Ask about this productRelated genes to: STAU1 Blocking Peptide
- Gene:
- STAU1 NIH gene
- Name:
- staufen double-stranded RNA binding protein 1
- Previous symbol:
- STAU
- Synonyms:
- PPP1R150
- Chromosome:
- 20q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-22
- Date modifiied:
- 2016-10-05
Related products to: STAU1 Blocking Peptide
Related articles to: STAU1 Blocking Peptide
- Dysregulation of integrins plays an important role in cancer metastasis, but its underlying mechanisms remain largely unexplored. Here we report that the RNA-binding protein STAU1 enhances mRNA stability of integrin β5 (ITGB5), forming a self-perpetuating loop that drives colorectal cancer (CRC) metastasis. STAU1 was significantly upregulated in CRC, particularly in metastatic tissues, and correlated with poor patient outcomes. STAU1 knockdown suppressed CRC cell metastasis in vitro and in vivo, while its overexpression promoted metastasis. ITGB5 mRNA was identified as a novel target of STAU1 and mediated its pro-metastatic effects. Mechanistically, STAU1 directly bound the 3' untranslated region of ITGB5 mRNA to stabilize it. We further identified transcription factor FOXP3 as a downstream effector of ITGB5 in CRC cells. STAU1-mediated ITGB5 upregulation increased FOXP3 phosphorylation at serine 418, which enhanced FOXP3 binding to the STAU1 promoter and activated its transcription, establishing a STAU1-ITGB5-FOXP3 positive feedback loop. This loop was augmented in CRC specimens from patients with distant metastasis. Our study elucidates a novel RBP-integrin regulatory axis in CRC metastasis and proposes the STAU1-ITGB5-FOXP3 loop as a prognostic biomarker and promising therapeutic target for metastatic CRC. - Source: PubMed
Publication date: 2026/03/06
Wang YingeLi DanxiuWei DanMiao GeLiu YanxingZhang WenyaoGuo XingxianYu JianingMa WanqiGuo ZhiyuWang ChenNie YongzhanCao TianyuJin HaifengZhao XiaodiLu Yuanyuan - Psychosis is a clinically heterogenous disorder associated with significant difficulties with social and occupational function (psychosocial disability; PD). While environmental and cognitive factors are identified predictors of PD, the genetic contribution remains unclear. Here, we investigated the hypothesis that objective social participation (SP) and occupational engagement are genetically influenced. We performed mixed-linear-model genome-wide association studies of these phenotypes in the UK Biobank (N∼404,500) and a series of post-hoc analyses including Mendelian randomization (MR) to interpret findings. SP was defined as the frequency of social visits and leisure activities based on response to questionnaires. Occupational engagement was represented by two variables: occupational function (OF) and the established Not in Education, Employment, and Training (NEET) measure, both derived from employment status responses. We identified 17 independent loci for SP, with a SNP-based heritability of 4.1%. A list of contributory genes included TNRC6B, STAU1, CDH7, GBE1, DDX27, and several known schizophrenia risk genes including CSE1L, ZNF536 and TCF4. The regulation of synaptic signalling was implicated in the biology of SP by gene-set analysis. SNP-based heritabilities for OF and NEET were 1.8% and 1.3% respectively and DRD2 was associated with both phenotypes by gene-based analysis. Reduced SP and occupational engagement demonstrated genetic correlations with an increased risk for neuropsychiatric disorders, socioeconomic deprivation, lower cognitive ability, loneliness, neuroticism and chronic pain. MR indicated that attention-deficit hyperactivity disorder and schizophrenia were likely causal for reduced occupational engagement. PD has a genetic component with shared genetic links and relationships with neuropsychiatric disorders and related traits. - Source: PubMed
Publication date: 2026/01/18
