Ask about this productRelated genes to: ANP32A Blocking Peptide
- Gene:
- ANP32A NIH gene
- Name:
- acidic nuclear phosphoprotein 32 family member A
- Previous symbol:
- C15orf1
- Synonyms:
- LANP, PP32, I1PP2A, PHAPI, MAPM, mapmodulin
- Chromosome:
- 15q23
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-13
- Date modifiied:
- 2015-11-05
Related products to: ANP32A Blocking Peptide
Related articles to: ANP32A Blocking Peptide
- This study aims to explore the plasma proteomic profiles of angiographically confirmed pmSAH and aSAH, and to identify candidate protein biomarkers for discriminating these subtypes on a biological level. - Source: PubMed
Publication date: 2026/08/14
Wang ChenchenHou DanHan YuweiHuo DaLi XiaomingLiang Guobiao - The highly pathogenic avian influenza virus (HPAIV) subtype H5N1 has been continuously circulating among wild bird populations and domestic poultry. It's ongoing circulation has led to outbreaks in poultry and U.S. dairy cattle populations, as well as sporadic severe infections in individuals engaged in poultry and dairy farming. These occurrences have raised concerns about the potential evolution of this virus into a pandemic strain. To elucidate the molecular determinants facilitating H5N1 cross-species adaptation and to evaluate its implications for public health, we conducted serials of sequence analysis and specific-site mutations on the viral polymerase subunit PB2 to determine its effect on polymerase activity and viral infectivity. The results showed that three mutations in the PB2 protein (E362G, D441N and M631L) were presented cooperative effects associated with enhanced viral replication in mammalian cells. Compared to the original isolated strain of the 2.3.4.4b clade, A/chicken/NL/FAV-0033/2021, these three mutations were predominantly identified in isolates obtained from cattle and other mammalian hosts between 2021 and 2024. The M631L mutation, identified as the primary determinant of increased polymerase activity in mammalian cells, significantly enhanced the binding affinity of PB2 to ANP32A. The mutation E362G and D441N did not increased polymerase activity and viral replication significantly but enhanced binding affinity of PB2 to ANP32A. The combined mutations with E362G, D441N and M631L resulted in a significantly increased polymerase activity and viral replication in H5N1 virus, and significantly elevated viral loads and aggravated pulmonary pathology in lungs of mice with H5N1 infection. These findings indicate that the PB2-M631L mutation constitutes a crucial molecular marker for the adaptation of H5N1 to mammalian hosts, whereas the E362G and D441N mutations likely function as supportive modulatory factors that optimize this host-adaptation process. - Source: PubMed
Publication date: 2026/07/29
Cui SiminHou XiaoningPu SiyuLuo JunhaoZhu HaijunHe PeiqingGao ChenGao RongbaoHan Jun - Influenza A and B viruses are considerable public health threats. Annual seasonal epidemics are driven by antigenic drift and cause an estimated 3-5 million severe cases and 290,000-650,000 deaths annually. The clinical presentation of seasonal influenza is typically an abrupt, uncomplicated acute respiratory illness with full recovery; however, it can lead to severe, life-threatening complications in individuals at high risk. Antigenic shift caused by reassortment of a seasonal influenza A virus with avian and/or swine influenza A viruses has led to unpredictable pandemics. The successful cross-species transmission of influenza A viruses requires key viral adaptations, including changes in receptor specificity and compatibility with host factors such as ANP32A. Host defence involves a layered innate response, which is antagonized by proteins, such as non-structural protein 1, and a robust adaptive immunity comprising cytotoxic CD8 T cells targeting conserved internal proteins and B cells producing neutralizing antibodies. Diagnosis primarily depends on highly sensitive PCR-based methods and multiplexed rapid antigen tests. Prevention involves annually updated seasonal vaccines (including inactivated, live attenuated and protein-based vaccines), while treatment relies on early use of neuraminidase and polymerase acidic protein inhibitors. Research priorities include the development of improved vaccines and a better understanding of influenza virus transmission from animals to humans. - Source: PubMed
Publication date: 2026/08/06
Neumann GabrieleCowling Benjamin JChen HualanStertz SilkeManicassamy BalajiBarr Ian GUyeki Timothy MKawaoka Yoshihiro - Primary sclerosing cholangitis (PSC) is an immune-mediated cholestatic liver disease. Its molecular etiology remains poorly defined, hindering the development of mechanism-based diagnostics and therapies. Therefore, this study aimed to identify key molecular drivers and causal biomarkers of PSC by integrating transcriptomics, machine learning, and genetic causal inference. - Source: PubMed
Publication date: 2026/03/20
Cheng PengfeiQiang YuanmingSun YiboDuan BinweiOuyang YaboLi Guangming - Acidic nuclear phosphoprotein 32A (ANP32A) is not only a core component of the inhibitor of histone acetyltransferases (INHAT) complex but also a crucial pleiotropic protein regulating cellular homeostasis and disease progression. Its extensive involvement in transcriptional regulation, apoptotic cascades, and signal transduction underpins its pivotal role across virology, neurobiology, and oncology. This review systematically elucidates the structure-function relationship of ANP32A, delineating its role as an essential host factor for viral replication and its complex involvement in neurodegenerative processes. Particular emphasis is placed on its context-dependent duality within oncology, where it exerts a pronounced "double-edged sword" effect by acting as either a tumor suppressor or an oncogene depending on the cellular milieu. Ultimately, this article aims to provide a theoretical foundation for the development of precision-targeted clinical interventions directed at ANP32A. - Source: PubMed
Publication date: 2026/07/20
Zhang ZhiqiLiu EnjieWang ZeyuanHuo YajunShang YifanDu HuiminYu JunLi Wencai