Ask about this productRelated genes to: TRAF3IP2 antibody
- Gene:
- TRAF3IP2 NIH gene
- Name:
- TRAF3 interacting protein 2
- Previous symbol:
- C6orf4, C6orf5, C6orf6, C6orf2
- Synonyms:
- DKFZP586G0522, ACT1, CIKS
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-15
- Date modifiied:
- 2019-04-23
- Gene:
- TRAF3IP2-AS1 NIH gene
- Name:
- TRAF3IP2 antisense RNA 1
- Previous symbol:
- TRAF3IP2-AS2, C6orf3, NCRNA00248
- Synonyms:
- C6UAS
- Chromosome:
- 6q21
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2011-04-28
- Date modifiied:
- 2014-11-18
Related products to: TRAF3IP2 antibody
Related articles to: TRAF3IP2 antibody
- Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder. It is marked by difficulties in social communication and the presence of repetitive behaviors. Research has found that disruptions in the body's circadian rhythm and dopamine signaling pathways can contribute to the development of this disorder. Long non-coding RNAs (lncRNAs) are important for regulating gene expression. They have been identified as potential risk genes and diagnostic markers for ASD. This observational (case-control) study aimed to investigate and compare the expression levels of three lncRNAs related to circadian rhythm, , , and LINC01138, and two lncRNAs linked to dopamine signaling, and , in the peripheral blood of 30 patients with ASD and 41 healthy controls using Real-time PCR. The results showed a significant increase in lncRNA expression in patients with ASD compared to healthy controls (P = 0.0048**). However, the expression level of , LINC01138, , and did not show any significant difference between these two groups (P > 0.05). Additionally, when analyzing by sex, affected males had significantly higher expression than control males (P = 0.002**). There was also a significant correlation between the expression of and and the age of ASD patients. Moreover, ROC curve analysis suggested that could serve as a diagnostic marker for ASD (AUC = 0.70 and P = 0.004). Overall, these findings indicate that dysregulation of in peripheral blood is associated with ASD. While the functional relevance of this peripheral signature to CNS pathophysiology remains to be established, may serve as a candidate for future peripheral biomarker discovery attempts. - Source: PubMed
Publication date: 2026/07/02
Ziaei AsalShirvani-Farsani ZeinabGhafouri-Fard Soudeh - Psoriasis is a chronic inflammatory skin disorder affecting approximately 2% of the global population, characterized by abnormal keratinocyte proliferation and dysregulated immune responses. This review examines the emerging role of long non-coding RNAs (lncRNAs) in psoriasis pathogenesis, highlighting their significance as regulatory molecules in disease initiation, progression, and chronicity. LncRNAs demonstrate distinct expression patterns in psoriatic lesions, with upregulated transcripts such as MALAT1, XIST, MIR31HG, and HOTAIR promoting keratinocyte hyperproliferation, inhibiting apoptosis, and amplifying inflammatory cascades through mechanisms including microRNA sponging and transcription factor modulation. These molecules primarily target key signaling pathways including NF-κB, STAT3, and PI3K/AKT. Conversely, downregulated lncRNAs like NEAT1, MEG3, and PRINS normally function as tumor suppressor molecules that maintain epidermal homeostasis through pro-apoptotic and anti-inflammatory mechanisms. Their reduced expression contributes to the pathological hyperproliferative phenotype characteristic of psoriatic skin. Importantly, genetic variants within lncRNA loci have been identified as significant contributors to psoriasis susceptibility and treatment responses across different populations. Single- nucleotide polymorphisms in genes such as TRAF3IP2-AS1, HOTAIR, and CDKN2B-AS1 demonstrate population-specific associations with disease risk and therapeutic outcomes, suggesting their potential utility as pharmacogenomic markers. The complex regulatory networks involving lncRNAs provide new insights into psoriasis pathogenesis and offer promising avenues for personalized treatment strategies. Integration of lncRNA profiling into clinical practice may enhance our understanding of disease heterogeneity and improve therapeutic outcomes for psoriatic patients. - Source: PubMed
Publication date: 2025/09/19
Danis JuditSzéll Márta - Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal solid malignancies. PDAC is characterized by prominent necrotic foci within the tumor and a high propensity for distant liver metastasis, leading to a poor prognosis. In this study, using patient-derived organoid models, single-cell RNA sequencing, and multiplex immunofluorescence staining of samples from patients with PDAC, in vivo TGFβ1 conditional knockout mouse models, and 3D in vitro models, we discovered that the formation of intratumoral necrotic foci in pancreatic cancer is closely associated with liver metastatic events. This process was triggered by the deficiency of the long noncoding RNA TRAF3IP2-AS1 that induced necroptosis, which was accompanied by an immunosuppressive microenvironment. Mechanistically, TRAF3IP2-AS1 blocked necroptosis by reducing the mRNA stability of MLKL through competitively binding to IGF2BP2. Loss of TRAF3IP2-AS1 also promoted necroptosis by promoting RIPK3 phosphorylation via interference with the ubiquitination of the phosphatase PPM1B that dephosphorylates RIPK3. Additionally, TRAF3IP2-AS1 deficiency promoted the release of TGFβ1 from tumor cells, which induced an M2-like immunosuppressive phenotype and the release of more TGFβ1. The elevated production of TGFβ1 created a feedback loop that promoted the transcription of TRAF3IP2-AS1 in tumor cells to balance necroptosis. Overall, these findings identify TRAF3IP2-AS1 as a key regulator of necroptosis and the formation of an immunosuppressive microenvironment in PDAC, providing potential therapeutic targets for treating liver metastasis in patients with pancreatic cancer. - Source: PubMed
Wu Yong-DingHuang Xiao-XiaoZhang Hao-XiangPan YuXie Cheng-KeLi GeLin Cai-FengLin Xin-QuanLi Zhi-YuanChen Yin-HaoHu Jian-FeiLin Hong-YiZhu Shun-CangWang Zu-WeiTian Yi-FengLi Qiao-WeiLiao Cheng-YuChen Shi - Excessive activity in the DNA damage repair (DDR) pathway causes genomic instability, leading to the development of hepatocellular carcinoma (HCC), the most common form of liver cancer. The long non-coding RNA (lncRNA) tumor necrosis factor receptor-associated factor 3 interacting protein 2 antisense RNA 1 (TRAF3IP2-AS1) acts as a tumor suppressor. MicroRNA (miR)-374a-5p is a target miRNA for TRAF3IP2-AS1, while SEL1L ERAD E3 ligase adaptor subunit (SEL1L) acts as a target gene of miR-374a-5p. Moreover, DDR-participating molecule ribosomal protein L6 (RPL6) interacts with SEL1L. In this study, we aimed to explore the role and mechanism of TRAF3IP3-AS1 in HCC. - Source: PubMed
Publication date: 2025/04/15
Wang YuWu Wen-ZeHu Yuan-WenYu Qian-QianGe Hai-LongYu Wei-XinMo FengChao ChenSun Dong-Lin - Disulfidptosis, a novel form of metabolism-related regulated cell death, is a promising intervention for cancer therapeutic intervention. Although aberrant expression of long-chain noncoding RNAs (lncRNAs) expression has been associated with pancreatic carcinoma (PC) development, the biological properties and prognostic potential of disulfidptosis-related lncRNAs (DRLs) remain unclear. - Source: PubMed
Publication date: 2025/02/22
Shi JiangminZhao LiangWang KaiLin JieqiongShen Jianwei