ANP32A

更新于：2025-05-07

基本信息

别名

Acidic leucine-rich nuclear phosphoprotein 32 family member A、acidic nuclear phosphoprotein 32 family member A、Acidic nuclear phosphoprotein pp32

+ [12]

简介

Multifunctional protein that is involved in the regulation of many processes including tumor suppression, apoptosis, cell cycle progression or transcription (PubMed:10400610, PubMed:11360199, PubMed:16341127, PubMed:18439902). Promotes apoptosis by favouring the activation of caspase-9/CASP9 and allowing apoptosome formation (PubMed:18439902). In addition, plays a role in the modulation of histone acetylation and transcription as part of the INHAT (inhibitor of histone acetyltransferases) complex. Inhibits the histone-acetyltranferase activity of EP300/CREBBP (CREB-binding protein) and EP300/CREBBP-associated factor by histone masking (PubMed:11830591). Preferentially binds to unmodified histone H3 and sterically inhibiting its acetylation and phosphorylation leading to cell growth inhibition (PubMed:16341127). Participates in other biochemical processes such as regulation of mRNA nuclear-to-cytoplasmic translocation and stability by its association with ELAVL1 (Hu-antigen R) (PubMed:18180367). Plays a role in E4F1-mediated transcriptional repression as well as inhibition of protein phosphatase 2A (PubMed:15642345, PubMed:17557114). (Microbial infection) Plays an essential role in influenza A, B and C viral genome replication (PubMed:30666459, PubMed:32694517, PubMed:33045004, PubMed:33208942). Mechanistically, mediates the assembly of the viral replicase asymmetric dimers composed of PB1, PB2 and PA via its N-terminal region (PubMed:33208942). Also plays an essential role in foamy virus mRNA export from the nucleus (PubMed:21159877).

关联

100 项与 ANP32A 相关的临床结果

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100 项与 ANP32A 相关的转化医学

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0 项与 ANP32A 相关的专利（医药）

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284

项与 ANP32A 相关的文献（医药）

2025-04-01·Advanced Science

Cell Sizes Matter for Industrial Bioproduction, a Case of Polyhydroxybutyrate

Article

作者: Guo, Wei‐Ke ; Zhang, Li‐Zhan ; Wu, Qiong ; Wang, Jia‐Le ; Chen, Guo‐Qiang ; Chen, Yi‐Ling ; Liu, Xu ; Wu, Fu‐Qing ; Yang, Ji‐Shuai ; Yan, Xu ; Zheng, Shuang

AbstractMost bacterial cells are 1–2 microns in size, limiting intracellular products like polyhydroxyalkanoates (PHA) accumulation. Cell size is regulated by key genes such as mreB and minCD, which encode cellular skeleton protein and control cell fission ring location, respectively. Their expression changes significantly affect microbial growth. This study successfully redesigns the ClpXP protein degradation system by deleting the sspB gene and using mutated SsrA tags with different degradation rates to control MreB degradation. Dynamic degradation of MreB allows non‐model bacterium Halomonas bluephagenesis to grow normally and increase cell size simultaneously. Combined with overexpression of minCD, H. bluephagenesis with progressive MreB degradation increases the cell size further, albeit with a reduced growth rate. H. bluephagenesis CYL0307, with the PHB granule‐associated protein PhaP1 deleted and phaABRe overexpressed in the MreB‐degraded strain, increases cell volume more than nine times compared to the original strain. CYL0307 produces 149 g L−1 cell dry weight containing 82% PHB after 44 h in a 5000 L bioreactor, with cells containing single large PHB granules, simplifying recovery and purification. These results provide a post‐translational gene regulation method in H. bluephagenesis and a strategy for enhancing PHB production via morphological engineering.

