Ask about this productRelated genes to: ROD1 antibody
- Gene:
- PTBP3 NIH gene
- Name:
- polypyrimidine tract binding protein 3
- Previous symbol:
- ROD1
- Synonyms:
- DKFZp781I1117
- Chromosome:
- 9q32
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2014-11-19
Related products to: ROD1 antibody
Related articles to: ROD1 antibody
- Non-small cell lung cancer (NSCLC) remains among the most lethal malignancies, with aggressive progression and limited survival. The binding of programmed cell death 1 ligand 1 (PD-L1) to its receptor PD-1, which is expressed on T cells, functions as a critical checkpoint that undermines anti-tumor immune defenses. Despite encouraging anti-tumor efficacy, PD-1 inhibition yields only modest objective response rates in clinical practice. This limitation stems, in part, from an incomplete elucidation of the molecular circuitry controlling PD-L1 expression within the tumor microenvironment. In this work, we delineated a previously unrecognized regulatory axis that modulates sensitivity to PD-1 blockade in NSCLC, centering on SplA/ryanodine receptor domain and SOCS box containing 1 (SPSB1), a substrate-recognition subunit of a Cullin-RING E3 ubiquitin ligase. SPSB1 is markedly upregulated in NSCLC, and its genetic depletion suppressed NSCLC cell proliferation In vitro. Paradoxically, this deletion triggered PD-L1 upregulation, resulting in functional exhaustion of cocultured T cells In vitro, attenuated anti-tumor immunity in vivo, and diminished therapeutic efficacy in immunocompetent murine models. Notably, combined PD-1 mAb and SPSB1 knockdown markedly attenuated tumor growth in immunocompetent mouse models. Mechanistically, SPSB1 ubiquitinated Krüppel-like factor 6 (KLF6), destabilizing the transcription factor, thereby relieving KLF6-mediated promotion of PD-L1 transcription. Upstream, polypyrimidine tract binding protein 3 (PTBP3) bound SPSB1 3'UTR, stabilizing its mRNA. Rescue experiments confirmed that the KLF6/PD-L1 axis is necessary to transmit the signal triggered by SPSB1 loss. In conclusion, this work establishes that SPSB1 suppression combined with PD-1 blockade may be a potential combinatorial strategy for NSCLC management. - Source: PubMed
Publication date: 2026/04/27
Dong ChenglaiZhu DeqiZhang JincaoLi BinZhao JiaGan ShaoyinShen Wei - The patients with intrahepatic cholangiocarcinoma (iCCA) are highly susceptible to recurrence after radical resection, while predicting recurrence remains challenging. Adjacent-to-tumor tissues (ATTs), as the main microenvironment for postoperative recurrence, exhibited superior predictive value for recurrence compared with tumor tissues. However, the postoperative recurrence prediction model based on iCCA ATTs characteristics has not been studied. This study aims to construct recurrence prediction model based on iCCA ATTs and discover possible beneficial postoperative treatment options. - Source: PubMed
Publication date: 2026/03/25
Ping RongyuZhao QianfuMa WenhaoWang HuqiangLiu WeirenYang Dong - Circular RNAs (circRNAs) perform critical functions in cancer biology, commonly serving as microRNA (miRNA) sponges to modulate gene expression. Nevertheless, their participation in gut microbiota-driven colorectal cancer (CRC) has yet to be substantially investigated. Fusobacterium nucleatum (F. nucleatum), a well-recognized oncogenic bacterium in the human gut, has been implicated in CRC development, but the underlying mechanisms are not fully defined. In this study, we identified a novel circRNA, circPTBP3, which is the most significantly upregulated circRNA upon F. nucleatum infection, and is significantly upregulated in CRC tissues. CircPTBP3 is preferentially transcribed over its host gene PTBP3 in response to F. nucleatum through activation of the transcription factor ETS1. Functional assays demonstrated that circPTBP3 enhances CRC cell proliferation and tumor growth in vitro and in vivo. Mechanistically, circPTBP3 acts as a molecular sponge for miR-760, thereby relieving its suppression of the downstream target gene PUM1. In clinical CRC specimens, circPTBP3 expression showed a positive correlation with F. nucleatum abundance, PUM1 expression, larger tumor sizes, advanced TNM stages, and a negative correlation with miR-760 levels. These findings establish for the first time that circPTBP3 functions as a pivotal mediator of F. nucleatum 's oncogenicity, and reveal a novel F. nucleatum-circPTBP3-miR-760-PUM1 regulatory axis that promotes CRC progression. CircPTBP3 may serve as a potential biomarker and therapeutic target in F. nucleatum-associated colorectal carcinogenesis. - Source: PubMed
