Dear Editor,The circulation of respiratory viruses,primarily the influenza virus,has been disrupted by the emergence of the COVID-19 pandemic and SARS-CoV-2.Epidemiological surveillance data during the COVID-19 pandem...Dear Editor,The circulation of respiratory viruses,primarily the influenza virus,has been disrupted by the emergence of the COVID-19 pandemic and SARS-CoV-2.Epidemiological surveillance data during the COVID-19 pandemic indicate a decline in the circulation of the influenza B Yamagata lineage in recent periods,suggesting a dynamic shift in the epidemiology of influenza B viruses(IBVs).展开更多
Of dietary monosaccharides,fructose is primarily metabolized by aldolase B(ALDOB)in the liver,whereas glucose is metabolized elsewhere in the body.It has been documented that overconsumption of dietary fructose,especi...Of dietary monosaccharides,fructose is primarily metabolized by aldolase B(ALDOB)in the liver,whereas glucose is metabolized elsewhere in the body.It has been documented that overconsumption of dietary fructose,especially industrial fructose,associates significantly with advanced inflammation in chronic hepatitis C(CHC)patients.However,little is known about whether impaired fructolysis might attribute to CHC hepatopathogenesis.Herein we found that the level of ALDOB protein was significantly reduced in CHC patients and mice that were persistently infected by hepatitis C virus(HCV).In vitro,HCV infection activated caspase-1,and caspase-3 to a lesser extent,which proteolyzed ALDOB and blocked fructose metabolism in hepatocytes.Downregulation of ALDOB attenuated HCV replication,indicating an intrinsic anti-HCV role for homeostatic fructolysis.On the other hand,reduced ALDOB caused intracellular fructose 1-phosphate accumulation that provoked severe cellular toxicity through intracellular ATP depletion and heightened glycation,which was aggravated by HCV infection.Taken together,these results have unveiled that inflammatory activation of caspase-1 impairs homeostatic fructolysis and exacerbates liver damage.展开更多
Strains from the Cryptococcus gattii species complex(CGSC)have caused the Pacific Northwest cryptococcosis outbreak,the largest cluster of lifethreatening fungal infections in otherwise healthy human hosts known to da...Strains from the Cryptococcus gattii species complex(CGSC)have caused the Pacific Northwest cryptococcosis outbreak,the largest cluster of lifethreatening fungal infections in otherwise healthy human hosts known to date.In this study,we utilized a pan-phenome-based method to assess the fitness outcomes of CGSC strains under 31 stress conditions,providing a comprehensive overview of 2,821 phenotype-strain associations within this pathogenic clade.Phenotypic clustering analysis revealed a strong correlation between distinct types of stress phenotypes in a subset of CGSC strains,suggesting that shared determinants coordinate their adaptations to various stresses.Notably,a specific group of strains,including the outbreak isolates,exhibited a remarkable ability to adapt to all three of the most commonly used antifungal drugs for treating cryptococcosis(amphotericin B,5-fluorocytosine,and fluconazole).By integrating pan-genomic and pan-transcriptomic analyses,we identified previously unrecognized genes that play crucial roles in conferring multidrug resistance in an outbreak strain with high multidrug adaptation.From these genes,we identified biomarkers that enable the accurate prediction of highly multidrug-adapted CGSC strains,achieving maximum accuracy and area under the curve(AUC)of 0.79 and 0.86,respectively,using machine learning algorithms.Overall,we developed a pan-omic approach to identify cryptococcal multidrug resistance determinants and predict highly multidrug-adapted CGSC strains that may pose significant clinical concern.展开更多
Hepatitis B virus(HBV),an enveloped DNA virus with a partially double-stranded DNA genome,causes transient and chronic hepatitis B in humans.A certain amount of chronic HBV infections eventually leads to liver cirrhos...Hepatitis B virus(HBV),an enveloped DNA virus with a partially double-stranded DNA genome,causes transient and chronic hepatitis B in humans.A certain amount of chronic HBV infections eventually leads to liver cirrhosis or hepatocellular carcinoma which is a major health problem worldwide[1,2].With tissue tropism and species-specific infection,the establishment of in vitro models permissive to HBV is critical in understanding the viral life cycle and designing curative therapies.The ideal cell model for in vitro infection studies is primary human hepatocytes(PHHs)[3].However,PHHis difficult to obtain andwith high cost.The donor diversity and high batch-to-batch variability of infection efficiency also limit its applicability.In 2012,sodium taurocholate co-transporting polypeptide(NTCP)was identified as a functional receptor for HBV entry[4].Thus,a new infection model based on NTCP-reconstituted HepG2 hepatocytes(HepG2-NTCP)was successfully established,which greatly promoted the understanding of HBV infection and replication[4].However,in this infection system,successful HBV infection stringently requires a high concentration of HBV viral particles,but still in most cases supports a low level of HBV replication[5].Thus,further optimization of infection cell models is an important demand in HBV research.展开更多
