PTP1B
- Known as:
- PTP1B
- Catalog number:
- 000331A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PTP1B
Related genes to: PTP1B
- 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
Related products to: PTP1B
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- Colorectal cancer remains a major clinical challenge, and dual targeting of PTPN1 and PTPN2 represents a promising strategy to modulate conserved phosphatase signaling relevant to tumor biology and immune regulation. Here, we identified and prioritized two compounds, HIT101308137 and HIT104293658, as dual compatible chemotypes for PTPN1 and PTPN2 through a structure guided workflow integrating pocket comparison, ligand based interaction hypothesis generation, and structure based evaluation under static and dynamic conditions. Sequence and structural analyses supported high conservation of the catalytic pocket, providing a feasible basis for dual target coverage. Screening and post docking tri metric prioritization nominated three shared candidates, of which HIT101308137 and HIT104293658 were further differentiated by microsecond molecular dynamics simulations and interaction occupancy profiling. In both targets, the candidates preserved an Arg centered anchoring pattern within the P loop, while exhibiting distinct binding behaviors: HIT101308137 maintained a more co crystal like, catalytic core coupled interaction network with stronger persistence of contacts associated with the WPD region, whereas HIT104293658 displayed a more entrance biased interaction distribution consistent with increased pose reorganization. In CCK 8 viability assays, HIT101308137 and HIT104293658 produced reproducible dose dependent reductions in viability in HCT116 and SW480 cells, while showing limited effects in NCM460 and FHC cells within the same concentration window. Together, these results nominate HIT101308137 and HIT104293658 as starting points for dual target optimization and provide a mechanistic rationale to enhance cellular potency while maintaining low impact on normal colonic epithelial cells. - Source: PubMed
Publication date: 2026/04/17
Huang ChaojieChen JingyunChen RuiCao Liping - The clinical management of bladder cancer is severely impeded by high recurrence rates and the rapid emergence of chemoresistance, necessitating the discovery of novel therapeutic agents with distinct mechanisms of action. Dehydrodiisoeugenol (DHE), a bioactive neolignan, exhibits potent anti-tumor efficacy, yet its direct molecular targets and mode of action remain elusive. : To deconvolute the mechanism of DHE, we integrated a phenotypic screening approach using 2D cell lines and 3D patient-derived organoids with a chemoproteomics-based activity-based protein profiling (ABPP) strategy. We synthesized a functionalized photoaffinity probe to capture the specific interactome of DHE under physiological conditions and validated targets via cellular thermal shift assays (CETSA), quantitative mass spectrometry, and 100 ns molecular dynamics (MD) simulations. : DHE exhibited potent dose-dependent cytotoxicity in bladder cancer cells, with IC50 values of 39.23 μM in T24 and 34.58 μM in 5637 cells. In 3D patient-derived organoids, DHE significantly reduced viability ( < 0.0001). Using a dual-filtering ABPP strategy, we identified 65 high-confidence candidate targets, prioritizing PTPN1 (PTP1B) as the primary functional interactor. Comparative molecular docking and 100 ns MD analyses showed that multiple stereoisomers of DHE could adopt plausible PTPN1-binding modes. Mechanistically, organoid proteomics indicated that DHE engagement with PTPN1 disrupts ER membrane homeostasis, thereby modulating the PI3K-Akt signaling axes. : These findings establish PTPN1 as a critical druggable vulnerability in bladder cancer and define the molecular basis for the therapeutic potential of DHE. This study highlights the power of combining chemoproteomics with physiological 3D models to accelerate the translation of natural products into precision cancer therapies. - Source: PubMed
Publication date: 2026/04/21
