TIAL1 antibody - C-terminal region (AVARP02048_T100)
- Known as:
- TIAL1 (anti-) - C-terminal region (AVARP02048_T100)
- Catalog number:
- avarp02048_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TIAL1 antibody - C-terminal region (AVARP02048_T100)
Related genes to: TIAL1 antibody - C-terminal region (AVARP02048_T100)
- Gene:
- TIAL1 NIH gene
- Name:
- TIA1 cytotoxic granule associated RNA binding protein like 1
- Previous symbol:
- -
- Synonyms:
- TIAR
- Chromosome:
- 10q26.11
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-01
- Date modifiied:
- 2019-01-07
Related products to: TIAL1 antibody - C-terminal region (AVARP02048_T100)
Related articles to: TIAL1 antibody - C-terminal region (AVARP02048_T100)
- Preeclampsia (PE) is a major pregnancy-specific disorder driven by impaired trophoblast function, placental hypoxia, and excessive oxidative stress. Ferroptosis has recently emerged as a key contributor to placental pathology; however, the upstream regulatory mechanisms that activate ferroptosis in trophoblasts remain incompletely defined. Circular RNAs (circRNAs) have been implicated in trophoblast dysfunction, yet the ferroptosis-related circRNA network in PE is largely unexplored. This study investigated whether circCOL3A1 regulates p53-mediated ferroptosis in trophoblasts and contributes to PE pathogenesis. CircCOL3A1 expression was examined in placental tissues and HTR-8/SVneo cells. Hypoxia and hypoxia/reoxygenation models were used to mimic PE-associated stress in vitro. Loss- and gain-of-function assays, ferroptosis measurements, RNA pull-down, RIP, FISH, and Actinomycin-D stability analyses were performed to elucidate the circCOL3A1/TIAL1/p53 axis. A reduced uterine perfusion pressure (RUPP) rat model was used to evaluate the in vivo effects of circCOL3A1 knockdown. CircCOL3A1 was significantly elevated in PE placentas and hypoxia-treated trophoblasts, exhibiting cytoplasmic localization and high structural stability. CircCOL3A1 knockdown restored trophoblast migration, invasion, viability, and reduced apoptosis under hypoxia. Silencing circCOL3A1 suppressed hypoxia-induced ferroptosis by reducing ROS, MDA, and iron levels while restoring GSH and GPX4. Mechanistically, circCOL3A1 bound the RNA-binding protein TIAL1 to enhance p53 mRNA stability, thereby promoting p53-dependent ferroptosis. In vivo, circCOL3A1 silencing lowered maternal blood pressure and proteinuria, reduced placental ferroptosis, and improved fetal survival in PE rats. CircCOL3A1 drives trophoblast ferroptosis through a TIAL1-dependent stabilization of p53, contributing to PE progression. Targeting the circCOL3A1/TIAL1/p53 axis may offer a promising therapeutic strategy for preeclampsia. - Source: PubMed
Wang HaidongYin LizhongZheng HaoyuShi ZhonghuaZhao Chun - Triple-negative breast cancer (TNBC) exhibits robust self-regulatory mechanisms against harsh microenvironmental stress, yet the precise molecular drivers remain elusive. Here, we identified circSCLT1 as a novel circular RNA with energy stress-responsive properties. Systematic in vitro and in vivo assays demonstrated that circSCLT1 promotes TNBC metastasis and radioresistance. Mechanistically, energy stress triggers HNRNPA1-dependent circSCLT1 biogenesis. Cytoplasmic circSCLT1 scaffolds a ternary complex with HNRNPA1 and CSDE1, blocking HNRNPA1 nuclear translocation and stabilizing IL1B via binding to its coding sequence (CDS). Additionally, the circSCLT1-containing complex displaces the E3 ubiquitin ligase TRIM25 from CSDE1 and redirects it toward TIAL1, thereby inducing K48-linked polyubiquitination and proteasomal degradation of TIAL1. Furthermore, circSCLT1 suppresses arginine dimethylation of HNRNPA1 by reinforcing the binding between CSDE1 and HNRNPA1, which in turn facilitates stress granule (SG) assembly under severe energy stress. These circSCLT1/HNRNPA1/CSDE1-containing SGs shield IL1B from autophagy-mediated degradation. Collectively, these actions amplify IL1B/NF-κB signaling, sustaining pro-survival networks that drive metastasis and radioresistance. Importantly, pharmacological inhibition of IL-1β secretion using disulfiram (DSF) synergizes with circSCLT1 silencing to markedly suppress tumor progression and extend survival in preclinical TNBC models. Our findings elucidate the oncogenic role of circSCLT1 in TNBC and underscore its potential as a novel therapeutic target, providing a rationale for combining IL-1β inhibition with circSCLT1-targeted therapy. - Source: PubMed
Publication date: 2026/05/04
