Inhibition of BET Family Proteins Suppresses African Swine Fever Virus Infection

Zhao, Yaru; Niu, Qingli; Yang, Saixia; Yang, Jifei; Zhang, Zhonghui; Geng, Shuxian; Fan, Jie; Liu, Zhijie; Guan, Guiquan; Liu, Zhiqing; Zhou, Jia; Hu, Haitao; Luo, Junyu; Yin, Hong

doi:10.1128/spectrum.02419-21

Cited by 8 publications

(3 citation statements)

References 56 publications

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“…BRD2 is reported to interact with many chromatin- and transcriptional activation-related proteins to regulate the transcription of diverse genes [ 32 , 33 , 34 ]. Importantly, several studies have shown that viruses hijacking BRD2 to enhance viral gene transcription is beneficial for viral replication [ 22 , 23 , 35 , 36 ]. Consistent with these findings, we previously found that the expression level of chBRD2 was obviously reduced in both NDV-infected cells and pEGFP-M-transfected cells, which facilitated vRNA synthesis and transcription [ 17 ].…”

Section: Discussionmentioning

confidence: 99%

“…[ 20 ]. In recent years, BRD2 has also been found to participate in the replication of multiple DNA or RNA viruses via interacting with viral proteins [ 21 , 22 , 23 , 24 ]. In our previous studies, we demonstrated that chicken BRD2 (chBRD2) was a novel interacting partner of NDV M protein [ 9 ], and the C-terminus (aa 264–313) of M protein was responsible for direct interaction with the extra-terminal (ET) domain (aa 619–683) of chBRD2 [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

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Mutation of Basic Residues R283, R286, and K288 in the Matrix Protein of Newcastle Disease Virus Attenuates Viral Replication and Pathogenicity

Duan

Shi

Xing

et al. 2023

IJMS

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The matrix (M) protein of Newcastle disease virus (NDV) contains large numbers of unevenly distributed basic residues, but the precise function of most basic residues in the M protein remains enigmatic. We previously demonstrated that the C-terminus (aa 264–313) of M protein interacted with the extra-terminal (ET) domain of chicken bromodomain-containing protein 2 (chBRD2), which promoted NDV replication by downregulating chBRD2 expression and facilitating viral RNA synthesis and transcription. However, the key amino acid sites determining M’s interaction with chBRD2/ET and their roles in the replication and pathogenicity of NDV are not known. In this study, three basic residues—R283, R286, and K288—in the NDV M protein were verified to be responsible for its interaction with chBRD2/ET. In addition, mutation of these basic residues (R283A/R286A/K288A) in the M protein changed its electrostatic pattern and abrogated the decreased expression of endogenic chBRD2. Moreover, a recombinant virus harboring these mutations resulted in a pathotype change of NDV and attenuated viral replication and pathogenicity in chickens due to the decreased viral RNA synthesis and transcription. Our findings therefore provide a better understanding of the crucial biological functions of M’s basic residues and also aid in understanding the poorly understood pathogenesis of NDV.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mutation of Basic Residues R283, R286, and K288 in the Matrix Protein of Newcastle Disease Virus Attenuates Viral Replication and Pathogenicity

Duan

Shi

Xing

et al. 2023

IJMS

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“…The bromodomain terminal (BET) family of proteins, including BRD2, BRD3, BRD4 and BRDT, are epigenetic readers of gene transcriptional regulation ( 54 ). Bromo dopamine-containing protein 4 (BRD4) is the most studied member of the BET family, which interprets the epigenetic code by binding to acetylated histones and non-histones, regulating a variety of cellular processes including cell cycle, cell differentiation and cell proliferation ( 55 ).…”

Section: Synergistic or Accelerating Roles Of Cirrhosis In The Mechan...mentioning

confidence: 99%

Sarcopenia in liver cirrhosis: perspectives from epigenetics and microbiota

Xu,

Pan,

Zhang

et al. 2023

Front. Med.

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Sarcopenia is characterized by the loss of muscle mass and function. It is well known that sarcopenia is often associated with aging, while in recent years, sarcopenia comorbid with chronic diseases such as cirrhosis has attracted widespread attention, whose underlying molecular mechanisms remain unclear. Since cirrhosis and sarcopenia are assumed to be closely interrelated in terms of pathogenesis, this review innovatively discussed the role of epigenetic modifications and microecological dysregulation in sarcopenia in the context of liver cirrhosis. Here we illustrated the relationship between sarcopenia and cirrhosis in the aspect of epigenetics, dysbiosis, and the crosstalk between gene modifications and intestinal microecology. Furthermore, the alterations in cirrhosis patients with sarcopenia, such as inflammatory response and oxidative stress, are found to present synergistic effects in the pathways of epigenetics and dysbiosis leading to sarcopenia. This review proposes that microbiome-based therapies are promising to break the vicious cycle between epigenetic modification and dysbiosis, providing strong support for the use of intestinal microecological interventions to prevent sarcopenia in cirrhotic patients.

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Genome-wide detection of runs of homozygosity and heterozygosity in Tunchang pigs

Liu,

Xu,

Chen

et al. 2024

animal

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Inhibition of BET Family Proteins Suppresses African Swine Fever Virus Infection

Cited by 8 publications

References 56 publications

Mutation of Basic Residues R283, R286, and K288 in the Matrix Protein of Newcastle Disease Virus Attenuates Viral Replication and Pathogenicity

Mutation of Basic Residues R283, R286, and K288 in the Matrix Protein of Newcastle Disease Virus Attenuates Viral Replication and Pathogenicity

Sarcopenia in liver cirrhosis: perspectives from epigenetics and microbiota

Genome-wide detection of runs of homozygosity and heterozygosity in Tunchang pigs

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