NAP1L1

更新于：2025-05-07

基本信息

别名

hNRP、MGC23410、MGC8688

+ [7]

简介

Histone chaperone that plays a role in the nuclear import of H2A-H2B and nucleosome assembly (PubMed:20002496, PubMed:21211722, PubMed:26841755). Participates also in several important DNA repair mechanisms: greatly enhances ERCC6-mediated chromatin remodeling which is essential for transcription-coupled nucleotide excision DNA repair (PubMed:28369616). Stimulates also homologous recombination (HR) by RAD51 and RAD54 which is essential in mitotic DNA double strand break (DSB) repair (PubMed:24798879). Plays a key role in the regulation of embryonic neurogenesis (By similarity). Promotes the proliferation of neural progenitors and inhibits neuronal differentiation during cortical development (By similarity). Regulates neurogenesis via the modulation of RASSF10; regulates RASSF10 expression by promoting SETD1A-mediated H3K4 methylation at the RASSF10 promoter (By similarity). (Microbial infection) Positively regulates Epstein-Barr virus reactivation in epithelial cells through the induction of viral BZLF1 expression. (Microbial infection) Together with human herpesvirus 8 protein LANA1, assists the proper assembly of the nucleosome on the replicated viral DNA.

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100 项与 NAP1L1 相关的临床结果

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100 项与 NAP1L1 相关的转化医学

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0 项与 NAP1L1 相关的专利（医药）

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项与 NAP1L1 相关的文献（医药）

2024-12-16·Animal Biotechnology

Weighted single step GWAS reveals genomic regions associated with economic traits in Murrah buffaloes

Article

作者: Gowane, Gopal ; Kumar, Ravi ; Joshi, Pooja ; George, Linda ; Verma, Archana ; Alex, Rani ; Vohra, Vikas

The objective of the present study was to identify genomic regions influencing economic traits in Murrah buffaloes using weighted single step Genome Wide Association Analysis (WssGWAS). Data on 2000 animals, out of which 120 were genotyped using a double digest Restriction site Associated DNA (ddRAD) sequencing approach. The phenotypic data were collected from NDRI, India, on growth traits, viz., body weight at 6M (month), 12M, 18M and 24M, production traits like 305D (day) milk yield, lactation length (LL) and dry period (DP) and reproduction traits like age at first calving (AFC), calving interval (CI) and first service period (FSP). The biallelic genotypic data consisted of 49353 markers post-quality check. The heritability estimates were moderate to high, low to moderate, low for growth, production, reproduction traits, respectively. Important genomic regions explaining more than 0.5% of the total additive genetic variance explained by 30 adjacent SNPs were selected for further analysis of candidate genes. In this study, 105 genomic regions were associated with growth, 35 genomic regions with production and 42 window regions with reproduction traits. Different candidate genes were identified in these genomic regions, of which important are OSBPL8, NAP1L1 for growth, CNTNAP2 for production and ILDR2, TADA1 and POGK for reproduction traits.

2024-11-01·Molecular Cancer Research

NAP1L1 Promotes Endometrial Cancer Progression via EP300-Mediated DDX5 Promoter Acetylation

