Min Zheng

ORCID: 0009-0003-9811-4937
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Animal Virus Infections Studies
  • Viral Infections and Immunology Research
  • Animal Disease Management and Epidemiology
  • interferon and immune responses
  • Viral gastroenteritis research and epidemiology
  • Virus-based gene therapy research
  • Influenza Virus Research Studies
  • Inflammasome and immune disorders
  • Herpesvirus Infections and Treatments
  • Heme Oxygenase-1 and Carbon Monoxide
  • Respiratory viral infections research
  • Bacteriophages and microbial interactions
  • RNA regulation and disease
  • Immune Cell Function and Interaction
  • Poxvirus research and outbreaks
  • RNA and protein synthesis mechanisms
  • Vector-Borne Animal Diseases
  • Autophagy in Disease and Therapy
  • SARS-CoV-2 and COVID-19 Research
  • Endoplasmic Reticulum Stress and Disease
  • Immunotherapy and Immune Responses
  • Epigenetics and DNA Methylation
  • Pancreatic function and diabetes
  • Immune Response and Inflammation
  • Congenital heart defects research

Guangxi Center for Disease Prevention and Control
2012-2025

Chinese Academy of Agricultural Sciences
2009-2024

Ministry of Agriculture and Rural Affairs
2024

Nanchang Center for Disease Control and Prevention
2024

Nanjing University of Chinese Medicine
2018-2024

Albert Einstein College of Medicine
2015-2023

Fujian Academy of Agricultural Sciences
2013-2023

Chinese Academy of Medical Sciences & Peking Union Medical College
2016-2023

Peking Union Medical College Hospital
2023

Guangdong Medical College
2023

Programmed cell death plays crucial roles in organismal development and host defense. Recent studies have highlighted mechanistic overlaps extensive, multifaceted crosstalk between pyroptosis, apoptosis, necroptosis, three programmed pathways traditionally considered autonomous. The growing body of evidence, conjunction with the identification molecules controlling concomitant activation all by pathological triggers, has led to concept PANoptosis. During PANoptosis, inflammatory occurs...

10.3389/fcimb.2020.00237 article EN cc-by Frontiers in Cellular and Infection Microbiology 2020-05-29

Cell death provides host defense and maintains homeostasis. Zα-containing molecules are essential for these processes. Z-DNA binding protein 1 (ZBP1) activates inflammatory cell death, PANoptosis, whereas adenosine deaminase acting on RNA (ADAR1) serves as an editor to maintain Here, we identify characterize ADAR1's interaction with ZBP1, defining its role in regulation tumorigenesis. Combining interferons (IFNs) nuclear export inhibitors (NEIs) ZBP1-dependent PANoptosis. ADAR1 suppresses...

10.1016/j.celrep.2021.109858 article EN cc-by Cell Reports 2021-10-01

Coronaviruses have caused several zoonotic infections in the past two decades, leading to significant morbidity and mortality globally. Balanced regulation of cell death inflammatory immune responses is essential promote protection against coronavirus infection; however, underlying mechanisms that control these processes remain be resolved. Here we demonstrate infection with murine mouse hepatitis virus (MHV) activated NLRP3 inflammasome form PANoptosis. Deleting components or downstream...

10.1074/jbc.ra120.015036 article EN cc-by Journal of Biological Chemistry 2020-08-06

Abstract Host-adaptive strategies, such as the E627K substitution in PB2 protein, are critical for replication of avian influenza A viruses mammalian hosts. Here we show that mutation PB2-K526R is present some human H7N9 isolates, nearly 80% H5N1 isolates from Indonesia and, conjunction with E627K, almost all seasonal H3N2 since 1970. Polymerase complexes containing PB2-526R derived H7N9, or exhibit increased polymerase activity. also enhances viral transcription and cells. In comparison...

10.1038/ncomms6509 article EN cc-by Nature Communications 2014-11-20

The mechanisms underlying pathophysiological states such as metabolic syndrome and obesity include endoplasmic reticulum (ER) stress aberrant inflammatory responses. ER results from the accumulation of misfolded proteins during conditions. However, precise by which modulates inflammation remain incompletely understood. In this study, we hypothesized that alone could represent a sufficient signal for modulation inflammasome-dependent cytokine We found several stress-inducing chemicals free...

10.1177/1753425913508593 article EN Innate Immunity 2013-11-11

Herpes virus type 1 (HSV-1) is one of the most widespread human pathogens and accounts for more than 90% cases herpes simplex encephalitis (HSE) causing severe permanent neurologic sequelae among surviving patients. We hypothesize such CNS deficits are due to HSV-1 infection neural progenitor cells (NPCs). In vivo, was found diminish NPC numbers in subventricular zone. Upon culture NPCs conditions that stimulate their differentiation, we resulted loss neuronal precursors with no significant...

