PhosphoSeek™ PTP1B Assay Kit
- Known as:
- PhosphoSeek™ PTP1B Assay Kit
- Catalog number:
- K707-400
- Product Quantity:
- 400 Assays
- Category:
- Peptides
- Supplier:
- Biovis
- Gene target:
- PhosphoSeek™ PTP1B Assay Kit
Related genes to: PhosphoSeek™ PTP1B Assay Kit
- Gene:
- PTPN1 NIH gene
- Name:
- protein tyrosine phosphatase non-receptor type 1
- Previous symbol:
- PTP1B
- Synonyms:
- -
- Chromosome:
- 20q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-13
- Date modifiied:
- 2019-02-14
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- Classic Hodgkin lymphoma is a highly curable B-cell malignancy; however, 10-30 % of patients experience primary refractory disease or early relapse. While PET/CT is a cornerstone in response-adapted therapy, it has notable limitations, including variable sensitivity, and inability to capture molecular heterogeneity or predict minimal residual disease. Emerging non-invasive techniques such as circulating tumour DNA (ctDNA) analysis, extracellular vesicle-associated biomarkers, and cytokine profiling offer new avenues for dynamic, real-time disease monitoring. Liquid biopsy through ctDNA analysis enables early relapse detection, characterization of clonal evolution, and personalized risk stratification. Additionally, tumour-associated macrophages, tumour-derived exosomes, and immune checkpoint markers such as PD-L1 and IL1β+ monocytes/macrophages have been identified as potential indicators of non-response. Advanced molecular profiling of Hodgkin Reed-Sternberg cells further reveals key genetic mutations (e.g., SOCS1, TNFAIP3, PTPN1) contributing to immune evasion, particularly in non-responders. Despite these advancements, a critical gap remains in the integration of these novel biomarkers into clinical practice. Current studies often lack stratification of high-risk subsets, limiting the development of targeted therapies. Bridging this gap through advanced molecular profiling, immune landscape assessments, and the incorporation of novel, non-invasive techniques alongside PET/CT will be crucial for refining risk models and optimizing outcomes for patients with refractory or relapsed disease. - Source: PubMed
Publication date: 2025/09/13
Alibrahim Mohamed NazemGloghini AnnunziataCarbone Antonino - Cyclosporine A (CsA) is a potent immunosuppressive agent that has been reported to cause various disorders, including hepatotoxicity. However, the precise molecular mediators involved in CsA-induced liver injury remain to be fully elucidated. The present study aspires to elucidate the transcription factors implicated in lipid metabolism in the context of hepatic injury induced by cyclosporine A (CsA), both independently and in conjunction with curcumin. A total of twenty-eight male adult Wistar rats were assigned into four groups, including control (Con), sham, cyclosporine A (CsA), and cyclosporine A (CsA) + curcumin (CsA+cur). The rats were administered CsA at a dosage of 30 mg/kg and curcumin at 40 mg/kg via a gastric tube for a duration of 28 days. RT-PCR and Masson trichrome staining were used to measure related changes. The results demonstrated that CsA exposure led to a substantial upregulation of protein tyrosine phosphatase 1B (PTP1B), fatty acid translocase CD36 (FAT/CD36), and sterol regulatory element-binding protein-1c (SREBP-1c) genes, along with a notable decrease in hepatocyte nuclear factor 4 Alpha (HNF4A) gene expression compared to the control and sham groups. Furthermore, CsA treatment led to a substantial elevation in plasma lipids (LDL, cholesterol, triglycerides) and liver enzymes (alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP)), in comparison to the control and sham groups. Furthermore, fibrotic changes were detected in the CsA group through Masson trichrome staining. Curcumin consumption resulted in a considerable improvement in histological disorders and molecular mediators involved in liver injury following CsA treatment. Consequently, these findings collectively suggest that CsA can exert deleterious effects on liver tissue, manifesting as lipid homeostasis disorders, as evidenced by alterations in FAT/CD36, PTP1B, and HNF4A gene expression. The findings of this study suggest that the use of curcumin, a natural antioxidant and anti-inflammatory agent, can mitigate the adverse effects of CsA on liver tissue by restoring lipid homeostasis. - Source: PubMed