Regulatory T(T_(reg))cells play an essential role in maintaining immune balance across various physiological and pathological conditions.However,the mechanisms underlying T_(reg)homeostasis remain incompletely underst...Regulatory T(T_(reg))cells play an essential role in maintaining immune balance across various physiological and pathological conditions.However,the mechanisms underlying T_(reg)homeostasis remain incompletely understood.Here,we report that RIPK1 is crucial for T_(reg) cell survival and homeostasis.We generated mice with T_(reg) cell-specific ablation of Ripk1 and found that these mice developed fatal systemic autoimmunity due to a dramatic reduction in the Treg cell compartment caused by excessive cell death.Unlike conventional T cells,Treg cells with Ripk1 deficiency were only partially rescued from cell death by blocking FADD-dependent apoptosis.However,simultaneous removal of both Fadd and Ripk3 completely restored the homeostasis of Ripk1-deficient Treg cells by blocking two cell death pathways.Thus,our study highlights the critical role of RIPK1 in regulating Treg cell homeostasis by controlling both apoptosis and necroptosis,thereby providing novel insights into the mechanisms of Treg cell homeostasis.展开更多
The dynamic remodeling of the cytoskeletal network of vimentin intermediate filaments supports various cellular functions,including cell morphology,elasticity,migration,organelle localization,and resistance against me...The dynamic remodeling of the cytoskeletal network of vimentin intermediate filaments supports various cellular functions,including cell morphology,elasticity,migration,organelle localization,and resistance against mechanical or pathological stress.Currently available chemicals targeting vimentin predominantly induce network reorganization and shrinkage around the nucleus.Effective tools for long-term manipulation of vimentin network dispersion in living cells are still lacking,limiting in-depth studies on vimentin function and potential therapeutic applications.Here,we verified that a commercially available small molecule,trametinib,is capable of inducing spatial spreading of the cellular vimentin network without affecting its transcriptional or Translational regulation.Further evidence confirmed its low cytotoxicity and similar effects on different cell types.Importantly,Trametinib has no impact on the other two cytoskeletal systems,actin filaments and the microtubule network.Moreover,Trametinib regulates vimentin network dispersion rapidly and efficiently,with effects persisting for up to 48 h after drug withdrawal.We also ruled out the possibility that Trametinib directly affects the phosphorylation level of vimentin.In summary,we identified an unprecedented regulator Trametinib,which is capable of spreading the vimentin network toward the cell periphery,and thus complemented the existing repertoire of vimentin remodeling drugs in the field of cytoskeletal research.展开更多
The rise of mRNA vaccine technology Vaccines stand as one of the most significant medical advancements,playing a crucial role in the prevention of infectious diseases and the improvement of global health.The triumph o...The rise of mRNA vaccine technology Vaccines stand as one of the most significant medical advancements,playing a crucial role in the prevention of infectious diseases and the improvement of global health.The triumph of smallpox vaccination stands as a towering achievement in the annals of healthcare,leading to the complete elimination of a oncedevastating disease and showcasing the efficacy of vaccination methods.展开更多
Ebolaviruses,such as the highly pathogenic Ebola virus(EBOV),belong to the family Filoviridae and have caused out-breaks of severe and fatal hemorrhagic fever over the past years.Bombali virus(BOMV)is a newly discover...Ebolaviruses,such as the highly pathogenic Ebola virus(EBOV),belong to the family Filoviridae and have caused out-breaks of severe and fatal hemorrhagic fever over the past years.Bombali virus(BOMV)is a newly discovered ebolavirus from bats with unknown potential to infect humans.For most ebolaviruses,the interaction between viral glycoprotein(GP)and host receptor Niemann-Pick C1(NPC1)is crucial for viral entry and determines host tropism.Here,we analyzed the BOMV GP-mediated virus entry into human cells using our recently developed EBOV transcription-and replication-competent virus-like particle(trVLP)system.We demonstrated that while BOMV GP can be efficiently incorporated into trVLPs,it is inefficient in mediating trVLP entry into human cells.However,BOMV GP-mediated virus entry into human cells can be significantly enhanced by a few mutations in the NPC1-binding domain of GP.Furthermore,we showed that these mutations increase the binding of BOMV-GP to human NPC1.In summary,our results suggested that although wild-type BOMV does not efficiently infect human cells,the emergence of mutations in viral GP may boost its ability to spill over to humans,highlighting the importance of monitoring BOMV GP evolution in preventing potential BOMV spillover events.展开更多
