PTPRCAP

Last update 23 Jan 2025

Basic Info

Synonyms

CD45-AP, CD45-associated protein, LPAP

+ [5]

Introduction-

100 Clinical Results associated with PTPRCAP

100 Translational Medicine associated with PTPRCAP

0 Patents (Medical) associated with PTPRCAP

Literatures (Medical) associated with PTPRCAP

31 Dec 2024·Renal Failure

Identification of common and specific fibrosis-related genes in three common chronic kidney diseases

Article

Author: Sun, Guannan ; Liu, Chao ; Dong, Zheyi ; Geng, Xiaodong ; Cai, Guangyan ; Chen, Xiangmei ; Shen, Wanjun ; Hong, Quan ; Fu, Zhangning

BACKGROUNDKidney fibrosis is the common final pathway of virtually all advanced forms of chronic kidney disease (CKD) including diabetic nephropathy (DN), IgA nephropathy (IgAN) and membranous nephropathy (MN), with complex mechanism. Comparative gene expression analysis among these types of CKD may shed light on its pathogenesis. Therefore, we conducted this study aiming at exploring the common and specific fibrosis-related genes involved in different types of CKD.METHODSKidney biopsy specimens from patients with different types of CKD and normal control subjects were analyzed using the NanoString nCounter® Human Fibrosis V2 Panel. Genes differentially expressed in all fibrotic DN, IgAN and MN tissues compared to the normal controls were regarded as the common fibrosis-related genes in CKD, whereas genes exclusively differentially expressed in fibrotic DN, IgAN or MN samples were considered to be the specific genes related to fibrosis in DN, IgAN and MN respectively. Quantitative real-time PCR (qRT-PCR) was performed to validate the expression of the selected genes.RESULTSProtein tyrosine phosphatase receptor type C (PTPRC), intercellular cell adhesion molecule-1 (ICAM1), vascular cell adhesion molecule-1 (VCAM1), interleukin 10 receptor alpha (IL10RA) and CC chemokine receptor 2 (CCR2) were identified as the potential common genes for kidney fibrosis in different types of CKD, while peroxisome proliferator-activated receptor alpha (PPARA), lactate oxidase (LOX), secreted phosphoprotein 1 (SPP1) were identified as the specific fibrosis-associated genes for DN, IgAN and MN respectively. qRT-PCR demonstrated that the expression levels of these selected genes were consistent with the NanoString analysis.CONCLUSIONSThere were both commonalities and differences in the mechanisms of fibrosis in different types of CKD, the commonalities might be used as the common therapeutic targets for kidney fibrosis in CKD, while the differences might be used as the diagnostic markers for DN, IgAN and MN respectively. Inflammation was highly relevant to the pathogenesis of fibrosis. This study provides further insight into the pathophysiology and treatment of fibrotic kidney disease.

01 Dec 2024·International Immunopharmacology

Single-cell sequencing reveals the heterogeneity of immune landscape in drug users with HIV infection

Article

Author: Gao, Kai-Cheng ; Mou, Tangwei ; Zhao, Yu ; Liang, Dan ; Jia, Jie ; Kuang, Yi-Qun

BACKGROUNDInjection drug use (IDU) leads to immune system dysfunction, thereby increasing the risk of opportunistic infection. There is a critical need to reveal the role of IDU in the immunopathogenesis of HIV infection.METHODSWe performed single-cell RNA sequencing (scRNA-seq) on peripheral blood mononuclear cells (PBMCs) derived from healthy control (HC) individuals, HIV-infected patients with IDU (HIV-IDU) and without IDU (HIV-nIDU). In addition, the Gene Set Enrichment Analysis (GSEA) was used to analyze the immunomodulatory effects of differential immune cells.RESULTSSeven types of cells were identified with specific expressions of maker genes. Specific subsets such as CD14⁺ monocytes, plasmacytoid dendritic cells (pDCs), plasma cells, and CD8⁺ T cells displayed a high degree of heterogeneity among HC, HIV-nIDU, and HIV-IDU. We identified signature genes for each subset in distinct groups, including CFP⁺ CD14⁺ monocytes, PTPRCAP⁺ pDCs, IGHD⁺ plasma cells, and IFITM1⁺ CD8⁺T cells from HIV-IDU, whereas these genes were not expressed in such cells from HIV-nIDU. Moreover, considerable heterogeneity in the function of these immune cells was observed across different groups, especially the elevated IFN-α/β signaling for CD14⁺ monocytes, histone H2A/2B and H3/4 pathway for pDCs, the creation of C4 and C2 activators for plasma cells, and drug metabolism cytochrome p450 for CD8⁺ T cells in HIV-IDU individuals.CONCLUSIONOur comprehensive analyses clarify the heterogeneous characteristics of the immune landscape between HIV-IDU and HIV-nIDU. These insights provide a deeper understanding of the IDU-mediated immunopathogenesis in HIV infection.

01 Dec 2024·Current Alzheimer Research

Molecular Mechanisms of GFAP and PTPRC in Alzheimer's Disease: An Analysis of Neuroinflammatory Response and Progression

Article

Author: Pang, Chaoyang ; Sun, Yue ; Taishi, Yezi ; Gao, Chonghao ; Huang, Jingyue ; Wang, Dongxiao ; Pang, Xinping ; Yang, Hongmei

Introduction:Alzheimer's disease (AD) is a complex neurological disorder that progressively worsens. Although its exact causes are not fully understood, new research indicates that genes related to non-neuronal cells change significantly with age, playing key roles in AD's pathology. METHOD: This study focuses on a protein network centered on Glial Fibrillary Acidic Protein (GFAP) and Protein Tyrosine Phosphatase Receptor Type C (PTPRC).Method:This study focuses on a protein network centered on Glial Fibrillary Acidic Protein (GFAP) and Protein Tyrosine Phosphatase Receptor Type C (PTPRC).The Key Findings of this Study Include:1. A significant correlation was observed between GFAP and PTPRC expression throughout AD progression, which links closely with clinical phenotypes and suggests their role in AD pathology. 2. A molecular network centered on GFAP and PTPRC, including Catenin Beta 1 (CTNNB1) and Integrin Beta 2 (ITGB2), showed distinct changes in interactions, highlighting its regulatory role in AD. 3. Analysis of GSE5281 data revealed a decline in the interaction strength within this network, pointing to potential desynchronization as a biomarker for AD. 4. SVM diagnostic models comparing GFAP expression and coupling values confirmed this desynchronization, suggesting it worsens with AD progression.Result:Based on these findings, it is hypothesized that as AD progresses, the GFAP- and PTPRCcentered molecular framework undergoes significant changes affecting key biological pathways. These changes disrupt immune regulation and cellular functions, increasing immune cell activation and inflammation in the brain. This may impair neuronal communication and synaptic functionality, exacerbating AD's pathology.Conclusion:To verify these findings, Support Vector Machine (SVM) diagnostic models and correlation analyses were used to examine changes in this network, indicating that its dysregulation significantly affects AD progression.

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