2025-03-01·Advanced Science

Evolutionary Pro‐To‐Thr Mutation in the Intrinsically Disordered Domain of ANP32 Family Members Modulates Their Target Binding Modes

Article

作者: Díaz‐Moreno, Irene ; Velázquez‐Cruz, Alejandro ; Casado‐Combreras, Miguel Á. ; Baños‐Jaime, Blanca ; De la Rosa, Miguel A. ; Velázquez‐Campoy, Adrián ; Uceda‐Mayo, Ana B. ; Corrales‐Guerrero, Laura ; Rivero‐Rodríguez, Francisco

AbstractGene duplication has allowed protein evolution toward novel functions and mechanisms. The differences between paralogous genes frequently rely on the sequence of disordered regions. For instance, in mammals, the chaperones ANP32A and ANP32B share a common evolutionary line and have some exchangeable functions based on their similar N‐terminal domains. Nevertheless, their C‐terminal low‐complexity‐acidic‐regions (LCARs) display substantial sequence differences, unveiling some degree of variability between them, in agreement with their different tissue‐specific expression patterns. These structural and computational results indicate that a substitution in the vicinity of the nuclear localization signal (NLS), of Pro in ANP32A for Thr in ANP32B, determines the overall compactness of the C‐terminal LCAR. The different structural properties of the disordered region affect the binding mode of ANP32 members to their targets. This type of divergent binding mode is exemplified with the extra‐mitochondrial cytochrome c (Cc), a well‐known ANP32B partner and which now determine also binds to ANP32A; and with the RNA binding protein HuR, whose export to the cytoplasm is mediated by ANP32 proteins under stress. Therefore, differential expression patterns of ANP32A or ANP32B may affect the regulation of Cc and HuR and can help to explain the distinct roles of these proteins in diseases.

2025-01-31·Journal of Virology

Chicken ANP32A-independent replication of highly pathogenic avian influenza viruses potentially leads to mammalian adaptation-related amino acid substitutions in viral PB2 and PA proteins

Article

作者: Fujimoto, Yoshikazu ; Ono, Etsuro ; Ozaki, Kinuyo

ABSTRACT Acidic nuclear phosphoprotein 32 family member A (ANP32A) is an important host factor that supports the efficient replication of avian influenza viruses (AIVs). To develop an antiviral strategy against Gs/Gd-lineage H5 highly pathogenic avian influenza (HPAI) viruses in chickens, we established chicken ANP32-knockout (chANP32A-KO) DF-1 cells and evaluated their antiviral efficacy through in vitro validation. The replication of all HPAI viruses tested in chANP32A-KO cells was significantly lower compared to that of wild-type DF-1 cells. However, when HPAI strains A/mountain hawk-eagle/Kumamoto/1/2007 (H5N1; MHE) and A/chicken/Aichi/2/2011 (H5N1; H5Aichi) were passed in chANP32A-KO cells, mutant viruses were generated, which exhibited comparable replication levels in both chANP32A-KO and wild-type DF-1 cells. Sequence analysis revealed that mammalian-adaptive amino acid mutations PB2_D256G and PA_T97I were present in the MHE mutant virus, and the PB2_E627K mutation was identified in the H5Aichi mutant virus. These mutations have also been reported to enhance the polymerase activity of AIVs in mammalian cells; however, the minigenome assay in the present study showed that the polymerase activity of mutant viruses in chANP32A-KO cells was not restored to levels comparable to those in wild-type DF-1 cells. These findings suggest that ANP32A-independent viral replication may induce amino acid substitutions associated with mammalian adaptation in AIVs. They also imply that the high efficiency of viral replication mediated by these amino acid mutations may not result from enhanced polymerase activity but rather involve other undefined mechanisms. IMPORTANCEDuring the host-switching of avian influenza viruses (AIVs) to mammalian hosts, introducing adaptive mutations into viral proteins is essential to ensure optimal functionality through virus-host protein interactions in mammalian cells. However, the mechanisms leading to adaptive mutations in viral proteins remain unclear. Among several host proteins that promote viral growth, acidic nuclear phosphoprotein 32 family member A (ANP32A) is known to be an important factor for efficient viral replication. Here, we generated mutant highly pathogenic avian influenza viruses capable of ANP32A-independent replication in a chicken-derived cell line. We demonstrated that several amino acid mutations found in the mutant viruses correspond to those associated with the mammalian adaptation of AIVs. These results suggest that ANP32A-independent viral replication is one of the mechanisms for introducing amino acid mutations that are reportedly involved in the mammalian adaptation of AIVs.

