Last update 01 Nov 2024

MYL

Last update 01 Nov 2024

Basic Info

Synonyms-

Introduction-

Drugs associated with MYL

CN116410310

Patent Mining

Target

MYL3

Mechanism-

Active Org.

PerGrande BioTech Development Co., Ltd.

Originator Org.

PerGrande BioTech Development Co., Ltd.

Active Indication

Infectious Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

EDG-6289

Target

MYLPF

Mechanism

MYLPF inhibitors

Active Org.-

Originator Org.

Edgewise Therapeutics, Inc.

Active Indication-

Inactive Indication

Cerebral Palsy [+5]

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MYL

100 Translational Medicine associated with MYL

0 Patents (Medical) associated with MYL

3,880

Literatures (Medical) associated with MYL

01 Dec 2024·Environmental Research

Insights into the developmental and cardiovascular toxicity of bixafen using zebrafish embryos and larvae

Article

Author: Xu, Wenping ; Zhang, Yang ; Fang, Fei ; Zhu, Yanjuan ; Cheng, Jiagao

Bixafen (BIX), a member of the succinate dehydrogenase inhibitor (SDHI) class of fungicides, has seen a surge in interest due to its expanding market presence and positive development outlook. However, there is a growing concern about its potential harm to aquatic life, largely due to its resistance to breaking down in the environment. In this study, we thoroughly examined the toxicological impact of BIX on zebrafish as a model organism. Our results revealed that BIX significantly hindered the development of zebrafish embryos, leading to increased mortality, hatching failures, and oxidative stress. Additionally, we observed cardiovascular abnormalities, including dilated cardiac chambers, reduced heart rate, sluggish blood circulation, and impaired vascular function. Notably, BIX also altered the expression of key genes involved in cardiovascular development, such as myl7, vmhc, nkx2.5, tbx5, and flt1. In summary, BIX was found to induce developmental and cardiovascular toxicity in zebrafish, underscoring the risks associated with SDHI pesticides and emphasizing the need for a reassessment of their impact on human health. These findings are crucial for the responsible use of BIX.

01 Dec 2024·Food Chemistry: X

Unveils key proteins in Xinjiang goat muscle linked to post-mortem meat quality: A TMT-based proteomic analysis

Article

Author: Zhang, Wei ; Al-Wraikat, Majida ; Liu, Yongfeng ; Zhu, Yanlei ; Abubaker, Mohamed Aamer ; Ma, Xiaolin ; Zhang, Rui ; Zhang, Duoduo ; Gu, Minghui ; Zhang, Shiquan ; Yu, Hong

An extensive proteomic analysis utilizing the tandem mass tag (TMT) method was conducted to investigate the changes in protein expression in the longissimus dorsi muscle of Xinjiang goats over various post-mortem intervals: immediately after death within 0 h, 12 h, 24 h and 48 h. The investigation carefully identified around 108 proteins that showed significant changes in expression during these intervals. Among these proteins, six were highlighted for their crucial roles in muscle growth and differentiation of muscle fibers post-mortem. These proteins, namely COL12A1, MRPL46, CTNNB1, MYH1, CAPZA1, and MYL9, have a direct effect on the meat's quality attributes, such as tenderness and color. Further discuss observed a progressive increase in the expression of proteins linked with oxidative metabolism (MSRB2, ENOX1, LOC102170282, GSTM1, and AOC3) as the post-mortem aging period extended, particularly between 24 h to 48 h. These proteins are instrumental in defining the color and flavor profiles of goat meat, underscoring the importance of precise processing and storage conditions to preserve meat quality during the critical aging phase. This enhanced understanding of protein expression dynamics offers significant implications for optimizing meat quality and provides a scientific basis for post-mortem handling practices in the goat meat industry.

01 Dec 2024·Biological Trace Element Research

Zinc as a Mediator Through the ROCK1 Pathway of Cognitive Impairment in Aluminum-Exposed Workers: A Clinical and Animal Study

Article

Author: Li, Xianlin ; He, Chanting ; Shang, Nan ; Zheng, Xiaojun ; Niu, Qiao ; Zhang, Lan ; Wang, ShanShan ; Zhang, Ling

Aluminum (Al) exposure was implicated in neurodegenerative diseases and cognitive impairment, yet the involvement of zinc (Zn) and its mechanism in Al-induced mild cognitive impairment (MCI) remains poorly understood. The objective is to explore the role of Zn in Al-induced cognitive impairment and its potential mechanisms. Montreal cognitive assessment (MoCA) test scores and serum Al, Zn from Al industry workers were collected. A mediation analysis was performed to evaluate the role of serum Zn among serum Al and MoCA test scores. Subsequently, an Al-exposure study was conducted on a rat model categorized into control, low-, medium-, and high-dose groups. After a Morris Water Maze test and detection of Al, Zn content in the hippocampus, integrated transcriptomic and proteomic analyses between the control group and the high-dose group were performed to identify the differentially expressed genes (DEPs), proteins (DEPs), and pathways. To corroborate these findings, quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting (WB) were selected to identify the gene and protein results. Zn overall mediates the relationship between serum Al and cognitive function (mediation effect 17.82%, effect value = - 0.0351). In the Al-exposed rat model, 734 DEGs, 18 miRNAs, 35 lncRNAs, 64 circRNAs, and 113 DEPs were identified between the high-dose group and the control group. Among them, ROCK1, DMD, and other four DEPs were identified as related to zinc finger proteins (ZNF). Co-enrichment analyses of the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) linked these changes to the RHOA/ROCK1 signaling axis. ZNF-related proteins Rock1, DMD, and DHX57 in the high-dose group were downregulated (p = 0.006, 0.003, 0.04), and the expression of Myl9, Rhoa, miR431, and miR182 was also downregulated (p = 0.003, 0.032, 0.032, and 0.046). These findings also show correlations between Al, Zn levels in the hippocampus, water maze performance, and expressions of Myl9, Rhoa, miR431, miR182, DMD, ROCK1, and DHX57, with both negative and positive associations. Based on the results, we determined that Zn was involved in Al-induced MCI in Al workers and Al-exposed rat models. Al exposure and interaction with Zn could trigger the downregulation of ZNF of ROCK1, DMD, and DHX57. miR431, miR182 regulate RHOA/ROCK1 was one of the Zn-involved pathways in Al-induced cognitive impairment.

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MYL

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