Publication date: 2026/03/31
Li ChunminLiu QianqianShen HangchangZou TianhuiFu LinnaChen Yingxuan - Immune activation enhances defense gene expression but often suppresses plant growth, creating a fundamental trade-off that limits durable resistance. While selective translation of defense mRNAs has been reported, how growth mRNAs are regulated after transcription during immune responses remains poorly understood. Here, using network-level analyses in Arabidopsis, we identify an RNA-binding protein-dependent mechanism that selectively destabilizes growth-related mRNAs upon immune activation. We show that polypyrimidine tract-binding protein 3 (PTBP3) recognizes a pyrimidine-rich RNA element, undergoes immune-induced condensation, and assembles an mRNA degradation hub that preferentially targets growth genes, including growth-regulating factors. Experimental disruption of this pathway-either by impairing PTBP3 function or by restoring growth gene expression-unexpectedly enhances disease resistance while improving growth resilience under immune stress. These findings reveal post-transcriptional control of growth mRNA stability as a regulatory layer shaping growth-defense balance and suggest a strategy for achieving stronger and safer plant immunity without constitutive defense activation. - Source: PubMed
Publication date: 2026/02/27
Zhou GuilongNiu RuixiaZhu SitaoWang HuiTang ZhijuanWang WanzhenXiong SiruiLong JiaweiZhou YuluTong YongjiaYang HongchunXu Guoyong - Total parenteral nutrition (TPN) provides medical nutrients intravenously to patients who cannot obtain proper nutrition through normal dietary means or enteral feeding. One significant concern is the risk of liver damage associated with long-term TPN use. In this study, the TPN-associated acute liver injury proteins and the molecular mechanisms underlying TPN oxidative stress were investigated through a quantitative proteomic survey. The proteomic changes between control and TPN infusion rats were analyzed by using the LC-MS/MS iTRAQ technology. Rats were randomly assigned to saline infusion (control group) and TPN infusion (infusion rate of 30 mL/kg/h for 3 h). At the end of treatment, total liver samples from rats of control and TPN infusion groups were separated by iTRAQ-based quantitative proteomic identification. The effects of the differentially expressed proteins on the potential mechanism of hepatocytes were examined through flow cytometry. Additionally, siRNA-based assessments were conducted to examine the role of the endoplasmic reticulum stress (ER stress) as well as in vivo apoptosis of TPN-related liver cells. The effect of TPN on the biochemical markers of acute liver injury in the experimental rats was examined following palmitic acid treatment of live cells. Forty-eight proteins were differentially expressed between untreated control and TPN infusion liver tissues. The abundances of Elovl5 and Ptbp3 proteins were observed in TPN infusion (P < 0.05). Palmitic acid treatment of liver cells increased cell cytotoxicity and generated ROS, and increased the level of Elovl5 and Ptbp3, validated in the TPN infusion in vivo. The treatment of hepatocytes resulted in the activation of the caspases 3, caspase 9, accompanied by the expression and release of apoptotic molecules, cytochrome c, Bcl-2, Bcl-XL, p-IRE1α, and TRAF2. Elovl5 and Ptbp3 knockdown significantly regulated palmitic acid-mediated cytotoxicity of liver cells, including inhibition of apoptosis and ROS generation. Palmitic acid-mediated apoptotic induction was accompanied by histone H3K4 trimethylation of Elovl5 and Ptbp3 promoters, leading to enhanced transcription through the sustained phosphorylation of ASK1/JNK/p38 pathways. The mechanism of palmitic acid-induced apoptosis cascade and ER stress in hepatocyte cells involves up-regulation of Elovl5 and Ptbp3. This study provides novel regulators underlying the effects of TPN on liver injury. - Source: PubMed
Publication date: 2025/10/10
Hsieh Yung-YuTsai Jai-JenTung Shui-YiLee Ko-ChaoCheng Kung-ChuanLee Kam-FaiHsieh Meng-ChiaoHuang Cheng-YiTeng Chih-ChuanShen Chien-HengKuo Hsing-Chun