Protein Tyrosine Phosphatase (PTP) PTPRG
- Known as:
- Protein Tyrosine Phosphatase (PTP) PTPRG
- Catalog number:
- E-3359
- Product Quantity:
- 20 ug
- Category:
- -
- Supplier:
- Bioner
- Gene target:
- Protein Tyrosine Phosphatase (PTP) PTPRG
Related genes to: Protein Tyrosine Phosphatase (PTP) PTPRG
- Gene:
- ACP1 NIH gene
- Name:
- acid phosphatase 1
- Previous symbol:
- -
- Synonyms:
- HAAP, LMW-PTP, LMWPTP
- Chromosome:
- 2p25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2017-09-15
- Gene:
- DUSP1 NIH gene
- Name:
- dual specificity phosphatase 1
- Previous symbol:
- PTPN10
- Synonyms:
- HVH1, CL100, MKP-1
- Chromosome:
- 5q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-03-03
- Date modifiied:
- 2015-09-11
- Gene:
- HACD1 NIH gene
- Name:
- 3-hydroxyacyl-CoA dehydratase 1
- Previous symbol:
- PTPLA
- Synonyms:
- CAP
- Chromosome:
- 10p12.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-22
- Date modifiied:
- 2016-01-15
- Gene:
- HACD2 NIH gene
- Name:
- 3-hydroxyacyl-CoA dehydratase 2
- Previous symbol:
- PTPLB
- Synonyms:
- -
- Chromosome:
- 3q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-22
- Date modifiied:
- 2016-01-15
- Gene:
- HACD3 NIH gene
- Name:
- 3-hydroxyacyl-CoA dehydratase 3
- Previous symbol:
- PTPLAD1
- Synonyms:
- B-ind1, HSPC121
- Chromosome:
- 15q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-11
- Date modifiied:
- 2016-01-15
Related products to: Protein Tyrosine Phosphatase (PTP) PTPRG
Related articles to: Protein Tyrosine Phosphatase (PTP) PTPRG
- Progress in defining the proteome of the developing human brain has lagged behind our understanding of the adult human brain, primarily due to challenges in tissue acquisition and in preservation of anatomical structure during experimental processing. Single-cell transcriptomics alone is an excellent resource for defining cellular identity, but has limited capacity to trace neuronal connectivity because proteins, the active molecules in interactions, may be transported significant distances from cell bodies and their site of synthesis. There are numerous protein-mediated transient interactions between cellular elements in the developing brain, such as between migrating cortical neurons and subplate, and thalamic projections and cortical progenitors. Anatomical approaches have identified specific cell populations that interact, allowing us to characterize the transient and dynamically changing early circuits. Proteomic data generation is now essential for ligand-receptor pair prediction and validation. Upon receipt of a single, exceptionally well-preserved 20 postconception week human brain hemisphere, we conducted fine dissections of 18 anatomically distinct brain regions, including the pia mater. These samples underwent in-depth analysis of both the total and posttranslationally modified proteomes, with the aim of creating a reference resource for investigators studying this critical stage of neurodevelopment. Here, we have presented an overview of the resulting dataset, compared the proteomic profiles across regions, and highlighted examples of variable posttranslational modifications within individual proteins. As expected, non-modified protein profiles revealed substantial differences across brain regions and structures. For instance, pia mater and thalamus were enriched for proteins involved in transcription and chromatin organization, which may suggest a higher proportion of dividing cells and/or significant epigenetic regulation in these areas at this developmental stage. In contrast, the cortical and hippocampal proteome reflected active synaptogenesis and cytoskeletal remodeling. While interregional differences in phosphorylated and acetylated peptides largely mirrored those observed in the non-modified proteome with respect to gene ontology categories, the glycosylated peptidome of the pia mater was markedly distinct. This divergence is driven by the secretion of extracellular matrix proteins and the region's intimate association with the basement membrane of the pia. Finally, by integrating our proteomic data with publicly available single-cell RNA sequencing datasets from the same developmental stage, we identified high-confidence ligand-receptor pairs (e.g., L1CAM:CD9, CNTN4:PTPRG, LGALS1:ITGB1) likely involved in thalamocortical interactions. - Source: PubMed
Publication date: 2026/05/03
Bandiera SBogetofte HJensen PHussain RNischal S ARihova LClowry G JLarsen M RMolnár ZCarlyle B C - Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and widespread cerebral pathology. Understanding cell-type-specific molecular mechanisms underlying AD is critical for identifying precise therapeutic targets. We applied a supervised machine learning approach to single-nucleus RNA sequencing data from the ROSMAP cohort, aggregating gene expression profiles into pseudobulk representations across six major brain cell types. Systematic evaluation of all possible cell-type combinations identified microglia and astrocytes as the most discriminative cell types for AD classification. A logistic regression model trained on 228 highly variable genes achieved robust classification performance on held-out ROSMAP samples (balanced