Zhai ZhaoWu FanSheng GuoliJia BinJia BolinDu PengZhang Yong - : EBV is an oncogenic virus linked to NPC and GC, driving cisplatin resistance. Resveratrol has anticancer activity, but its targets and mechanisms against EBV-positive cancers remain unclear. : We assessed resveratrol's cytotoxicity in EBV-positive cells via functional assays, identified targets by chemical similarity search and molecular docking, and validated PTPN1 via in vitro experiments and nude mouse xenograft models. : Resveratrol inhibited EBV-positive cell viability in a time- and concentration- dependent manner, with IC50 values ranging from 35.85 to 145.7 μM across different cell lines at 24-72 h. Apoptosis rates increased by approximately 2- to 4-fold after 80 μM resveratrol treatment for 24 h. Resveratrol directly targeted PTPN1 (docking score = -4.89) and promoted its degradation via the proteasome pathway, as MG132 reversed this effect. Notably, resveratrol synergized with cisplatin (combination index < 1) to reverse cisplatin resistance in both in vitro and in vivo models. Furthermore, resveratrol induced EBV lytic reactivation through ROS production, as evidenced by the increased expression of BZLF1, BMRF1, and BALF2, which was attenuated by the ROS scavenger NAC. : Our findings identify PTPN1 as a direct anticancer target of resveratrol in EBV-positive cancers. Resveratrol enhances the therapeutic efficacy of cisplatin via PTPN1 proteasomal degradation and induces EBV lytic reactivation through ROS accumulation. These findings provide a mechanistic basis for the development of novel combination therapies targeting EBV-associated malignancies. - Source: PubMed
Publication date: 2026/04/09
Liu NaLi YueshuoTang MinCao YaShang LiShi Feng - Our research endeavored to formulate a patient-specific prognostic algorithm and elucidate the interconnection between critical genetic polymorphisms at PTPN1 loci and the predisposition to small vessel pathologies in Han Chinese subjects presenting with T2DM. From January 1, 2019, to June 30, 2024, a total of 3,847 patients with T2DM were enrolled in this cross-sectional case-control study. They were grouped into four groups by means of fundus examination and renal function assessment: the T2DM alone group (T2DM group), the T2DM combined with diabetic retinopathy (DR) group (T2DM + DR group), the T2DM combined with diabetic nephropathy (DN) group (T2DM + DN group), and the T2DM combined with DR + DN group (T2DM + DR +DN group). The genotypes of four SNP loci (rs968289, rs6067484, rs2206521, rs754118) of the PTPN1 gene were detected by PCR-RFLP. To evaluate the association between SNP loci and microvascular complications, multivariate logistic regression analysis was employed, followed by LASSO regression for variable selection to develop a nomogram prediction model. The rs968289-GG genotype demonstrated a statistically significant link to the risk of DR (adjusted OR = 1.47, 95%CI: 1.15-1.88, P = 0.002); the rs6067484-CC genotype exhibited a significant relationship with the risk of DN (adjusted OR = 1.58, 95%CI: 1.21-2.06, P < 0.001); The rs2206521-AA genotype significantly correlated with the risk of DR + DN co-morbidity (adjusted OR = 1.69, 95%CI: 1.28-2.24, P < 0.001). The column-line graphical model constructed based on nine independent predictors had AUCs of 0.823 and 0.808 in the training and validation sets, with sensitivity and specificity of 76.4%/78.9% and 74.2%/80.1%, respectively. Significant associations were observed between specific genotypic variants at the PTPN1 gene's rs968289, rs6067484 and rs2206521 loci and microvascular complication risk in Chinese Han T2DM patients. The column-line graph prediction model integrating genetic markers and clinical indicators has good discriminative ability and clinical utility, providing an important tool for individualized risk assessment and precise prevention of diabetic microvascular complications. - Source: PubMed
Publication date: 2026/05/01
Dong QianXu HuanXu PengjieShen DanqingLiu Jiang - PTPN1 and PTPN2 are interesting targets for immuno-oncology due to their ability to modulate IFNγ signaling and T-cell activity. We report the discovery of benzothiophene difluoromethyl phosphonate (DFMP) inhibitors with potent dual PTPN1/PTPN2 activity. Structure-based design and a late-stage Ir-catalyzed C-H borylation enabled C5/C7-disubstituted designs that produced a marked inflection in potency. Systematic vector optimization improved potency, selectivity, and pharmacokinetic properties. Mechanistic studies identified SLC19A1 as a key transporter mediating cellular uptake. Lead compound exhibited good potency, high selectivity, favorable PK, and dose-dependent pSTAT1 induction in a MC38 mouse model. These results establish compound as promising structurally differentiated tool to study PTPN1/N2 inhibition and underscore the importance of SLC19A1 in the transport of DFMPs. - Source: PubMed
Publication date: 2026/04/29
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