MYPT

Last update 08 May 2025

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100 Clinical Results associated with MYPT

100 Translational Medicine associated with MYPT

0 Patents (Medical) associated with MYPT

1,175

Literatures (Medical) associated with MYPT

01 Aug 2025·Computational Biology and Chemistry

The potential mechanisms by which Xiaoyao Powder may exert therapeutic effects on thyroid cancer were examined at various levels

Article

Author: Lei, Xiaoli ; Huang, Yanqin ; Zhang, Xinying ; Huang, Jiaxi ; Wang, Feifei

BACKGROUNDThyroid cancer (TC) is the most prevalent endocrine malignancy, with a rising incidence necessitating safer treatment strategies to reduce overtreatment and its side effects. Xiaoyao Powder (XYP), a widely used herbal formula, shows promise in treating TC. This study aims to investigate the mechanisms by which XYP may affect TC.METHODSThe components of XYP were identified through database retrieval, and targets related to TC were collected to construct a target network for key screening. GEO dataset samples analyzed immune cells and identified significantly differentially expressed core genes (SDECGs). Based on SDECG expression and clustering, samples were classified for comparison. WGCNA was employed to identify gene modules linked to clinical characteristics. ML models screened characteristic genes and constructed a nomogram validated using another GEO dataset. MR methods explored causal relationships between genes and TC.RESULTSThe top ten active components of XYP were identified, along with 27 SDECGs that exhibited significant differences in immune cell infiltration between TC patients and normal controls. The nomogram effectively predicted TC risk, validated through ROC curves. Key characteristic genes included SMIM1, PPP1R16A, KIAA1462, DNAJC22, and EFNA5.CONCLUSIONXYP may treat TC by regulating SMIM1, PPP1R16A, KIAA1462, DNAJC22, EFNA5, and associated immune pathways; this provides theoretical support for its potential mechanisms.

01 Apr 2025·Physiological Reports

Effects of Rho inhibitors on membrane depolarization‐induced contraction of male rat caudal arterial smooth muscle

Article

Author: Ishii‐Nozawa, Reiko ; Aida, Kazuki ; Mita, Mitsuo

AbstractWe previously reported that depolarization of the vascular smooth muscle plasma membrane activates the Ca2+‐dependent proline‐rich tyrosine kinase 2 (Pyk2) upstream of the RhoA/Rho‐associated kinase (ROCK) pathway, leading to phosphorylation of the myosin‐targeting subunit of myosin light chain phosphatase (MYPT1) and the 20 kDa light chain of myosin (LC20). However, the mechanism whereby Pyk2 activates RhoA remains unclear. It is conceivable that Rho guanine nucleotide exchange factors (RhoGEFs) may link activated Pyk2 to RhoA activation through phosphorylation and activation of RhoGEFs. In this study, we investigated the activation of RhoA and RhoGEFs in membrane depolarization‐induced contraction of rat caudal arterial smooth muscle. Rhosin, a RhoA inhibitor, concentration‐dependently inhibited both the phasic and tonic components of the 60 mM K+‐induced contraction, and the inhibition was particularly prominent in the tonic contraction. On the contrary, Y16, a RhoGEF inhibitor, had little inhibitory effect. Moreover, phosphorylation of MYPT1 was increased at Thr697 and Thr855 by 60 mM K+ stimulation for 15 min, and this increase in MYPT1 phosphorylation was inhibited in the presence of Rhosin, but not Y16. We conclude that Pyk2 activated in response to Ca2+ entry induced by depolarization may cause activation of Y16‐insensitive RhoGEFs and RhoA, resulting in sustained contraction.

01 Apr 2025·American Journal of Respiratory Cell and Molecular Biology

SOX17 Prevents Endothelial–Mesenchymal Transition of Pulmonary Arterial Endothelial Cells in Pulmonary Hypertension through Mediating TGF-β/Smad2/3 Signaling

Article

Author: Zhou, Wei ; Pan, Zongfu ; Yuan, Mengnan ; Hu, Xiaoping ; Huang, Ping ; Zhang, Yiwen ; Zhan, Zibo ; Zheng, Shuilian ; Cheng, Yili ; Cai, Anqi ; Zou, Xiaozhou ; Liu, Ting

Endothelial-to-mesenchymal transition (EndMT) has been reported to contribute to pulmonary vascular remodeling in patients with pulmonary hypertension (PH). Our study demonstrates that SOX17, a member of the SOX (SRY-Box) transcription factor family, plays a role in regulating pulmonary arterial homeostasis through extracellular vesicles in an autocrine and paracrine manner. However, the role of SOX17 in mediating EndMT of pulmonary arterial endothelial cells (PAECs) and its intracellular mechanisms remain unclear. Here we present evidence showing that downregulation of SOX17 expression is accompanied by significant pulmonary arterial EndMT and activation of the TGF-β/Smad2/3 signaling pathway in patients with idiopathic PH and rats with PH induced by Sugen 5416/hypoxia. In primary human PAECs, canonical TGF-β (transforming growth factor-β) signaling inhibits the expression of SOX17. Overexpression of SOX17 reverses TGF-β- and hypoxia-induced EndMT. These findings suggest that SOX17 is essential for human PAECs to undergo TGF-β-mediated EndMT. Mechanistically, our data demonstrate that SOX17 prevents TGF-β-induced EndMT by suppressing ROCK1 (Rho-associated kinase 1) expression through binding to the specific promoter region of ROCK1, thereby inhibiting MYPT1 (myosin phosphatase target subunit 1) and MLC (myosin light chain) phosphorylation. Furthermore, we show that Tie2-Cre rats with endothelial cell-specific overexpression of SOX17 are protected against Sugen/hypoxia-induced EndMT and subsequent pulmonary vascular remodeling. Consistent with the in vitro results, compared with Tie2-Cre rats treated with Sugen/hypoxia alone, rats overexpressing SOX17 exhibited reduced levels of ROCK1 as well as decreased phosphorylation levels of MYPT1 and MLC. Overall, our studies unveil a novel TGF-β/SOX17/ROCK1 pathway involved in regulating PAECs' EndMT process, and we propose the targeting of SOX17 as a potential therapeutic strategy for alleviating pulmonary vascular remodeling in PH.

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