Relevant bibliographies by topics / FOXP2, alternative splicing, PTBP1

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  1. Journal articles
  2. Dissertations / Theses
  3. Conference papers

Academic literature on the topic 'FOXP2, alternative splicing, PTBP1'

Author: Grafiati
Published: 11 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "FOXP2, alternative splicing, PTBP1"

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Babenko, Vladimir N., Galina T. Shishkina, Dmitriy A. Lanshakov, Ekaterina V. Sukhareva, and Nikolay N. Dygalo. "LPS Administration Impacts Glial Immune Programs by Alternative Splicing." Biomolecules 12, no. 2 (2022): 277. http://dx.doi.org/10.3390/biom12020277.

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We performed transcriptome analysis in the hippocampus 24 h after lipopolysaccharide (LPS) administration. We observed glial-specific genes, comprised of two-thirds of all differentially expressed genes (DEGs). We found microglial DEGs that were the most numerous in LPS group. On the contrary, differential alternative splicing (DAS) analysis revealed the most numerous DAS events in astrocytes. Besides, we observed distinct major isoform switching in the Ptbp1 gene, with skipping of exon 8 in LPS group. Ptbp1 usually considered a pluripotency sustaining agent in brain embryonic development, acc
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Hinkle, Emma R., Hannah J. Wiedner, Eduardo V. Torres, et al. "Alternative splicing regulation of membrane trafficking genes during myogenesis." RNA 28, no. 4 (2022): 523–40. http://dx.doi.org/10.1261/rna.078993.121.

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Alternative splicing transitions occur during organ development, and, in numerous diseases, splicing programs revert to fetal isoform expression. We previously found that extensive splicing changes occur during postnatal mouse heart development in genes encoding proteins involved in vesicle-mediated trafficking. However, the regulatory mechanisms of this splicing-trafficking network are unknown. Here, we found that membrane trafficking genes are alternatively spliced in a tissue-specific manner, with striated muscles exhibiting the highest levels of alternative exon inclusion. Treatment of dif
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Méreau, Agnès, Vincent Anquetil, Hubert Lerivray, et al. "A Posttranscriptional Mechanism That Controls Ptbp1 Abundance in the Xenopus Epidermis." Molecular and Cellular Biology 35, no. 4 (2014): 758–68. http://dx.doi.org/10.1128/mcb.01040-14.

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The output of alternative splicing depends on the cooperative or antagonistic activities of several RNA-binding proteins (RBPs), like Ptbp1 and Esrp1 inXenopus. Fine-tuning of the RBP abundance is therefore of prime importance to achieve tissue- or cell-specific splicing patterns. Here, we addressed the mechanisms leading to the high expression of theptbp1gene, which encodes Ptbp1, inXenopusepidermis. Two splice isoforms ofptbp1mRNA differ by the presence of an alternative exon 11, and only the isoform including exon 11 can be translated to a full-length protein.In vivominigene assays revealed
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Zhu, Huayuan, Xiaotong Li, Xinqi Zheng, et al. "PTBP1 Regulates Alternative Splicing of Apoptotic Protein: Implications in CLL and Ibrutinib Resistance." Blood 134, Supplement_1 (2019): 1290. http://dx.doi.org/10.1182/blood-2019-126945.

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Introduction : Ibrutinib, an oral, selective inhibitor of Bruton's tyrosine kinase (BTK), dramatically improved Progression-free survival (PFS) and Overall survival (OS) compared with immunochemotherapy in CLL both in first line and relapsed/refractory patients. However, some patients did progress on ibrutinb with dismal outcome. The underlying mechanism remains to be investigated beyond evolving of BTK and/or PLCg2 mutation, the dysfunction of apoptotic protein and mitochondrial apoptotic dependencies may be involves in ibrutinib resistance. PTBP1 (Polypyrimidine tract binding protein 1), a s
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Li, Nana, Haibo Du, Rui Ren, Yanfei Wang, and Zhigang Xu. "Alternative Splicing of Cdh23 Exon 68 Is Regulated by RBM24, RBM38, and PTBP1." Neural Plasticity 2020 (July 25, 2020): 1–11. http://dx.doi.org/10.1155/2020/8898811.

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Alternative splicing plays a pivotal role in modulating the function of eukaryotic proteins. In the inner ear, many genes undergo alternative splicing, and errors in this process lead to hearing loss. Cadherin 23 (CDH23) forms part of the so-called tip links, which are indispensable for mechanoelectrical transduction (MET) in the hair cells. Cdh23 gene contains 69 exons, and exon 68 is subjected to alternative splicing. Exon 68 of the Cdh23 gene is spliced into its mRNA only in a few cell types including hair cells. The mechanism responsible for the alternative splicing of Cdh23 exon 68 remain
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Bushra, Samira, Ying-Ni Lin, Atefeh Joudaki, et al. "Neural Isoforms of Agrin Are Generated by Reduced PTBP1−RNA Interaction Network Spanning the Neuron−Specific Splicing Regions in AGRN." International Journal of Molecular Sciences 24, no. 8 (2023): 7420. http://dx.doi.org/10.3390/ijms24087420.