Li ZhengSun XiaorongZheng JuanSun XingyaoYang LiyingXing Ligang - The Hippo pathway is an evolutionarily conserved signaling cascade whose dysregulation is implicated in a wide range of diseases. While many RNA-binding proteins (RBPs) regulate this pathway through canonical functions such as modulating mRNA stability and translation, the potential for RBP-mediated regulation via non-canonical, RNA-binding-independent mechanisms remains poorly defined. Here, we report that the RBP TIAL1 exhibits oncogenic properties in hepatocellular carcinoma, promoting cancer cell proliferation, migration, and invasion. Mechanistically, TIAL1 directly interacts with the core Hippo component SAV1, disrupting the MST1-SAV1 interaction and thereby suppressing Hippo signaling and activating YAP. Notably, this regulatory function is independent of the RNA-binding activity of TIAL1. Furthermore, extracellular stimuli such as energy surplus and EGF significantly upregulate TIAL1 expression, linking microenvironmental cues to Hippo pathway dysregulation. Together, our results reveal a previously unrecognized, RNA-binding-independent mode of RBP-mediated regulation, in which TIAL1 serves as a molecular integrator that conveys extracellular signals to the Hippo pathway to drive hepatocellular carcinoma progression, providing potential avenues for therapeutic intervention. - Source: PubMed
Publication date: 2026/04/24
Dai QianlongLou LeiZhu XiaojieZhao HaotianCai ZixinWei PengchengZhong YaxianPeng ShuchangHu XinyueSun RuohanTang XiaotianPeng KaiHe YanwenGu FengDeng XiyunZhou YingqunZhou JunhuaWang YirongXue LeiGuo Xiaowei - Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) immune escape strategies include general inhibition of host gene expression referred to as host shutoff. Viral nonstructural protein 1 (Nsp1) is the main host shutoff factor that blocks protein translation and induces messenger RNA (mRNA) cleavage and degradation. Viral mRNAs are resistant to the translation shutoff and cleavage induced by Nsp1, and the 5' leader sequence present in all viral mRNAs has been shown to confer resistance. However, the exact molecular mechanism for escape from Nsp1 host shutoff has not been demonstrated. In our previous work, we analyzed the effects of Nsp1 on the expression and function of cellular proteins important for stress granule formation. We discovered that the host transcript for the TIA1 cytotoxic granule-associated RNA-binding protein-like 1 (TIAL1, commonly referred to as TIAR) is resistant to SARS-CoV-2 Nsp1 host shutoff. In this work, using reporter shutoff assays, we examined sequence and structural features of the TIAR 5' untranslated region (UTR) and discovered that the first 23 nt of the TIAR transcript are both necessary and sufficient to confer resistance to the Nsp1. Furthermore, our work revealed that the lack of guanosines within a window of 10-18 nt downstream from the 5' end is a defining feature of Nsp1-resistant transcripts shared between the SARS-CoV-2 leader sequence and the TIAR 5' UTR. Our findings are consistent with the model in which sequence features of 5' UTRs, rather than their secondary structure, confer resistance to Nsp1 host shutoff to both viral and cellular mRNAs. - Source: PubMed
Publication date: 2026/02/17
Galbraith CalebStolz MadeleineTersteeg ScottAndrews EmilyPatel Trushar RKhaperskyy Denys A - RNAs and RNA-binding proteins (RBPs) play crucial roles in stress granule (SG) dynamics, yet the specific interactions between SG-associated circular RNAs (circRNAs) and RBPs in esophageal squamous cell carcinoma (ESCC) remain unclear. In this study, we identified m6A-modified circG3BP1 as a potential prognostic biomarker in ESCC. Under cisplatin-induced stress, IGF2BPs facilitate the m6A-dependent translocation of circG3BP1 to SGs, where it functions as a scaffold to enhance TIAR-CAPRIN1 interactions, thereby promoting SG nucleation. SG formation suppresses the translation of senescence-associated mRNAs, such as p21, delaying chemotherapy-induced cellular senescence and contributing to cisplatin resistance in ESCC cells. Clinically, elevated circG3BP1 expression is associated with cisplatin resistance in patients with ESCC. These findings reveal a previously uncharacterized m6A-dependent mechanism by which circG3BP1 promotes SG-mediated chemoresistance, providing a promising potential biomarker and therapeutic target for ESCC treatment. - Source: PubMed
Publication date: 2025/09/30
Chen Ri-XinMo Ao-TianXu Shui-DanWu Jun-HanDeng Min-HuaXie Shu-HuanZhuang Wei-TaoDuan Jin-LingYang HanLin PengHe ZheTang Ji-MingZhou Hai-YuBen Xiao-SongQiao Gui-BinXie Dan