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Last update 08 May 2025

TEP1

Last update 08 May 2025

Basic Info

Synonyms

p240, p80 telomerase homolog, telomerase associated protein 1

+ [8]

Introduction

Component of the telomerase ribonucleoprotein complex that is essential for the replication of chromosome termini (PubMed:19179534). Also a component of the ribonucleoprotein vaults particle, a multi-subunit structure involved in nucleo-cytoplasmic transport (By similarity). Responsible for the localizing and stabilizing vault RNA (vRNA) association in the vault ribonucleoprotein particle. Binds to TERC (By similarity).

Drugs associated with TEP1

CN117736338

Patent Mining

Target

KGF-2 x TEP1

Mechanism-

Active Org.

Wenzhou Medical College

Originator Org.

Wenzhou Medical College

Active Indication

Neurologic Manifestations

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with TEP1

100 Translational Medicine associated with TEP1

0 Patents (Medical) associated with TEP1

740

Literatures (Medical) associated with TEP1

31 Dec 2025·Artificial Cells, Nanomedicine, and Biotechnology

IRES activation: HK2 and TPI1 glycolytic enzymes play a pivotal role in non-neuronal cell survival under hypoxia

Article

Author: Devi, Sushma ; Hussain, Mahboob-Ul- ; Arora, Poonam ; Rahamathulla, Mohamed ; Banday, Muddasir Sharief ; Kumar, Manish ; Shivanandappa, Thippeswamy Boreddy ; Najar, Imtiyaz Ahmed ; Pasha, Ismail ; Ismail, Rehana ; Ahmed, Mohammed Muqtader

Hypoxia-induced brain damage can cause consciousness, memory failure and death. HK2 and TPI1 were investigated to see how they change hypoxia sensitivity in neurons and non-neurons. Hypoxia sensitivity is determined by the differential overexpression of both important glycolytic enzymes in neuronal and non-neuronal cells. C6 glioma cells expressed greater HK2 and TPI1 protein than neuro 2A cells, which were more sensitive to hypoxia-induced cell death by MTT and lactate dehydrogenase leakage assay. After 48 h of hypoxia, C6 glioma cells displayed substantial protein upregulation of HK2 and TPI1 glycolytic proteins but not mRNA. Hypoxia did not raise HK2 and TPI1 mRNA transcription, pointing at post-transcriptional protein regulation. Using di-cistronic and promoter-less di-cistronic assays, we discovered significant IRES regions in HK2 and TPI1 mRNA's 5'UTR, more active in C6 glioma cells with polypyrimidine tract binding (PTB) protein. We concluded that non-neuronal cells varied in HK2 and TPI1 overexpression, altering their vulnerability to hypoxia-induced cell death. Adjusting HK2, TP1 and PTB levels may prevent hypoxia-induced brain cell death. These results offer new information on glycolytic enzyme modulation under hypoxia, crucial for comprehending cell survival in hypoxic situations. This could affect situations like neurodegenerative illnesses or ischaemic injuries, where hypoxia-induced cell death is crucial.

01 Apr 2025·Journal of the American Academy of Dermatology

A randomized phase III study to compare efficacy and safety of BAT2206 (proposed ustekinumab biosimilar) with reference ustekinumab in patients with moderate to severe plaque psoriasis

Article

Author: Qi, Yunpeng ; Mekokishvili, Lally ; Yang, Xiaolei ; Zheng, Min ; Dong, Qingfeng ; Man, Xiaoyong ; Pulka, Grażyna ; Żebrowska, Agnieszka ; Deng, Yunhua ; Zaharieva, Katya ; Gu, Cailing

BACKGROUNDBAT2206 is a proposed biosimilar to reference ustekinumab (UST; Stelara).OBJECTIVESTo compare the efficacy and safety of BAT2206 with UST at 2 treatment periods, ie, a 28-week initial treatment period 1 (TP1) and a 24-week secondary TP2. This article describes the results of TP1.METHODSIn this randomized, double-blind, phase III study, adult patients with moderate to severe plaque psoriasis were randomized (1:1) to receive 45 or 90 mg of BAT2206 or UST until week 28 in TP1, depending on their baseline body weight. The primary end point was the percent change from baseline in Psoriasis Area and Severity Index score to week 8 or 12. The secondary end points included safety, pharmacokinetics, and immunogenicity parameters.RESULTSIn all, 278 patients were each randomized into the BAT2206 or UST groups. At weeks 8 and 12, the least squares mean difference (standard error) for percent change from baseline in Psoriasis Area and Severity Index score was 0.964 (1.8952) and 1.774 (1.4912), respectively, and the least squares mean difference confidence intervals all completely fell within the predefined equivalence margins. Comparable results were observed between the treatment groups for secondary end points.LIMITATIONSOwing to the length limit, this article only described the findings from TP1.CONCLUSIONSBAT2206 and UST were comparable in terms of efficacy, safety, pharmacokinetics, and immunogenicity.

01 Apr 2025·Molecular and Cellular Biochemistry

Endothelium Piezo1 deletion alleviates experimental varicose veins by attenuating perivenous inflammation

Article

Author: Zhao, Jiani ; Wang, Wei ; Ling, Jin ; Liu, Shuai ; Liu, Yu ; Xiong, Yacheng

Previous large-scale genetic studies have prioritized the causal genes piezo type mechanosensitive ion channel component 1 (PIEZO1) and castor zinc finger 1 (CASZ1) associated with varicose veins (VVs). This study aims to evaluate their roles in both clinical and experimental VVs. In this study, we investigated abundance of PIEZO1 and CASZ1 in both varicose and normal veins from the same patients. Yoda1 (a selective PIEZO1 agonist, 2.6 mg/kg/day) or vehicle was administered intraperitoneally for 3 weeks to evaluate the effect of PIEZO1 activation on experimental VVs. Subsequently, endothelial Piezo1 deletion mice (Piezo1^iΔEC mice) were generated to explored the role of endothelial PIEZO1 on VVs. Laser speckle imaging, flow cytometry, cell tracing with Evans blue or rhodamine-6G, and histopathological staining were utilized to evaluate the pathophysiology of VVs. Our results showed that mRNA expression of PIEZO1, but not CASZ1, was abundant and increased in clinical VVs. The Piezo1^tP1-td mice revealed endothelium-specific expression of PIEZO1 in mice veins. By establishing iliac vein ligation-induced VVs in mice, Yoda1 exacerbated experimental VVs with increased inflammatory cell infiltration. Subsequently, endothelial Piezo1 deletion (Piezo1^iΔEC mice) alleviated experimental VVs and vascular remodeling by directly reducing vascular permeability and leukocyte-endothelium interactions compared to the control (Piezo1^fl/fl mice). PIEZO1 is highly expressed in clinical VVs, meanwhile, activation or inhibition of PIEZO1 exerts a remarkable effect on experimental VVs. Furthermore, Piezo1 may constitute a potential therapeutic approach for the medical treatment of VVs.

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TEP1

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