In fluorescence microscopy,computational algorithms have been developed to suppress noise,enhance contrast,and even enable super-resolution(SR).However,the local quality of the images may vary on multiple scales,and t...In fluorescence microscopy,computational algorithms have been developed to suppress noise,enhance contrast,and even enable super-resolution(SR).However,the local quality of the images may vary on multiple scales,and these differences can lead to misconceptions.Current mapping methods fail to finely estimate the local quality,challenging to associate the SR scale content.Here,we develop a rolling Fourier ring correlation(rFRC)method to evaluate the reconstruction uncertainties down to SR scale.To visually pinpoint regions with low reliability,a filtered rFRC is combined with a modified resolution-scaled error map(RSM),offering a comprehensive and concise map for further examination.We demonstrate their performances on various SR imaging modalities,and the resulting quantitative maps enable better SR images integrated from different reconstructions.Overall,we expect that our framework can become a routinely used tool for biologists in assessing their image datasets in general and inspire further advances in the rapidly developing field of computational imaging.展开更多
The aldo-keto reductase 1B(AKR1B)subfamily was initially known for its association with the pathogenesis of secondary diabetic complications such as retinopathy,neuropathy,nephropathy,and cataracts.Unfortunately,over ...The aldo-keto reductase 1B(AKR1B)subfamily was initially known for its association with the pathogenesis of secondary diabetic complications such as retinopathy,neuropathy,nephropathy,and cataracts.Unfortunately,over the past few decades,all drug development efforts targeting this family have failed for one reason or another.Recently,a growing body of evidence showing the deep involvement of AKR1B in metabolic reprogramming and production of signaling metabolites has led to a re-evaluation of their role in the pathogenesis of several immunometabolism-related diseases,such as gastrointestinal diseases,psoriasis,congenital disorders of glycosylation,carcinogenesis,even progression,and acquired chemoresistance.Therefore,in this review,we will summarize the current knowledge of AKR1B,highlighting their potential function in regulating immune cell function and then inflammatory complications.We will also explore how discovering this new insight into this old enzyme is essential for envisioning potential therapeutic strategies to prevent or treat inflammatory diseases.展开更多
文摘Dear Editor,The circulation of respiratory viruses,primarily the influenza virus,has been disrupted by the emergence of the COVID-19 pandemic and SARS-CoV-2.Epidemiological surveillance data during the COVID-19 pandemic indicate a decline in the circulation of the influenza B Yamagata lineage in recent periods,suggesting a dynamic shift in the epidemiology of influenza B viruses(IBVs).
基金the National Natural Science Foundation of China(81530067,31621061,31300716)the Ministry of Science and Technology(2015CB554304)+2 种基金the Hubei Provincial Natural Science Foundation(2013CFB487)Shandong Laboratory Microecological Biomedicine(JNL-2023002B)the Fundamental Research Funds for the Central Universities(2022ZFJH003).
文摘Of dietary monosaccharides,fructose is primarily metabolized by aldolase B(ALDOB)in the liver,whereas glucose is metabolized elsewhere in the body.It has been documented that overconsumption of dietary fructose,especially industrial fructose,associates significantly with advanced inflammation in chronic hepatitis C(CHC)patients.However,little is known about whether impaired fructolysis might attribute to CHC hepatopathogenesis.Herein we found that the level of ALDOB protein was significantly reduced in CHC patients and mice that were persistently infected by hepatitis C virus(HCV).In vitro,HCV infection activated caspase-1,and caspase-3 to a lesser extent,which proteolyzed ALDOB and blocked fructose metabolism in hepatocytes.Downregulation of ALDOB attenuated HCV replication,indicating an intrinsic anti-HCV role for homeostatic fructolysis.On the other hand,reduced ALDOB caused intracellular fructose 1-phosphate accumulation that provoked severe cellular toxicity through intracellular ATP depletion and heightened glycation,which was aggravated by HCV infection.Taken together,these results have unveiled that inflammatory activation of caspase-1 impairs homeostatic fructolysis and exacerbates liver damage.