项与 ANP32A 相关的新闻（医药）

2023-10-12

·生物谷

晚讯 |2019 年医学或生理学诺奖得主论文被撤、加州成为首个禁止在食品中使用四种添加剂的州

1、2019 年医学或生理学诺奖得主第 10 篇论文被撤，已有多达 56 篇论文受质疑根据撤稿观察（Retraction Watch）报道，10 月 2 日，2019 年诺贝尔生理学或医学奖得主格雷格·塞门扎（Gregg L. Semenza）因数据和图像问题撤回了他的第 10 篇论文。这篇被撤回的论文于 2013 年发表于《分子癌症研究》（Molecular Cancer Research），主要内容是关于缺氧诱导的乳腺癌转移，目前在 Web of Science 上已被引用 181 次。论文相关的通知显示，“应作者们的要求，这篇文章已被撤回”。撤稿原因是论文内一张图像存在作假，图像中几个部分比预期设想的更为相似。据悉，去年格雷格·塞门扎曾一次性撤回发表于《美国科学院院刊》（PNAS）的 4 篇论文。而在 2019 年之前，就有人指出他在 PubPeer 上发表的论文可能存在复制或篡改图像的问题。目前，PubPeer 上涉及塞门扎的争议论文数量已达到 56 篇。2、借助多次基因编辑，或可以让鸡不再患禽流感据《科学》新闻（Science news）消息，近期，英国爱丁堡大学等多个机构的科学家通过长达 30 年的努力，成功实现了通过基因编辑技术，制造出对禽流感病毒具有抵抗力的鸡。甲型流感病毒（influenza A virus，IAV）主要依赖鸡体内的蛋白 ANP32A 进行感染。研究人员使用 CRISPR/Cas9 技术对对应的基因纯合子进行了编辑，替换了蛋白 ANP32A 中的 2 个氨基酸，阻止了病毒的聚合酶相互作用，使得禽流感病毒不能在利用鸡的这种蛋白质进行感染。3、渐冻症治疗的一小步：全球第四款药物获批近日，从上海交通大学医学院附属瑞金医院海南医院（以下简称“瑞金海南医院”）获悉，医院对肌萎缩性侧索硬化症（ALS）新药Tofersen的伦理会已经通过，预计一两个月后可直接落地使用。4、FDA警告复方氯胺酮用于精神病治疗的危险性美国食品和药物管理局警告消费者使用氯胺酮复方制剂的风险，氯胺酮常被用于治疗精神疾病。复方产品的安全性和有效性未经 FDA 评估。它们也不像已批准的药品那样受到监管，因此风险更大。5、英国每年有两百多万人死于癌症《英国癌症杂志》（British Journal of Cancer）今天发表的最新研究报告显示，英国每年因癌症损失的生命年数超过 200 万年。伦敦国王学院的研究人员与英国癌症研究中心合作开展的这项研究表明，由于确诊人数多、存活率低，总损失年数的五分之一来自肺癌（每年超过 50 万）。肠癌每年造成 21.3 万多人死亡，乳腺癌每年造成约 19.7 万人死亡。6、加州成为首个禁止在食品中使用四种添加剂的州加利福尼亚州已成为第一个禁止在食品中添加四种常见化学物质的州，这些化学物质与健康问题有关。据 NBC 新闻报道，尽管加文-纽森州长签署的这项法律只在本州禁止使用这些添加剂，但这些化学物质有可能从全国各地的产品中去除。这些化学物质是红色染料 3 号、溴酸钾、溴化植物油和丙基苯甲酸酯。据 NBC 新闻报道，这四种化学物质目前都已获得美国食品和药物管理局的批准，但在欧盟和世界其他一些地区却是非法的。7、邦顺制药完成B+轮融资，持续推进核心管线获批上市和商业化2023年10月12日，生物医药创新药公司杭州邦顺制药有限公司（以下简称“邦顺制药”）宣布完成B+轮融资，本轮融资由华睿投资独家投资，这是公司在年初完成B轮融资后的又一次重要融资事件。8、万玛生物获得战略投资，可提供免疫细胞及干细胞储存服务近日，锦艺集团控股(00565.HK)公告，公司间接全资附属公司旭福有限公司("旭福")与杜刘东("创始人股东")订立不具法律约束力意向书，据此，旭福拟以(但不限于)股权、贷款或可换股债券等形式投资河北万玛生物医药有限公司("目标公司"，及其附属公司，"目标集团")以及创始人股东拟与旭福订立可能交易。本文仅用于学术分享，转载请注明出处。若有侵权，请联系微信：bioonSir 删除或修改！

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