Ask about this productRelated genes to: PTBP2 antibody
- Gene:
- PTBP2 NIH gene
- Name:
- polypyrimidine tract binding protein 2
- Previous symbol:
- -
- Synonyms:
- brPTB, nPTB, PTB, PTBLP
- Chromosome:
- 1p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-25
- Date modifiied:
- 2014-11-19
Related products to: PTBP2 antibody
Related articles to: PTBP2 antibody
- Chronic oxidative stress is a major contributor to neuronal aging. Due to the lack of homologous recombination (HR) DNA damage repair, high oxygen consumption in neurons causes DNA damage accumulation with age, resulting in a decline in neuronal function, senescence-like phenotypes and onset of neurodegenerative diseases. Here, we identify increased as a stress-inducible negative regulator of neuronal gene expression and senescence-protectant genes. Oxidative stress robustly increases expression in ShSY-5Y differentiated neurons and primary mouse cortical neurons, coinciding with the loss of neuronal genes, including neuronal , and activation of stress-responsive genes. Knockdown of in fibroblasts reduces the expression of key senescence genes. Transcriptomic analyses revealed that overexpression results in coordinated shift in gene expression characterized by repression of neuronal commitment genes and activation of stress and senescence genes. Mechanistically, induction is regulated by stress induced CTCF binding at the promoter. Together, our findings suggest that alteration in levels of acts as a molecular switch between neuronal function and survival, providing insight into transcriptional adaptations associated with aging. - Source: PubMed
Publication date: 2026/04/04
Priyanka PriyankaGamliel AmirTaylor HavilahOhgi KennethRosenfeld Michael G - Polypyrimidine Tract Binding Protein 2 (Ptbp2) binds to polypyrimidine clusters in pre-mRNA molecules and plays a vital role in alternative splicing, especially during neuronal development and maturation. Our study shows that Ptbp2 binds to the 3' UTR of DNA polymerase kappa (Polk), leading to its stabilization and increased expression. While Polk's role in DNA repair is known, its post-transcriptional regulation remains largely unclear. We observed a correlation between increased Ptbp2 levels and higher Polk expression in clinical samples of Chronic Myeloid Leukemia (CML). Knocking out Ptbp2 in CML cell lines and patient samples decreased Polk levels; when treated with hydroxyurea, these samples exhibited increased DNA damage, evidenced by long comet tails and elevated γH2AX foci, a DNA damage marker; however, re-expressing Polk in Ptbp2-KO cells restored the phenotype. Disruption of the DNA repair pathway is a hallmark of cancer and is closely linked to genomic instability. Polk was found to interact with MRE11 of the MRN complex, regulating the activation of the ATM-CHK2 signaling pathway. Cells with high levels of Ptbp2 and Polk showed increased sister chromatid exchanges and BrdU incorporation in ex vivo tests, while multinucleated cells with multipolar spindles appeared in in vivo tests. Our results confirm the key role of the Ptbp2-Polk-MRE11 axis in promoting genomic instability and supporting the survival of cells with higher malignancy. - Source: PubMed
Publication date: 2026/02/10
Lama ShristiBarik BibhudevIs SajithaSarkar TannisthaChanda SayantanBehera MonalisaGuha PayelBehera Subhankar PriyadarshiBiswas SutapaMohapatra SonaliBiswas GhanashyamChakraborty Soumen - Damage following ischemic stroke is worsened by microglial activation and subsequent neuroinflammation. Polypyrimidine tract binding protein 2 (Ptbp2) can influence the chemotaxis and repolarization of cancer-related macrophages; however, its specific role in microglial polarization and the underlying mechanisms are not yet fully understood. This study aimed to elucidate the neuroprotective mechanisms of Ptbp2 and examine its effects on microglial activation, neuroinflammation, and glucose metabolism following cerebral ischemia. Mice model of ischemic stroke was developed using temporary middle cerebral artery occlusion (tMCAO). Adeno-associated viruses were used for overexpression and knockdown in C57 mice, and microglial polarization, blood-brain barrier (BBB) integrity, and glycolytic parameters in the peri-infarct cortex were evaluated. RNA sequencing (RNA-seq) was performed on mouse brain tissues. To investigate the underlying mechanisms, the mouse brain microvascular endothelial cell line bEnd.3 and BV2 microglial cell line were used. The protective effect of Ptbp2 on BBB integrity following stroke was evaluated by targeted overexpression and knockdown. We found that Ptbp2 overexpression reduced microglia-mediated neuroinflammation and BBB damage while inhibiting pathological glycolysis, according to findings from both in vitro and in vivo studies. Additionally, Ptbp2 level was significantly downregulated in patients with stroke compared to controls, and was inversely correlated with the severity of neural impairment. Our study unveils novel immunomodulatory mechanisms in stroke and highlights Ptbp2 and its regulatory network as potential therapeutic targets for stroke. - Source: PubMed
Publication date: 2026/01/30
Xu WentingLi LinlinZhou MengjiaZhang CongZhang Xiangjian - Direct lineage reprogramming represents a promising strategy to convert somatic cells into neurons, offering regenerative potential. While transcription factor-based approaches have been extensively studied, the role of post-transcriptional regulation, particularly alternative splicing (AS), in neuronal fate acquisition remains poorly defined. Here, we demonstrate that the concurrent knockdown of the splicing regulator PTBP2 and the barrier protein p53 enhances the neuronal conversion of human retinal pigment epithelial (hRPE-19) cells when combined with ASCL1 and miR-9/9*-124 (AMnp). Transcriptomic and splicing analyzes reveal that PTBP2 depletion induces widespread AS changes, most notably promoting near-complete inclusion of exon 36 in the ANK2 gene, which encodes a key regulator of axon initial segment assembly. Functional and rescue assays confirm that loss of exon 36 significantly impairs neuronal induction, whereas re-expression restores neuronal conversion efficiency, establishing ANK2 isoform switching as a mechanistic requirement for reprogramming. Moreover, photoreceptor markers expression in AMnp-reprogrammed neurons suggests partial photoreceptor-like features potentially reflecting residual epigenetic memory, with chromatin remodeling potentially cooperating with splicing to influence subtype specification. These findings identify the PTBP2-ANK2 splicing axis as an isoform-specific molecular switch for RPE-to-neuron conversion, offering a strategy to enhance the precision and efficiency of neuronal reprogramming. - Source: PubMed
Ma Yun-XiZhang Yan-KeLi JunZhu Bing-Lin - Single-cell analysis has refined our understanding of cellular heterogeneity in glioma, yet RNA alternative splicing, a critical layer of transcriptome regulation, remains underexplored at single-cell resolution. Here, we present a pan-glioma single-cell alternative splicing analysis in both tumor and immune cells through integrating seven SMART-seq2 datasets of human gliomas to uncover overlooked isoform-level regulations shaping glioma progression and immune responses. - Source: PubMed
Publication date: 2025/12/12
Song XiaoTiek DeannaLu MinghuiYu XiaozhouWu RunxinWalker MayaHe QiuSisbarro DerekHu BoCheng Shi-Yuan