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Agrin is a heparan sulfate proteoglycan essential for the clustering of acetylcholine receptors at the neuromuscular junction. Neuron−specific isoforms of agrin are generated by alternative inclusion of three exons, called Y, Z8, and Z11 exons, although their processing mechanisms remain elusive. We found, by inspection of splicing cis−elements into the human AGRN gene, that binding sites for polypyrimidine tract binding protein 1 (PTBP1) were extensively enriched around Y and Z exons. PTBP1−silencing enhanced the coordinated inclusion of Y and Z exons in human SH−SY5Y neuronal cells, even tho
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Pina, Jeffrey M., Luis A. Hernandez, and Niroshika M. Keppetipola. "Polypyrimidine tract binding proteins PTBP1 and PTBP2 interact with distinct proteins under splicing conditions." PLOS ONE 17, no. 2 (2022): e0263287. http://dx.doi.org/10.1371/journal.pone.0263287.

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RNA binding proteins play an important role in regulating alternative pre-mRNA splicing and in turn cellular gene expression. Polypyrimidine tract binding proteins, PTBP1 and PTBP2, are paralogous RNA binding proteins that play a critical role in the process of neuronal differentiation and maturation; changes in the concentration of PTBP proteins during neuronal development direct splicing changes in many transcripts that code for proteins critical for neuronal differentiation. How the two related proteins regulate different sets of neuronal exons is unclear. The distinct splicing activities o
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Fochi, Stefania, Pamela Lorenzi, Marilisa Galasso, et al. "The Emerging Role of the RBM20 and PTBP1 Ribonucleoproteins in Heart Development and Cardiovascular Diseases." Genes 11, no. 4 (2020): 402. http://dx.doi.org/10.3390/genes11040402.

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Alternative splicing is a regulatory mechanism essential for cell differentiation and tissue organization. More than 90% of human genes are regulated by alternative splicing events, which participate in cell fate determination. The general mechanisms of splicing events are well known, whereas only recently have deep-sequencing, high throughput analyses and animal models provided novel information on the network of functionally coordinated, tissue-specific, alternatively spliced exons. Heart development and cardiac tissue differentiation require thoroughly regulated splicing events. The ribonuc
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Liu, Pan, Guo-Chao He, Yu-Zhen Tan, et al. "PTBP1 is a Novel Poor Prognostic Factor for Glioma." BioMed Research International 2022 (March 8, 2022): 1–11. http://dx.doi.org/10.1155/2022/7590997.

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Objective. Polypyrimidine tract-binding protein 1 (PTBP1) is an RNA-binding protein, which plays a role in pre-mRNA splicing and in the regulation of alternative splicing events. However, little was known about the correlation between PTBP1 and glioma and its prognostic significance in glioma patients. Our aim was to investigate the expression, functional role, and prognostic value of PTBP1 in glioma. Methods. We explored the expression of PTBP1 protein using immunohistochemistry in 150 adult malignant glioma tissues and 20 normal brain tissues and evaluated its association with clinicopatholo
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Zhu, Wei, Bo-lun Zhou, Li-juan Rong, et al. "Roles of PTBP1 in alternative splicing, glycolysis, and oncogensis." Journal of Zhejiang University-SCIENCE B 21, no. 2 (2020): 122–36. http://dx.doi.org/10.1631/jzus.b1900422.

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Dissertations / Theses on the topic "FOXP2, alternative splicing, PTBP1"

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Guidi, Mònica. "Micro RNA-Mediated regulation of the full-length and truncated isoforms of human neurotrophic tyrosine kinase receptor type 3 (NTRK 3)." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7114.

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Neurotrophins and their receptors are key molecules in the development of the<br/>nervous system. Neurotrophin-3 binds preferentially to its high-affinity receptor<br/>NTRK3, which exists in two major isoforms in humans, the full-length kinaseactive<br/>form (150 kDa) and a truncated non-catalytic form (50 kDa). The two<br/>variants show different 3'UTR regions, indicating that they might be differentially<br/>regulated at the post-transcriptional level. In this work we explore how<br/>microRNAs take part in the regulation of full-length and truncated NTRK3,<br/>demonstrating that the two isof
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Ferrarini, Federica. "PTBP1 regulates autism-associated FOXP2 gene by Alternative Splicing." Doctoral thesis, 2020. http://hdl.handle.net/11562/1018864.

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Il "gene del linguaggio" Forkhead Box P2 (FOXP2) codifica per un fattore di trascrizione e diverse mutazioni nella regione codificante sono state correlate con il disturbo della parola e del linguaggio di tipo 1 (SPCH1). Esperimenti di linkage disequilibrium e genome wide association hanno associato FOXP2 anche a disturbi dello sviluppo neuronale, tra i quali i disturbi dello spettro autistico (ASDs). Tuttavia non sono note mutazioni nella regione codificante di FOXP2 in pazienti ASD, portando all'ipotesi di possibili difetti a livello post-trascrizionale. A tal proposito, mentre sono disponib
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Conference papers on the topic "FOXP2, alternative splicing, PTBP1"

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Kim, Jung-Hyun, Joshua K. Stone, Jianfeng Li, et al. "Abstract LB-204: SON controls the oncogenic alternative splicing program in glioblastoma by regulating PTBP1/2 switch and RBFOX2 activity." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-lb-204.

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