基金financially supported by the National Key R&D Program of China(2021YFC2302100)the National Natural Science Foundation of China(82370005 and 82172291)+8 种基金the National Key R&D Program of China(2022YFC2303000 and 2021YFC230000)the CAS Interdisciplinary Innovation Team,the Beijing Research Center for Respiratory Infectious Diseases Project(BJRID2024-008 and BJRID2024-011)the R&D Program of Beijing Municipal Education Commission(KM202410025012)the Reform and Development Program of Beijing Institute of Respiratory Medicine(Ggyfz202328 and Ggyfz202418)the National Key R&D Program of China(2020YFA0907200)Shanghai Science and Technology Innovation Action Plan 2023“Basic Research Project”(23JC1404201)the Shanghai‘‘Belt and Road’’Joint Laboratory Project(22490750200)the National Natural Science Foundation of China(82370005)National High Level Hospital Clinical Research Funding(2022-PUMCH-C-052).
文摘Strains from the Cryptococcus gattii species complex(CGSC)have caused the Pacific Northwest cryptococcosis outbreak,the largest cluster of lifethreatening fungal infections in otherwise healthy human hosts known to date.In this study,we utilized a pan-phenome-based method to assess the fitness outcomes of CGSC strains under 31 stress conditions,providing a comprehensive overview of 2,821 phenotype-strain associations within this pathogenic clade.Phenotypic clustering analysis revealed a strong correlation between distinct types of stress phenotypes in a subset of CGSC strains,suggesting that shared determinants coordinate their adaptations to various stresses.Notably,a specific group of strains,including the outbreak isolates,exhibited a remarkable ability to adapt to all three of the most commonly used antifungal drugs for treating cryptococcosis(amphotericin B,5-fluorocytosine,and fluconazole).By integrating pan-genomic and pan-transcriptomic analyses,we identified previously unrecognized genes that play crucial roles in conferring multidrug resistance in an outbreak strain with high multidrug adaptation.From these genes,we identified biomarkers that enable the accurate prediction of highly multidrug-adapted CGSC strains,achieving maximum accuracy and area under the curve(AUC)of 0.79 and 0.86,respectively,using machine learning algorithms.Overall,we developed a pan-omic approach to identify cryptococcal multidrug resistance determinants and predict highly multidrug-adapted CGSC strains that may pose significant clinical concern.
基金supported by the National Natural Science Foundation of China(32222022,92354301,92054104)Key Research and Development Program,Ministry of Science and Technology of China(2022YFC2303502,2021YFC2300204)Natural Science Foundation of Shanghai(23ZR1470900).
文摘Hepatitis B virus(HBV),an enveloped DNA virus with a partially double-stranded DNA genome,causes transient and chronic hepatitis B in humans.A certain amount of chronic HBV infections eventually leads to liver cirrhosis or hepatocellular carcinoma which is a major health problem worldwide[1,2].With tissue tropism and species-specific infection,the establishment of in vitro models permissive to HBV is critical in understanding the viral life cycle and designing curative therapies.The ideal cell model for in vitro infection studies is primary human hepatocytes(PHHs)[3].However,PHHis difficult to obtain andwith high cost.The donor diversity and high batch-to-batch variability of infection efficiency also limit its applicability.In 2012,sodium taurocholate co-transporting polypeptide(NTCP)was identified as a functional receptor for HBV entry[4].Thus,a new infection model based on NTCP-reconstituted HepG2 hepatocytes(HepG2-NTCP)was successfully established,which greatly promoted the understanding of HBV infection and replication[4].However,in this infection system,successful HBV infection stringently requires a high concentration of HBV viral particles,but still in most cases supports a low level of HBV replication[5].Thus,further optimization of infection cell models is an important demand in HBV research.
基金supported by the following grants:National Key Research and Development Program of China(2021YFA1301402)Shanghai Municipal Science and Technology Major Project(ZD2021CY001)+4 种基金National Key Research and Development Program of China(2021YFE0200900,2022YFA0807300)National Natural Science Foundation of China(82101833,82073901)Three-year Action Plan for Shanghai TCM Development and Inheritance Program[ZY(2021-2023)-0103]Top-level Clinical Discipline Project of Shanghai Pudong District(grant/award number:PWYgf 2021-01)Training Plan for Discipline Leaders of Shanghai Pudong New Area Health Commission(grant/award number:PWRd2020-09).
