STRN

Last update 08 May 2025

Basic Info

Synonyms

PPP2R6A, striatin, STRN

+ [1]

Introduction

Calmodulin-binding scaffolding protein which is the center of the striatin-interacting phosphatase and kinase (STRIPAK) complexes (PubMed:18782753). STRIPAK complexes have critical roles in protein (de)phosphorylation and are regulators of multiple signaling pathways including Hippo, MAPK, nuclear receptor and cytoskeleton remodeling. Different types of STRIPAK complexes are involved in a variety of biological processes such as cell growth, differentiation, apoptosis, metabolism and immune regulation (Probable).

100 Clinical Results associated with STRN

100 Translational Medicine associated with STRN

0 Patents (Medical) associated with STRN

243

Literatures (Medical) associated with STRN

01 May 2025·American Journal of Surgical Pathology

High-Grade Papillary Thyroid Carcinoma, Diffuse Sclerosing Subtype

Article

Author: Ganly, Ian ; Ghossein, Ronald A. ; Shaha, Ashok R. ; Scholfield, Daniel W. ; Qin, Howard ; Xu, Bin

High-grade differentiated thyroid carcinoma is a novel classification defined by elevated mitotic count (MC) of ≥5/2 mm2 and/or tumor necrosis. It may assume a phenotype of papillary thyroid carcinoma, diffuse sclerosing subtype (PTC-DS), and can be termed HGPTC-DS. A detailed clinicopathologic review was conducted on a large series of 18 cases of HGPTC-DS. A control group of 41 PTC-DSs with genomic data was also included. Histologically, HGPTC-DS showed typical features of PTC-DS and HG areas, often exhibiting solid architecture of uniform squamoid cells admixed with tumor necrosis, frequently the comedo type. All HGDTC-DSs had tumor necrosis. The MC was often low (median 1/2 mm2). PTC nuclear features were retained and no nuclear pleomorphism was seen. HGPTC-DS was often subjected to misdiagnosis. Among the 7 external cases, the initial diagnosis was anaplastic carcinoma in 1 and PTC in 5. Compared with PTC-DS, HGPTC-DS was associated with positive resection margin, AJCC eighth edition pT3b and pT4a/4b disease, gross extrathyroidal extension (ETE), a higher number of regional lymph nodes metastasis, a larger size of nodal metastasis, decreased recurrence-free survival (RFS) and regional recurrence-free survival (P<0.05). Among the 9 HGPTC-DSs sequenced, 5 harbored RET fusions, 2 had STRN::ALK fusion, and 1 had BRAF p.V600E mutation. In conclusion, HGPTC-DS is a rare high-grade carcinoma characterized by uniform squamoid area with comedo-type tumor necrosis, high pT stage, gross ETE, large volume nodal metastasis, poor RFS, and RRFS. Given its rarity, it may be subjected to misdiagnosis as PTC and anaplastic carcinoma.

01 Mar 2025·Acta Physiologica

Striatin protein's role in human cardiomyocytes: Connection to electrical dysregulation and sudden cardiac death

Author: Hamdani, Nazha ; El‐Battrawy, Ibrahim ; Akin, Ibrahim

17 Feb 2025·Cancer Research

HBV Remodels PP2A Complexes to Rewire Kinase Signaling in Hepatocellular Carcinoma

Article

Author: Gordan, John D. ; Von Dollen, John ; Shokat, Kevan M. ; Eckhardt, Manon ; Jang, Gwendolyn M. ; Che, Li ; Theis, Fabian J. ; Lim, Huat Chye ; Ideker, Trey ; Xu, Zhong ; Levin, Rebecca S. ; Li, Xiaolei ; Singh, Ananya ; Yoon, Alex ; Pitea, Adriana ; Chen, Xin ; Krogan, Nevan J. ; McCarthy, Elizabeth ; Kelley, Robin K. ; Zhang, Wei ; Swaney, Danielle L. ; Choi, Alex L. ; Hu, Junjie ; Turnham, Rigney E. ; Webber, James T. ; Bandyopadhyay, Sourav ; Chan, Gary K.L.

AbstractHepatitis B virus (HBV) infections promote liver cancer initiation by inducing inflammation and cellular stress. Despite a primarily indirect effect on oncogenesis, HBV is associated with a recurrent genomic phenotype in hepatocellular carcinoma (HCC), suggesting that it impacts the biology of established HCC. Characterization of the interaction of HBV with host proteins and the mechanistic contributions of HBV to HCC initiation and maintenance could provide insights into HCC biology and uncover therapeutic vulnerabilities. In this study, we used affinity purification mass spectrometry to comprehensively map a network of 145 physical interactions between HBV and human proteins in HCC. A subset of the host factors targeted by HBV proteins were preferentially mutated in non–HBV-associated HCC, suggesting that their interaction with HBV influences HCC biology. HBV interacted with proteins involved in mRNA splicing, mitogenic signaling, and DNA repair, with the latter set interacting with the HBV oncoprotein X (HBx). HBx remodeled the PP2A phosphatase complex by excluding striatin regulatory subunits from the PP2A holoenzyme, and the HBx effects on PP2A caused Hippo kinase activation. In parallel, HBx activated mTOR complex 2, which can prevent YAP degradation. mTOR complex 2–mediated upregulation of YAP was observed in human HCC specimens and mouse HCC models and could be targeted with mTOR kinase inhibitors. Thus, HBV interaction with host proteins rewires HCC signaling rather than directly activating mitogenic pathways, providing an alternative paradigm for the cellular effects of a tumor-promoting virus.Significance: Integrative proteomic and genomic analysis of HBV/host interactions illuminated modifiers of hepatocellular carcinoma behavior and key signaling mechanisms in advanced disease, which suggested that HBV may have therapeutically actionable effects.

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