Ask about this productRelated genes to: PTBP1 antibody
- Gene:
- PTBP1 NIH gene
- Name:
- polypyrimidine tract binding protein 1
- Previous symbol:
- PTB
- Synonyms:
- HNRPI, HNRNP-I, PTB2, PTB3, PTB-1, PTB4, pPTB
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-29
- Date modifiied:
- 2015-03-26
Related products to: PTBP1 antibody
Related articles to: PTBP1 antibody
- Hepatic stellate cell (HSC) activation is the key step in liver fibrogenesis characterized by excessive extracellular matrix (ECM) accumulation, which is based on fibrogenic factors-induced changes in gene expression in HSCs. The post-transcriptional gene-expression regulation plays a crucial role in regulation of gene expression by controlling mRNA fate through RNA binding proteins (RBPs), RBPs are essentially involved in the process of HSC activation and liver fibrogenesis. Since the activated HSCs possess the characteristics of neuron and the roles of multifunctional polypyrimidine tract binding protein 1 (PTBP1), a key RBP in inhibiting neuron differentiation, in HSC activation and liver fibrosis are elusive, this research aimed to investigate the effects of PTBP1 on HSC activation and liver fibrosis. - Source: PubMed
Publication date: 2026/06/26
Xu FeifanZhou Yajun - 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 - Breast cancer is the most common malignant tumor worldwide, and its high heterogeneity limits the efficacy of current clinical therapies. R-spondin 2 (RSPO2) expression is closely associated with breast cancer subtypes, but the precise mechanisms by which it drives disease progression, particularly its relationship with ferroptosis, remain unclear. - Source: PubMed
Publication date: 2026/06/09
Jiang ShuyunMa HongweiDu ZhanweiMa ZhijunWang Xiaowu - Long noncoding RNAs (lncRNAs), widely regarded as nonprotein-coding transcripts longer than 200 nucleotides in length, play active roles in tumorigenesis, including in colorectal cancer (CRC). The abnormally elevated lncRNA small nucleolar RNA host gene 9 (SNHG9) in CRC samples was observed in The Cancer Genome Atlas (TCGA) database. However, the biological role and potential mechanism of SNHG9 in CRC development remain elusive. Herein, 49 paired CRC tissues and matched adjacent normal tissues were obtained to examine SNHG9 levels. Biological functions related to cell proliferation, migration and invasion were evaluated using CCK-8, colony formation, and Transwell assays and western blot analysis. RNA pull-down and RNA immunoprecipitation (RIP) assays were used to verify the SNHG9/PTBP1/PRMT7 regulatory axis. Interestingly, our data revealed that increasing levels of SNHG9 in CRC tissues and cells were positively correlated with poor prognosis and tumour metastasis, while depletion of SNHG9 caused the suppression of cell proliferation, migration, and invasion. Moreover, cytoplasmic SNHG9 enhanced the mRNA stability of PRMT7 by directly binding to PTBP1 through the "lncRNA‒RNA binding protein (RBP)" complex. The regulatory function of SNHG9 on PRMT7 was also validated via rescue functional assays. In summary, our data demonstrated that SNHG9 may play an oncogenic role in CRC tumorigenesis by stabilizing PRMT7 by recruiting PTBP1. This could be a prognostic biomarker and therapeutic target for CRC. - Source: PubMed
Liang Chengbai - This study explored the mechanism of FTO in regulating neuron apoptosis in hypoxic-ischemic brain damage (HIBD) models via PDCD5. - Source: PubMed
Publication date: 2026/06/08
Yin TaiyongZou MinshuLiu DaliShao CuiLi ShuangshuangYuan HuiXu Hongtao