Ask about this productRelated genes to: PTBP1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: PTBP1 Blocking Peptide
- Tau is a protein associated with microtubules principally expressed in neuronal cells, where it plays a fundamental role in cytoskeleton stabilization and axonal transport. Several diseases collectively named tauopathies, such as Alzheimer's disease, have been associated with an imbalance in the expression of alternative spliced Tau transcripts and the accumulation of hyperphosphorylated Tau, causing dysfunction and death of neuronal cells. Therefore, understanding the Tau exon splicing mechanisms may contribute to elucidating molecular factors that could underlie the development of neurodegenerative disorders. The aim of this study was to define the role of selected splicing factors in regulating Tau exon expression in cell lines and neuronal organoids. We demonstrated the role of the RNA-binding motif protein 20 (RBM20) splicing factor in regulating Tau exon 6 and exon 10, applying RNA-binding assay and qPCR analyses. Furthermore, we demonstrated that Tau expression was regulated during cerebral organoid differentiation, recapitulating in vivo Tau expression. These results suggest the feasibility of using brain organoid technology to study Tau alternative splicing during neural development, confirming that 3D cellular models could be used to study and characterize pathological processes taking place in Tau-related pathologies. - Source: PubMed
Publication date: 2026/04/29
Corsi AndreaValentino AngelaBruno Maria GiusyMenichetti GiacomoBelpinati FrancescaPereira Marta PValenti Maria TeresaRuggiero AlessandraTrabetti ElisabettaBombieri CristinaRomanelli Maria Grazia - Human pluripotent stem cells (hPSCs) present considerable potential for regenerative medicine; however, the standardization and large-scale production of these cells are hindered by an incomplete understanding of the molecular mechanisms governing self-renewal. The long non-coding RNA ESRG is integral to maintaining hPSC self-renewal, with its depletion leading to reduced levels of nucleophosmin 1 (NPM1) protein, thereby compromising the self-renewal capacity of hPSCs. Mechanistically, ESRG physically interacts with NPM1, and a reduction in ESRG/NPM1 expression results in elevated bone morphogenetic protein 4 (BMP4) levels and decreased polypyrimidine tract-binding protein 1 (PTBP1) levels, which in turn destabilize TGF-β1 mRNA and attenuate TGF-β signaling activity. Notably, treatment with the TGF-β agonist SRI-011381 partially rescues the self-renewal defects caused by ESRG or NPM1 knockdown. Collectively, our findings elucidate that the ESRG-NPM1-BMP4-PTBP1 axis governs hPSC self-renewal by post-transcriptionally regulating TGF-β1 mRNA stability and sustaining TGF-β signaling. This study enhances the understanding of the molecular regulatory network underlying hPSC self-renewal maintenance and validates ESRG as a promising target for improving the in vitro expansion of hPSCs. - Source: PubMed
Publication date: 2026/05/11
Liao ZilingZhao CongWang LeiLiu WeidongTeng JiajingXie WenOuyang JinhaoYao ChaoyanHuan QianpingLei XuanFu YuXuanZhou BoJiang XingjunRen Caiping - Mast cell (MC) degranulation is associated with allergic rhinitis (AR) progression. Although circMIRLET7BHG has been identified as a promoter of AR development, its potential regulatory role in MC degranulation during AR progression has not been clarified. To address this, MCs (LAD2) were co-cultured with ovalbumin (OVA)-induced human nasal mucosa epithelial cells (HNEpC), and an AR mouse model was generated through OVA stimulation. The expression levels of circMIRLET7BHG and interleukin-33 (IL-33) were assessed by qRT-PCR, while cytokine production in MCs was quantified using ELISA. MC degranulation was evaluated by toluidine blue staining, and western blotting was employed to detect the expression of polypyrimidine tract-binding protein 1 (PTBP1) and proteins related to mitochondrial fusion and fission. The interactions of PTBP1 with circMIRLET7BHG and IL-33 were verified by RNA immunoprecipitation and RNA pull-down assays, and IL-33 mRNA stability was determined using the actinomycin D