Publication date: 2025/02/01
Shirpoor ASamadi MGholizadeh-Ghaleh Aziz SNaderi R - Over 80% of patients with pancreatic cancer experience cachexia, characterized by severe muscle and fat loss. While all the mechanistic understanding comes from preclinical models, the translatable nature of these findings to humans remains a critical gap due to the limited knowledge of human cachexia biology. - Source: PubMed
Publication date: 2025/09/04
Narasimhan AshokZhong XiaolingCounts Brittany RYoung AndrewCao ShaWan JunLiu ShengKoniaris Leonidas GZimmers Teresa A - Vitiligo is an autoimmune disorder with a complex genetic and epigenetic aetiology, characterised by progressive skin depigmentation. Recent advancements in artificial intelligence (AI) have greatly impacted the understanding, diagnosis, and treatment of vitiligo. The genetic basis of vitiligo is linked to multiple single nucleotide polymorphisms (SNPs) in genes associated with immune function, apoptosis, and melanogenesis, necessitating the integration of AI for more efficient diagnostic tools and personalised therapies. Genome-wide association studies (GWAS) have identified approximately 50 vitiligo-susceptibility genes, including PTPN1, PTPN22, NLRP1, FASLG, and TYR. These genes influence the immune response and melanocyte function, with the transcription factor Nuclear Factor kappa B (NF-kB), playing a central role in inflammatory responses and redox signaling induced by oxidative stress, in conjunction with antioxidant enzymes such as GPx, GST, SOD, and CAT. AI technologies offer a promising avenue for diagnosing vitiligo by combining genetic, clinical, and imaging data, allowing for more accurate classification and personalised treatment strategies. By analysing vast datasets, AI algorithms can identify patterns within complex genetic markers and clinical features, facilitating earlier and more precise detection of vitiligo. Furthermore, AI-driven approaches can optimise therapeutic monitoring, enabling real-time treatment efficacy and disease progression assessment. Integrating AI in vitiligo genetic diagnostics can revolutionise the monitoring of the disorder, improving patient outcomes through personalised, data-driven interventions. - Source: PubMed
Kocić HristinaLotti TorelloJevtović-Stoimenov TatjanaWollina UweValle YanLukić StevoKlisić Aleksandra - Resveratrol (RSV), a polyphenol found in a variety of berries and wines, is known for its anti-inflammatory, anticancer, and antioxidant properties. It has been suggested that RSV may play a role in the regulation of metabolic disorders, including diabetes and insulin resistance. However, in recent years, it has been reported to completely inhibit Akt kinase function in liver cells. Akt is a central protein involved in the metabolic function of insulin and is regulated by the phosphatidylinositol-3-kinase (PI3K) pathway. In this study, we examined the effect of RSV on insulin-induced insulin receptor (IR) phosphorylation and proteins involved in the PI3K/Akt pathway in a hepatic cell model, clone 9 (C9), and in hepatoma cells, Hepa 1-6 (H1-6). In both cell lines, RSV inhibited tyrosine phosphorylation of IR and insulin-induced activation of Akt. We also evaluated the effect of RSV on the activation of protein tyrosine phosphatase 1B (PTP1B), which is associated with IR dephosphorylation, and found that RSV increased PTP1B-Tyr phosphorylation in a time- and concentration-dependent manner. Furthermore, we found that the protein kinase C (PKC) inhibitors BIM and Gö6976 prevented the inhibition of Akt phosphorylation by RSV and increased the phosphorylation of Ser/Thr residues in IR, suggesting that PKC is involved in the inhibition of the insulin pathway by RSV. Thus, classical PKC isoforms impair the PI3K/Akt pathway at the IR and GSK3 and GS downstream levels; however, IRS-Tyr phosphorylation remains unaffected. These results suggest that RSV can lead to insulin resistance by activating PTP1B and PKC, consequently affecting glucose homeostasis in hepatic cells. - Source: PubMed
Publication date: 2025/08/01
Hernández-González Karla DVinchira-Lamprea Monica AHernandez-Aranda JudithOlivares-Reyes J Alberto