10.1002/glia.22689 article EN Glia 2014-05-07

HSV-1 is the leading cause of sporadic viral encephalitis, with mortality rates approaching 30% despite treatment antiviral drug choice, acyclovir. Permanent neurologic deficits are common in patients that survive, but mechanism to this pathology poorly understood, impeding clinical advancements reduce CNS morbidity. Using magnetic resonance imaging and type I IFN receptor-deficient mouse chimeras, we demonstrate gains access murine brain stem subsequently ependymal cells, enlargement...

10.4049/jimmunol.1203265 article EN The Journal of Immunology 2013-02-05

Nonstructural protein 1 (NS1) of influenza virus is a key virulence element with multifunctional roles in replication and potent antagonist host immune response. Deletion NS1 (DelNS1) would create safer more extensively immunogenic live attenuated (LAIV) vaccine. However, DelNS1 viruses are very difficult to grow regular vaccine-producing systems, which has hampered the application LAIV vaccines humans. We have developed two master backbones deleted-NS1 viral genomes from A or B contain...

10.1128/mbio.02180-19 article EN cc-by mBio 2019-09-16

Abstract Influenza virus utilizes host splicing machinery to process viral mRNAs expressed from both M and NS segments. Through genetic analysis functional characterization, we here show that the segment of H7N9 contains a unique G540A substitution, located within previously undefined exonic enhancer (ESE) motif present in NEP mRNA influenza A viruses. supports replication mammalian cells while retaining ability avian cells. Host regulator, SF2, interacts with this ESE regulate NEP/NS1...

10.1038/ncomms14751 article EN cc-by Nature Communications 2017-03-21

Viruses and hosts have coevolved for millions of years, leading to the development complex host–pathogen interactions. Influenza A virus (IAV) causes severe pulmonary pathology is a recurrent threat human health. Innate immune sensing IAV triggers chain host responses. has adapted evade defense mechanisms, counteract these evasion strategies. However, molecular mechanisms governing balance between viral poorly understood. Here, we show that protein DEAD-box helicase 3 X-linked (DDX3X)...

10.1016/j.jbc.2021.100579 article EN cc-by Journal of Biological Chemistry 2021-01-01

<i>Salvia miltiorrhiza</i> (Danshen), a traditional Chinese herbal medicine, is commonly used for the prevention and treatment of cardiovascular disorders including atherosclerosis. However, mechanisms responsible vasoprotective effects Danshen remain largely unknown. Salvianolic acid B (Sal B) represents one most bioactive compounds that can be extracted from water-soluble fraction Danshen. We investigated Sal on inflammatory response in murine macrophages. both induced expression heme...

10.1124/jpet.111.190736 article EN Journal of Pharmacology and Experimental Therapeutics 2012-03-22

ABSTRACT The nonstructural protein (NS1) of influenza A virus performs multiple functions in the life cycle. Proteomic screening for cellular proteins which interact with NS1 identified RAP55, is one components processing bodies (P-bodies) and stress granules. To verify whether interacts P-bodies, interactions between NS1, other P-body-associated (Ago1, Ago2, DCP1a) were confirmed using coimmunoprecipitation colocalization assays. Overexpression RAP55 induced RAP55-associated granule...

10.1128/jvi.00647-12 article EN Journal of Virology 2012-09-13

Abstract A novel coronavirus (COVID-2019) was first identified in Wuhan, Hubei Province, and then spreads to the other Provinces of China. COVID-2019 reported share same receptor, Angiotensin-converting enzyme 2 (ACE2), with SARS-CoV. But infection rate is much higher than The biophysical structural evidence showed that binds ACE2 10~20 times affinity TMPRSS2 cleaves facilitates entry virus into host cells. presence SLC6A19 may block access cutting site on weaken Here based public...

10.21203/rs.3.rs-16992/v1 preprint EN cc-by Research Square (Research Square) 2020-03-12

The mitochondrial permeability transition pore (mPTP) is a channel in the inner membrane whose sustained opening response to elevated matrix Ca 2+ concentrations triggers necrotic cell death. molecular identity of mPTP unknown. One proposed candidate ATP synthase, canonical function generate most multicellular organisms. Here, we present mitochondrial, cellular, and vivo evidence that, rather than serving as mPTP, synthase inhibits this pore. Our studies confirm previous work showing...

10.1073/pnas.2303713120 article EN cc-by Proceedings of the National Academy of Sciences 2023-12-13
Coming Soon ...