Last update 01 Nov 2024

MYH9

Last update 01 Nov 2024

Basic Info

Synonyms

Cellular myosin heavy chain, type A, DFNA17, EPSTS

+ [13]

Introduction

Cellular myosin that appears to play a role in cytokinesis, cell shape, and specialized functions such as secretion and capping. Required for cortical actin clearance prior to oocyte exocytosis (By similarity). Promotes cell motility in conjunction with S100A4 (PubMed:16707441). During cell spreading, plays an important role in cytoskeleton reorganization, focal contact formation (in the margins but not the central part of spreading cells), and lamellipodial retraction; this function is mechanically antagonized by MYH10 (PubMed:20052411).

Drugs associated with MYH9

NMMHC IIA Inhibitor Compoud-006(Protheragen, Inc.)

Target

MYH9

Mechanism

MYH9 inhibitors

Active Org.

Protheragen, Inc.

Originator Org.

Protheragen, Inc.

Active Indication

Thrombosis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

NMMHC IIA Inhibitors

Target

MYH9

Mechanism

MYH9 inhibitors

Active Org.

Protheragen, Inc.

Originator Org.

Protheragen, Inc.

Active Indication

Thrombosis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

WO2022093121

Patent Mining

Target

MYH9

Mechanism-

Active Org.

Agency for Science, Technology & Research

Originator Org.

Agency for Science, Technology & Research

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MYH9

100 Translational Medicine associated with MYH9

0 Patents (Medical) associated with MYH9

1,146

Literatures (Medical) associated with MYH9

31 Dec 2024·Human vaccines & immunotherapeutics

Genomic insights into mRNA COVID-19 vaccines efficacy: Linking genetic polymorphisms to waning immunity.

Article

Author: Chiou, Shih-Hwa ; Hsieh, Min-Jia ; Chen, Yu-Chun ; Chiang, Pin-Hsuan ; Hsieh, Ai-Ru ; Tsai, Ping-Hsing ; Ho, Hsiang-Ling ; Liang, Kung-Hao ; Zhuang, Zi-Qing ; Kao, Zih-Kai

Genetic polymorphisms have been linked to the differential waning of vaccine-induced immunity against COVID-19 following vaccination. Despite this, evidence on the mechanisms behind this waning and its implications for vaccination policy remains limited. We hypothesize that specific gene variants may modulate the development of vaccine-initiated immunity, leading to impaired immune function. This study investigates genetic determinants influencing the sustainability of immunity post-mRNA vaccination through a genome-wide association study (GWAS). Utilizing a hospital-based, test negative case-control design, we enrolled 1,119 participants from the Taiwan Precision Medicine Initiative (TPMI) cohort, all of whom completed a full mRNA COVID-19 vaccination regimen and underwent PCR testing during the Omicron outbreak. Participants were classified into breakthrough and protected groups based on PCR results. Genetic samples were analyzed using SNP arrays with rigorous quality control. Cox regression identified significant single nucleotide polymorphisms (SNPs) associated with breakthrough infections, affecting 743 genes involved in processes such as antigenic protein translation, B cell activation, and T cell function. Key genes identified include CD247, TRPV1, MYH9, CCL16, and RPTOR, which are vital for immune responses. Polygenic risk score (PRS) analysis revealed that individuals with higher PRS are at greater risk of breakthrough infections post-vaccination, demonstrating a high predictability (AUC = 0.787) in validating population. This finding confirms the significant influence of genetic variations on the durability of immune responses and vaccine effectiveness. This study highlights the importance of considering genetic polymorphisms in evaluating vaccine-induced immunity and proposes potential personalized vaccination strategies by tailoring regimens to individual genetic profiles.

31 Dec 2024·Cancer Biology & Therapy

Epigenetic silencing ZSCAN23 promotes pancreatic cancer growth by activating Wnt signaling

Article

Author: Gao, Aiai ; Zhang, Meiying ; Du, Qian ; Guo, Mingzhou ; He, Tao

Pancreatic ductal adenocarcinoma (PDAC) is the most malignant tumor. Zinc finger and SCAN domain-containing protein 23 (ZSCAN23) is a new member of the SCAN domain family. The expression regulation and biological function remain to be elucidated. In this study, we explored the epigenetic regulation and the function of ZSCAN23 in PDAC. ZSCAN23 was methylated in 60.21% (171/284) of PDAC and its expression was regulated by promoter region methylation. The expression of ZSCAN23 inhibited cell proliferation, colony formation, migration, invasion, and induced apoptosis and G1/S phase arrest. ZSCAN23 suppressed Panc10.05 cell xenograft growth in mice. Mechanistically, ZSCAN23 inhibited Wnt signaling by interacting with myosin heavy chain 9 (MYH9) in pancreatic cancer cells. ZSCAN23 is frequently methylated in PDAC and may serve as a detective marker. ZSCAN23 suppresses PDAC cell growth both in vitro and in vivo.

31 Dec 2024·Virulence

Mechanism of PRRSV infection and antiviral role of polyphenols

Review

Author: Zhang, Chunlei ; Pang, Yipeng ; Gong, Xingyu ; Fang, Xingtang ; Chen, Xi ; Wang, Yanhong ; Amona, Fructueux Modeste

Porcine reproductive and respiratory syndrome (PRRS) is associated with the endemic outbreak of fever, anorexia, and abortion in pregnant sows, resulting in an enormous economic impact on the global swine industry. Current mainstream prophylactic agents and therapies have been developed to prevent PRRSV infection; however, they have limited efficacy. Therefore, there is an urgent need to develop novel antiviral strategies to prevent PRRSV infection and transmission. The identification of new PRRSV entry mediators, such as MYH9 and HSPA8; viral apoptotic mimicry; and TIM-induced macropinocytosis, to facilitate infection has led to a novel molecular understanding of the PRRSV infection mechanism, which can be utilized in the development of prophylactic agents and therapies for PRRSV infection. Polyphenols, complex chemical molecules with abundant biological activities derived from microorganisms and plants, have demonstrated great potential for controlling PRRSV infection via different mechanisms. To explore new possibilities for treating PRRSV infection with polyphenols, this review focuses on summarizing the pathogenesis of PRRSV, reviewing the potential antiviral mechanisms of polyphenols against PRRSV, and addressing the challenges associated with the widespread use of polyphenols.

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MYH9

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