Ask about this productRelated genes to: TIA1 Blocking Peptide
- Gene:
- TIA1 NIH gene
- Name:
- TIA1 cytotoxic granule associated RNA binding protein
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-01
- Date modifiied:
- 2016-10-05
Related products to: TIA1 Blocking Peptide
Related articles to: TIA1 Blocking Peptide
- RNA-binding proteins (RBPs) are essential regulators of all aspects of RNA metabolism, including splicing, stability, localisation, translation, and degradation. Through their ability to recognise specific cis-elements in target transcripts, often via RNA-recognition motifs or other conserved domains, RBPs enable rapid cellular adaptation to stress and maintain proteostasis, particularly in post-mitotic tissues with limited transcriptional flexibility. Accumulating evidence positions RBPs as both modulators and drivers of the molecular hallmarks of ageing, including genomic instability, loss of proteostasis, mitochondrial dysfunction, cellular senescence, and chronic inflammation. This review synthesises peer-reviewed studies on the multifaceted roles of RNA-binding proteins in organismal ageing and age-related diseases. Key themes include the tissue- and age-dependent changes in expression of turnover and translation regulatory RBPs such as HuR (ELAVL1), AUF1 (HNRNPD), TIA-1, and tristetraprolin (ZFP36), which alter the stability of mRNAs encoding cell-cycle regulators, pro-inflammatory cytokines, and stress-response proteins. Systematic downregulation of core splicing factors, including PTBP1 and several heterogeneous nuclear ribonucleoproteins, drives widespread senescence-associated splicing alterations in pathways governing cell division, autophagy, DNA repair, and mitochondrial function, suggesting a causal contribution to the senescent phenotype. Prion-like RBPs such as TDP-43 and FUS exhibit age-dependent mislocalisation, nuclear depletion, and cytoplasmic aggregation, contributing to splicing defects, impaired RNA transport, and neurodegeneration in amyotrophic lateral sclerosis, frontotemporal dementia, and limbic-predominant age-related TDP-43 encephalopathy. Interactions between RBPs and non-coding RNAs, together with disrupted liquid-liquid phase separation dynamics, further exacerbate age-related decline. By integrating mechanistic studies from cellular and animal models with observations in human cohorts, this review underscores RBPs as central nodes linking multiple ageing hallmarks and highlights their potential as biomarkers and therapeutic targets to promote healthy ageing. Limitations of current models and priorities for future translational research are discussed. - Source: PubMed
Publication date: 2026/06/07
Alves Ferreira João MiguelTukaiev SergiiGiannouli Vaitsa - NBO therapy has demonstrated a neuroprotective effect on ischemic stroke. This study investigated the role of HIF-1α in regulating SG formation and NLRP3 inflammasome activation following I/R injury in NBO-induced neuroprotection. - Source: PubMed
Publication date: 2026/06/19
Guo SichaoCheng ZheAl Tekreeti AbdullahLi FengwuDing YuchuanGeng Xiaokun - Mitochondrial dysfunction, characterized by reduced mitophagy, excessive mitochondrial elongation, and elevated reactive oxygen species production, is a hallmark of cellular senescence. However, the molecular mechanisms linking impairment of redox balance to mitophagy suppression during senescence remain poorly understood. In this study, we identified TIA-1, an RNA-binding protein, as a positive regulator of FUNDC1 expression, a key receptor for ubiquitin-independent mitophagy. Sodium butyrate and ultraviolet-B irradiation triggered oxidative stress-associated senescence in HaCaT cells, leading to reduced TIA-1 expression, decreased FUNDC1 levels, impaired mitophagy flux, excessive mitochondrial elongation, and upregulation of senescence markers. Conversely, ectopic expression of TIA-1 restored FUNDC1 levels, enhanced mitophagy, improved mitochondrial function, and reduced senescence marker expression. Ribonucleoprotein immunoprecipitation assays confirmed that TIA-1 directly interacts with FUNDC1 mRNA, and subsequent analyses indicated that TIA-1 enhances FUNDC1 expression primarily through translational control. Together, these findings establish TIA-1 as a pivotal regulator of mitochondrial homeostasis during cellular stress, acting through FUNDC1 to sustain mitophagy and limit senescence. Targeting TIA-1 may offer new strategies to mitigate mitochondrial dysfunction and restore redox balance in aging and age-related diseases. - Source: PubMed
Publication date: 2026/06/05
Cha SeonghoJung MyeongwooTak HyosunRyu SeungyeonHan SukyoungChae DongwooKim JiyoonJeong Seung MinKim WookLee Eun Kyung - In the 5th edition of the WHO classification, Epstein-Barr virus (EBV)-positive nodal T/NK-cell lymphoma (EBV nTNKL) is a newly defined, poor-prognosis disease originating from cytotoxic T cells. Here, we report a rare case of lymphoma arising in immune deficiency/dysregulation with an immunophenotype of EBV nTNKL that emerged during treatment for follicular lymphoma (FL). A 71-year-old woman was diagnosed with FL grade 3A and received chemotherapy with rituximab. Despite treatment, the disease relapsed repeatedly. During follow-up, she presented with fever and lymphadenopathy. An axillary lymph node biopsy revealed a diffuse proliferation of abnormal lymphocytes expressing CD3, CD4, TIA-1, granzyme B, and EBER, consistent with the EBV nTNKL immunophenotype. CHOP therapy was administered; however, disease control proved difficult, and the patient died 5 weeks after diagnosis. This case exemplifies a rare occurrence of EBV-associated lymphoma arising during the course of B-cell lymphoma. Our experience underscores that rapid clinical deterioration (e.g., fever, hepatosplenomegaly, or B symptoms) during the course of FL should prompt consideration of EBV-associated lymphoma in the differential diagnosis, alongside histologic transformation. Further case reports and molecular analyses should help improve diagnostic accuracy and establish treatment strategies for this rare and aggressive disease. - Source: PubMed
Maeda YusakuHarada TakeshiHori TaikiSumitani RyoheiOura MasahiroSogabe KimikoYagi HikaruFujii ShiroNakamura ShingenMiki HirokazuKageyama TakeshiMatsuoka Ken-Ichi - Alternative RNA splicing is a fundamental mechanism for enhancing proteomic diversity, and its dysregulation is a hallmark of cancer progression. However, the dynamic regulatory networks controlling oncogenic splicing events remain poorly understood. Our previous work identified the inclusion of CLSTN1 exon 11 as critical for the epithelial-to-mesenchymal transition (EMT). Here, we demonstrate that this splicing event promotes breast cancer metastasis by enhancing cell migration, invasion, and the generation of circulating tumor cells (CTCs) in vivo. To translate this finding into a therapeutic strategy, we developed splice-switching antisense oligonucleotides (ASOs) that effectively reverse exon 11 inclusion and suppress cancer cell migration. Furthermore, through systematic screening, we identified the RNA-binding protein TIA1 as a key suppressor of exon 11 inclusion. TIA1 inhibits EMT and metastasis, but its function is antagonized during EMT by phosphorylation mediated by the kinase DAPK3, which is upregulated in this process. This work defines a novel DAPK3-TIA1-CLSTN1 splicing axis that drives breast cancer metastasis, revealing new layers of post-transcriptional regulation and presenting promising therapeutic avenues for targeting pro-metastatic splicing. - Source: PubMed
Publication date: 2026/06/01
Sun YaxuanFeng RongrongZhou XunXu WuqinDu HuiminHu XiezongChen LiangCai YongpingHu Xiaohui