immune- and inflammation-related genes remains poorly understood. This study aims to investigate whether METTL14 is involved in regulating the expression of genes associated with tumor necrosis factor (TNF), interferon (IFN), interleukin (IL), and MHC class I in NPC cells. - Source: PubMed
Zhou ZhihaoWang JingShen LingjunHan LiuxinLi QiwenWu AibingLi JingLiang ZumingZhu LitongHe DanhuaZhou YingHuang ShihaoZhao ZhanlinCong JingePeng ZhitaoZhao PingYe ShunaBai BinyiHong XuanjiaDai GuanqiLei YeZhao WentaoJia JunshuangLin XiaolinXiao DongZhang YuqinLin Taoyan - Human membrane-bound CD137 (mCD137) is a well-known costimulatory molecule; however, it is alternatively spliced into two transcripts (sCD137-1, 2) whose function is not yet known. Here, we show that sCD137 isoforms lack the CRD4 region and form unique structures compared to mCD137. Human activated Tregs produce both CD137 splice isoforms, which are rapidly upregulated after cell activation, and identify an activated Treg phenotype along with FOXP3, CTLA4, and sCTLA4. We engineered recombinant Fc-Hu-sCD137 variants, which are immunosuppressive, inhibiting IFN-γ secretion and proliferation in purified CD4 and CD8 T cells in an APC-independent manner. These effects are mediated by the downregulation of S6 and 4EBP1 of the mTOR complex 1 pathway. Human sCD137 variants, in contrast to the membrane-bound form, are immunosuppressive and may be a novel treatment for inflammation and autoimmunity. - Source: PubMed
Publication date: 2025/11/07
Rojas ManuelHeuer Luke SZhang WeiciSweeney NicolleRamírez-Santana CarolinaLeung Patrick S CLam AlvinKamat ShraddhaMendelsohn Andrew RHuang ManleyYu BoAckerman PaulinaWei QishengLarrick James WChen Yi-GuangRidgway William M - This study aimed to investigate the role of Collagen triple helix repeat protein 1 (CTHRC1) in Wilms' tumor (WT) progression and elucidate its molecular mechanism in promoting WT malignancy through regulation of M2-type tumor-associated macrophages (M2-TAMs) infiltration and polarization. - Source: PubMed
Publication date: 2025/07/08
Zhuo YingquanFeng XiaoyunZhang WenqiDu JunSun XuLuo XiWang WeiJiang HuaGu Huajian - Owing to the desmoplastic stroma constituted by cancer-associated fibroblasts (CAFs), few immune cells infiltrate the pancreatic ductal adenocarcinoma (PDAC). Gabapentin can impede the production of ketoacids by CAFs to support cancer cells. However, in our study, we discovered a dose-dependent increase in transforming growth factor β1 (TGF-β1) levels in cancer cells in response to gabapentin. This reverse increase of TGF-β1 contributes to 'Gabapentin-resistance', leading to the antitumor effects on PDAC cell lines are negatively negotiated in the presence of pancreatic stellate cells. Pirfenidone synergistically inhibited the growth and apoptosis resistance of PDAC when combined with Gabapentin. In a mouse orthotopic PDAC model, Fe-mediated coordination nanodrugs, which contain gabapentin, pirfenidone and the natural polyphenol (EGCG), efficiently promoted the infiltration of naïve CD8 T cells (CD44CD62L) and the accumulation of inflammatory CAFs (α-SMAIL-6). This led to a nearly two-fold increase in survival compared to the control. Furthermore, we identified a new subpopulation as Hmox1iCAFs following treatment with our nanodrugs. Hmox1iCAFs overexpressed the Cxcl10 receptor (Sdc4) and facilitated functional CD8 T-cell infiltration through the Tnfsf9-Tnfrsf9 axis. Overall, our nanodrugs reshape the phenotype of CAFs and enhance functional CD8 T-cell infiltration into tumors, holding the potential to be a safe and promising therapy for PDAC. - Source: PubMed
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