assay. Co-culture of LAD2 cells with OVA-induced HNEpC demonstrated that circMIRLET7BHG knockdown inhibited MC degranulation by suppressing mitochondrial fission. Mechanistically, circMIRLET7BHG enhanced IL-33 mRNA stability through its interaction with PTBP1. IL-33 overexpression promoted mitochondrial fission and accelerated MC degranulation, whereas this effect was reversed upon circMIRLET7BHG knockdown. In OVA-induced AR mouse models, circMIRLET7BHG overexpression increased epithelial thickness, eosinophil infiltration, and apoptosis, thereby aggravating allergic symptoms by enhancing mitochondrial fission and MC degranulation via upregulation of IL-33 expression. In conclusion, these findings demonstrate that circMIRLET7BHG promotes AR progression by enhancing mitochondrial fission and MC degranulation through regulation of the PTBP1/IL-33 axis, suggesting a potential novel therapeutic target for AR treatment. - Source: PubMed
Publication date: 2026/02/27
Zhan JiabinLi RuiLiang YisenLuo DanZhou YuWei Xin - Right ventricular failure (RVF) is the major cause of mortality in pulmonary arterial hypertension (PAH), and even mild inflammatory stress can precipitate rapid decompensation. Here we report that the long noncoding RNA TCONS_00052110 (TCONS) is upregulated in the right ventricle (RV) under inflammatory stress and may modulate stress-associated responses. In adult male Sprague-Dawley rats with monocrotaline-induced PAH, a low-dose lipopolysaccharide challenge precipitated acute RVF. Mechanistically, TCONS physically associates with polypyrimidine tract-binding protein 1 (PTBP1) and is associated with a prolonged PTBP1 protein half-life, consistent with reduced PTBP1 protein turnover. Elevated PTBP1 skews pyruvate kinase muscle (PKM) isoforms toward PKM2, favoring a PKM2-dominant metabolic state consistent with glycolysis-related remodeling. These changes are accompanied by mitochondrial injury and cytosolic cytochrome c release in vivo and in vitro. Using a cardiomyocyte-enriched AAV9-cTnT strategy, knockdown of TCONS was associated with normalization of the PKM2/PKM1 balance, attenuation of mitochondrial injury, preservation of RV functional indices after inflammatory challenge, and improved survival. Reanalysis of patient-derived datasets from PAH lung tissue and RV tissue spanning compensation-to-decompensation revealed enrichment of inflammatory and glycolysis-related pathways concordant with the TCONS-PTBP1 axis, supporting contextual relevance. These findings support a model of a post-transcriptional link between inflammatory stress, glycolysis-related remodeling, and mitochondrial injury in PAH-related RVF, warranting validation in human RV tissue. - Source: PubMed
Publication date: 2026/04/29
Gao XiaoweiYang YueGuo LizheWang LuQian LiQin GangLuo HuiCao YananWang E - Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) plaques, neurofibrillary tangles, and chronic neuroinflammation. Genome-wide association studies (GWAS) have identified microglial dysfunction as central to AD pathogenesis, with CD33 emerging as a critical genetic risk factor. This review explores the dual roles of CD33 isoforms, CD33M (pro-pathogenic) and CD33m (protective), in modulating microglial activity, Aβ clearance, and neuroinflammatory responses. We dissect the molecular mechanisms underlying isoform formation, including genetic polymorphisms (e.g., rs3865444, rs12459419) and splicing regulation by hnRNPA/B, PTBP1, and SRSF1. Additionally, we highlight the antagonistic interplay between CD33 and TREM2, emphasizing their convergence on DAP12 signaling and downstream pathways. Emerging therapeutic strategies targeting CD33, such as isoform-specific immunotherapies, small-molecule splicing modulators, and Siglec-glycan interactions, are critically evaluated for their potential to mitigate AD pathology. By integrating recent preclinical and clinical advancements, this review underscores the necessity of precision approaches to harness CD33's therapeutic potential while addressing challenges like blood-brain barrier penetration and species-specific discrepancies. - Source: PubMed
Publication date: 2026/04/29
Li Xiao-YanZhang YuRan ZhaoLuo Jia-XinYu Xiao-QinLu Mei-Hong