文摘Regulatory T(T_(reg))cells play an essential role in maintaining immune balance across various physiological and pathological conditions.However,the mechanisms underlying T_(reg)homeostasis remain incompletely understood.Here,we report that RIPK1 is crucial for T_(reg) cell survival and homeostasis.We generated mice with T_(reg) cell-specific ablation of Ripk1 and found that these mice developed fatal systemic autoimmunity due to a dramatic reduction in the Treg cell compartment caused by excessive cell death.Unlike conventional T cells,Treg cells with Ripk1 deficiency were only partially rescued from cell death by blocking FADD-dependent apoptosis.However,simultaneous removal of both Fadd and Ripk3 completely restored the homeostasis of Ripk1-deficient Treg cells by blocking two cell death pathways.Thus,our study highlights the critical role of RIPK1 in regulating Treg cell homeostasis by controlling both apoptosis and necroptosis,thereby providing novel insights into the mechanisms of Treg cell homeostasis.
基金supported by the National Natural Science Foundation of China(92354301,32222022,32300569,and 92054104)R&D Program of Guangzhou National Laboratory(GZNL2023A03004)+2 种基金Key Research and Development Program,the Ministry of Science and Technology of China(2022YFC2303502 and 2021YFC2300204)the Natural Science Foundation of Shanghai(23ZR1470900)Youth Innovation Promotion Association,Chinese Academy of Sciences.
文摘The dynamic remodeling of the cytoskeletal network of vimentin intermediate filaments supports various cellular functions,including cell morphology,elasticity,migration,organelle localization,and resistance against mechanical or pathological stress.Currently available chemicals targeting vimentin predominantly induce network reorganization and shrinkage around the nucleus.Effective tools for long-term manipulation of vimentin network dispersion in living cells are still lacking,limiting in-depth studies on vimentin function and potential therapeutic applications.Here,we verified that a commercially available small molecule,trametinib,is capable of inducing spatial spreading of the cellular vimentin network without affecting its transcriptional or Translational regulation.Further evidence confirmed its low cytotoxicity and similar effects on different cell types.Importantly,Trametinib has no impact on the other two cytoskeletal systems,actin filaments and the microtubule network.Moreover,Trametinib regulates vimentin network dispersion rapidly and efficiently,with effects persisting for up to 48 h after drug withdrawal.We also ruled out the possibility that Trametinib directly affects the phosphorylation level of vimentin.In summary,we identified an unprecedented regulator Trametinib,which is capable of spreading the vimentin network toward the cell periphery,and thus complemented the existing repertoire of vimentin remodeling drugs in the field of cytoskeletal research.
基金supported by the National Science and Technology Major Projects(2021YFC2301304,2021YFC2300704)the National Natural Science Foundation of China(32270695,32270719)。
文摘The rise of mRNA vaccine technology Vaccines stand as one of the most significant medical advancements,playing a crucial role in the prevention of infectious diseases and the improvement of global health.The triumph of smallpox vaccination stands as a towering achievement in the annals of healthcare,leading to the complete elimination of a oncedevastating disease and showcasing the efficacy of vaccination methods.
基金supported by the grants from Key Research and Development Program,Ministry of Science and Technology of China(2022YFC2303300,2021YFC2300204)Shanghai Municipal Science and Technology Major Project(ZD2021CY001)+3 种基金Strategic Priority Research Program of the Chinese Academy of Sciences(XDB29010205)Shanghai International Science and Technology Cooperation Program(21430713900)Program of Shanghai Academic/Technology Research Leader(22XD1403800)to J.Z.Advanced Customer Cultivation Project of Wuhan National Biosafety Laboratory,Chinese Academy of Sciences to J.Z.and H.Y.