accuracy 0.87, AUC 0.89) and generalized to an independent cohort from the Seattle Alzheimer's Disease Brain Cell Atlas (balanced accuracy 0.86, AUC 0.92), demonstrating cross-cohort reproducibility that remains uncommon in computational AD research. Among the 72 genes selected by the model, microglial PTPRG exhibited the highest absolute coefficient. Gene Set Enrichment Analysis (GSEA) revealed that microglia-expressed genes were enriched for chronic immune activation and inflammatory signaling, while astrocyte-associated genes implicated protein homeostasis stress and HSF1-mediated chaperone pathways. Weighted Gene Co-expression Network Analysis (WGCNA) further showed that PTPRG operates within fundamentally different gene network contexts in AD and NCI microglia, with AD networks characterized by inflammatory dysregulation and NCI networks reflecting homeostatic immune surveillance. Cell-cell communication analysis identified established AD risk genes including APOE, GRN, PSEN1, and CLU among the top neuronal ligands predicted to regulate microglial PTPRG, positioning it as a convergence point for disease-relevant neuronal signals. Correlation analysis further revealed that excitatory and inhibitory neurons couple to microglial PTPRG through distinct biological processes, implicating divergent mechanisms of AD-associated microglial dysregulation. Collectively, these findings establish microglial PTPRG as a central hub integrating neuronal signaling and inflammatory dysregulation in AD pathology. - Source: PubMed
Publication date: 2026/04/10
Marchi AgataAnwer DanishKerkhoven EduardMontaldo Nicola PietroGilis JeroenPolster Annikka - Lung cancer is a leading cause of cancer mortality, with non-small cell lung cancer (NSCLC) comprising the majority of cases. This study aims to investigate the functional role of long non-coding RNA (lncRNA) PTPRG antisense RNA 1 (PTPRG-AS1) in NSCLC progression using in vitro models, focusing on its potential as a regulator of key oncogenic processes and its interaction with the IGF-1/PI3K/AKT signaling pathway to identify novel therapeutic targets. PTPRG-AS1 expression in NSCLC cell lines (A549, H1299, NCI-H226) and normal lung cells (Beas-2B) was analyzed using RT-qPCR. PTPRG-AS1 was silenced with siRNA, and its effects on cell proliferation, migration, invasion, colony formation, apoptosis, and angiogenesis-related factors were evaluated. Western blot analysis assessed components of the PI3K/AKT pathway. LncRNA PTPRG-AS1 was significantly upregulated in NSCLC cells, particularly in H1299. Our results showed that PTPRG-AS1 knockdown inhibited cell proliferation, migration, and invasion, while promoting cell apoptosis. IGF-1 treatment reversed these effects. PTPRG-AS1 knockdown reduced levels of angiogenesis-related factors, including VEGF and bFGF. Additionally, silencing PTPRG-AS1 decreased expression of key PI3K/AKT pathway components, while exogenous IGF-1 reactivated this signaling cascade. PTPRG-AS1 plays a critical role in NSCLC progression by modulating the IGF-1/PI3K/AKT signaling pathway. Targeting PTPRG-AS1 offers a promising therapeutic strategy for NSCLC, warranting further investigation into its clinical implications. - Source: PubMed
Publication date: 2026/03/30
Su GongzhangYang ShanFan BoJiang ZhishengGeng YingcaiCao Ming - This article provides a comprehensive review of the molecular and neurodevelopmental mechanisms underlying schizophrenia, with a particular focus on the roles of protein tyrosine phosphatases (PTPs). Schizophrenia is a neurodevelopmental disorder with a complex etiology involving genetic and environmental factors and characterized by diverse clinical symptoms. The review synthesizes recent advances in understanding how dysregulation of specific PTPs, including PTP1B, PTP receptor gamma (PTPRG), PTPN5 (encoding striatal-enriched PTP [STEP]), and PTP receptor type A (PTPRA), contributes to disrupted synaptic signaling, neurotransmitter dysfunction, and neurodevelopmental abnormalities observed in schizophrenia. Key findings include evidence that altered phosphorylation states, impaired myelination, and aberrant modulation of N-methyl-D-aspartate (NMDA) and dopamine receptor function are central to disease pathophysiology. The review also examines the therapeutic potential of targeting PTP1B and other phosphatases, highlighting promising animal model data while emphasizing the need for additional clinical research. Collectively, the article underscores the importance of phosphatase signaling pathways in the pathogenesis and potential treatment of schizophrenia. - Source: PubMed
Publication date: 2026/01/27
Murugesan KarthikaRebellow DelvyKasagga AlousiousMon Aye MAnwar Summayya - Nerve injuries severely impair quality of life, with the limited axonal regenerative capacity in mammals hindering functional recovery. Dorsal root ganglion (DRG) neurons serve as an essential model for the identification of axonal regeneration regulators as their peripheral axonal branches are regeneration permissive after axotomy while their central axonal branches are regeneration incompetent. - Source: PubMed
Publication date: 2025/11/13
Zhao QianZhang LanYang PengLi JingjingYi Sheng