Doherty EvieLaighneach AodánCasburn MiaQuilligan FergusDonohoe GaryCannon Dara MMorris Derek W - About 25% of long noncoding RNAs (lncRNAs) contain Alu elements, yet their functional significance remains largely unexplored. We previously found that lnc-APUE was upregulated in hepatocellular carcinoma (HCC) and correlated with high recurrence rates. However, the pathogenic roles of lnc-APUE upregulation in tumor metastasis and its underlying mechanism are still unknown. Here, we showed that an Alu element in lnc-APUE could base-pair with the Alu element in 3'-untranslated region of E-cadherin coding gene (CDH1), triggering CDH1 mRNA decay and E-cadherin loss, consequently enhancing hepatoma cell migration and invasion. These effects of lnc-APUE were abrogated by deleting or mutating its Alu element, or by silencing STAU1 or UPF1, two key components of the STAU1-mediated mRNA decay (SMD) pathway. Mouse xenograft models revealed that overexpression of wild-type lnc-APUE, but not Alu-deleted lnc-APUE, reduced E-cadherin levels and promoted tumor metastasis, whereas silencing lnc-APUE had opposite effects. Furthermore, TGFβ1 stimulation induced SMAD2 binding to the lnc-APUE promoter, activating its transcription. Silencing lnc-APUE blocked TGFβ1-driven migration and invasion, identifying lnc-APUE as a downstream target and critical mediator of TGFβ1 signaling. Collectively, we define a new TGFβ1/SMAD/lnc-APUE/E-cadherin axis: TGFβ1 activates lnc-APUE to promote cancer metastasis through Alu element-driven STAU1-mediated CDH1 mRNA decay and subsequent E-cadherin downregulation. - Source: PubMed
Publication date: 2026/02/03
Li Song-YangHuang Jia-HuiYang Jin-ELi Yi-HangHong Juan-ZhenWang Ting-TingChi Ying-LeiWu Meng-ZhiWang WeiZhu YingZhuang Shi-Mei - Increasing evidence shows that RNA-binding proteins play crucial roles in modulating the blood-tumor barrier (BTB) permeability in glioblastoma (GB). In this study, we identified elevated expression of Musashi RNA-binding protein 2 (MSI2) and Long intergenic nonprotein coding RNA 667 (LINC00667) in glioma co-cultured endothelial cells. MSI2 enhanced the stability of LINC00667, and its knockdown elevated the BTB permeability. In contrast, transcription factor interferon regulatory factor 6 (IRF6) exhibited reduced expression in glioma co-cultured endothelial cells, and its over-expression elevated the BTB permeability. Mechanistically, LINC00667 facilitated IRF6 mRNA degradation through Staufen1-mediated mRNA decay pathway. IRF6 inhibited the transcriptions of key tight junction associated proteins (ZO-1, occludin, and claudin-5) through promoter binding. That is, MSI2 knockdown down-regulated the expression of LINC00667, thereby diminishing its ability to degrade IRF6 through the Staufen1-mediated mRNA decay pathway. This led to IRF6 accumulation, which transcriptionally suppressed ZO-1, occludin and claudin-5 expression, ultimately increasing BTB permeability. Furthermore, both individual and combined modulation of MSI2 knockdown, LINC00667 knockdown and IRF6 over-expression enhanced BTB permeability to doxorubicin, thereby increasing the apoptosis rate of GB cells. Collectively, the MSI2/LINC00667/IRF6 pathway plays an important role in modulating BTB permeability, offering potential targets for new molecular therapies in GB. - Source: PubMed
Publication date: 2026/01/23
Gao RuiRuan XueleiXue YixueWang PingWang DiE TiangeLiu XiaobaiLiu Libo - Antibody-small interfering RNA (siRNA) conjugates present an opportunity to expand the siRNA therapy to extrahepatic tissues. However, their investigation is now only confined to a limited number of targets, partially owing to some flaws in structures. Here, we described a modular design of bifunctional antibody that tethers siRNA without conjugation, yielding a diligent one-to-one antibody-siRNA pairing structure feasible for target expansion, charge masking, and further functionalization. Focusing on a noncationic siRNA-recruiting module, Staufen1 dsRBD34, we demonstrated that bifunctional antibodies recruit siRNA independent of base modification and enable target gene silencing on multiple cell types at a stoichiometry (1/1). Notably, by functionalizing siRNA terminus with small-molecule enhancers, the silencing potency of this pairing system can be augmented by seven times (IC50 from 200 to 28 nM) through the endosome-to-cytosol import. Affinity maturation by arginine scanning yields the 32 times higher affinity of dsRBD34 to siRNA, but the augment led to neither stronger silencing nor higher stability in mouse plasma as compared to p19 protein. The competition from sulfated GAGs in circulations can alter the pharmacokinetics of pairs and prevent a practical assessment of their potential in vivo. Altogether, bifunctional antibodies here possess notable properties, but ultrahigh-affinity dsRNA-binding domain is necessary to realize applications. - Source: PubMed
Liu YahuiZheng YanXu RuolinQuan YananTai Wanyi