文摘Ebolaviruses,such as the highly pathogenic Ebola virus(EBOV),belong to the family Filoviridae and have caused out-breaks of severe and fatal hemorrhagic fever over the past years.Bombali virus(BOMV)is a newly discovered ebolavirus from bats with unknown potential to infect humans.For most ebolaviruses,the interaction between viral glycoprotein(GP)and host receptor Niemann-Pick C1(NPC1)is crucial for viral entry and determines host tropism.Here,we analyzed the BOMV GP-mediated virus entry into human cells using our recently developed EBOV transcription-and replication-competent virus-like particle(trVLP)system.We demonstrated that while BOMV GP can be efficiently incorporated into trVLPs,it is inefficient in mediating trVLP entry into human cells.However,BOMV GP-mediated virus entry into human cells can be significantly enhanced by a few mutations in the NPC1-binding domain of GP.Furthermore,we showed that these mutations increase the binding of BOMV-GP to human NPC1.In summary,our results suggested that although wild-type BOMV does not efficiently infect human cells,the emergence of mutations in viral GP may boost its ability to spill over to humans,highlighting the importance of monitoring BOMV GP evolution in preventing potential BOMV spillover events.
基金supported by the National Natural Science Foundation of China(grant no.T2222009 to H.L.,grant no.32227802 to L.C.,grant no.81925022 to L.C.,grant no.92054301 to L.C.,grant no.62305083 to W.Z.,grant no.12174208 to P.L.,grant no.32301257 to S.Z.,grant no.32222022 to Y.J.,grant no.32071458 to H.M.)the National Key Research and Development Program of China(grant no.2022YFC3400600 to L.C.)+4 种基金the Natural Science Foundation of Heilongjiang Province(grant no.YQ2021F013 to H.L.)the Beijing Natural Science Foundation(grant no.Z20J00059 to L.C.)the Guangdong Major Project of Basic and Applied Basic Research(grant no.2020B0301030009 to P.L.)the China Postdoctoral Science Foundation(grant no.2023T160163 to W.Z.,grant no.2022M720971 to W.Z.)the Heilongjiang Provincial Postdoctoral Science Foundation(grant no.LBH-Z22027 to W.Z.).L.C.acknowledges support from the High-performance Computing Platform of Peking University。
文摘In fluorescence microscopy,computational algorithms have been developed to suppress noise,enhance contrast,and even enable super-resolution(SR).However,the local quality of the images may vary on multiple scales,and these differences can lead to misconceptions.Current mapping methods fail to finely estimate the local quality,challenging to associate the SR scale content.Here,we develop a rolling Fourier ring correlation(rFRC)method to evaluate the reconstruction uncertainties down to SR scale.To visually pinpoint regions with low reliability,a filtered rFRC is combined with a modified resolution-scaled error map(RSM),offering a comprehensive and concise map for further examination.We demonstrate their performances on various SR imaging modalities,and the resulting quantitative maps enable better SR images integrated from different reconstructions.Overall,we expect that our framework can become a routinely used tool for biologists in assessing their image datasets in general and inspire further advances in the rapidly developing field of computational imaging.
基金supported by grants from the National Key Research and Development Program of China(2022YFC2303504)the National Natural Science Foundation of China(92157106,32270917,82003361)+2 种基金the Shanghai Municipal Sci-ence and Technology Major Project(2019SHZDZX02)the Shanghai Committee of Science and Technology,China(22ZR1469900)supported by Youth Innovation Promo-tion Association of CAS,China(YIPA2023291).
文摘The aldo-keto reductase 1B(AKR1B)subfamily was initially known for its association with the pathogenesis of secondary diabetic complications such as retinopathy,neuropathy,nephropathy,and cataracts.Unfortunately,over the past few decades,all drug development efforts targeting this family have failed for one reason or another.Recently,a growing body of evidence showing the deep involvement of AKR1B in metabolic reprogramming and production of signaling metabolites has led to a re-evaluation of their role in the pathogenesis of several immunometabolism-related diseases,such as gastrointestinal diseases,psoriasis,congenital disorders of glycosylation,carcinogenesis,even progression,and acquired chemoresistance.Therefore,in this review,we will summarize the current knowledge of AKR1B,highlighting their potential function in regulating immune cell function and then inflammatory complications.We will also explore how discovering this new insight into this old enzyme is essential for envisioning potential therapeutic strategies to prevent or treat inflammatory diseases.
基金the Key Research and Development Program,Ministry of Science and Technology of China(2022YFC2303502 and 2021YFC2300204)the Chinese Academy of Sciences-Vice Presidency Science and Technology Silk Road Science Fund(GJHZ2021138)+2 种基金the National Natural Science Foundation of China(32222022,92054104,31970660,31925025,and 22293033)the Strategic Priority Research Program of the Chinese Academy of Sciences(XDB29050201)the R&D Program of Guangzhou Laboratory(SRPG22-002)。