Article

作者: Zhu, Xiangfei ; Lu, Xiaoyuan ; Shao, Zhiying ; Li, Yishan ; Chen, Youguo

AbstractEndometrial cancer is one of the predominant tumors of the female reproductive system. In this current study, we investigated the functions and related mechanisms of nucleosome assembly protein 1 like 1 (NAP1L1)/ DEAD-box helicase 5 (DDX5) in endometrial cancer. This retrospective study analyzed the medical records of patients with endometrial cancer, collected tissue samples for NAP1L1 and DDX5 staining, and conducted survival analysis using the Kaplan–Meier method. To evaluate the impact of NAP1L1 and/or DDX5 on cellular processes in endometrial cancer cells, several techniques were employed. These included Cell Counting Kit-8 assay, wound healing assay, Transwell assay, as well as overexpression or knockdown of target gene expression. Additionally, chromatin immunoprecipitation, dual luciferase reporter gene, and coimmunoprecipitation (Co-IP) assay were utilized to confirm the interaction between NAP1L1, E1A-binding protein p300 (EP300), and DDX5. Furthermore, qRT-PCR, Western blot, and Co-IP assay were performed to analyze the modulation of NAP1L1/DDX5 in Wnt/β-catenin. NAP1L1 and DDX5 expression were upregulated in endometrial cancer tissues, and correlated with poor prognosis. NAP1L1/DDX5 promoted endometrial cancer cell proliferation, migration, and invasion. NAP1L1 promotes acetylation and transcription by recruiting EP300 to the DDX5 promoter. DDX5 could activate Wnt/β-catenin signal by binding to β-catenin. In animal models, knockdown of NAP1L1 inhibits endometrial cancer tumor growth and lung metastasis. To sum up, our study demonstrated that NAP1L1 promoted the malignant phenotypes of endometrial cancer cells via recruiting EP300 to promote DDX5 acetylation, thus activating the Wnt/β-catenin signaling pathway.Implications: Our research findings indicate that targeting the NAP1L1/EP300/DX5 axis might be a new potential treatment option for endometrial cancer.

2024-04-23·Blood Advances

Structural variants involving MLLT10 fusion are associated with adverse outcomes in pediatric acute myeloid leukemia

Article

作者: Buteyn, Nathaniel ; Kolb, E. Anders ; Gamis, Alan S. ; Abla, Oussama ; Hirsch, Betsy ; Harmon, Lauren M. ; Wen, Hong ; Gerbing, Robert B. ; Ries, Rhonda E. ; Triche, Tim ; Farrar, Jason E. ; Alonzo, Todd ; Deshpande, Aniruddha J. ; Raimondi, Susana ; Cooper, Todd ; Aplenc, Richard ; Meshinchi, Soheil

AbstractMLLT10 gene rearrangements with KMT2A occur in pediatric acute myeloid leukemia (AML) and confer poor prognosis, but the prognostic impact of MLLT10 in partnership with other genes is unknown. We conducted a retrospective study with 2080 children and young adults with AML registered on the Children’s Oncology Group AAML0531 (NCT00372593) and AAML1031 trials (NCT01371981). Transcriptome profiling and/or karyotyping were performed to identify leukemia-associated fusions associated with prognosis. Collectively, 127 patients (6.1%) were identified with MLLT10 fusions: 104 (81.9%) with KMT2A::MLLT10, 13 (10.2%) with PICALM::MLLT10, and 10 (7.9%) X::MLLT10: (2 each of DDX3X and TEC), with 6 partners (DDX3Y, CEP164, SCN2B, TREH, NAP1L1, and XPO1) observed in single patients. Patients with MLLT10 (n = 127) demonstrated adverse outcomes, with 5-year event-free survival (EFS) of 18.6% vs 49% in patients without MLLT10 (n = 1953, P < .001), inferior 5-year overall survival (OS) of 38.2% vs 65.7% (P ≤ .001), and a higher relapse risk of 76% vs 38.6% (P < .001). Patients with KMT2A::MLLT10 had an EFS from study entry of 19.5% vs 12.7% (P = .628), and an OS from study entry of 40.4% vs 27.6% (P = .361) in those with other MLLT10 fusion partners. Patients with PICALM::MLLT10 had an EFS of 9.2% vs 20% in other MLLT10− without PICALM (X::MLLT10; P = .788). Patients with PICALM::MLLT10 and X::MLLT10 fusions exhibit a DNA hypermethylation signature resembling NUP98::NSD1 fusions, whereas patients with KMT2A::MLLT10 bear aberrations primarily affecting distal regulatory elements. Regardless of the fusion partner, patients with AML harboring MLLT10 fusions exhibit very high–risk features and should be prioritized for alternative therapeutic interventions.

项与 NAP1L1 相关的新闻（医药）

2024-04-02

·今日头条

抑制肿瘤进展！贵州医科大学左石/陈腾祥发现肝细胞癌靶向治疗策略

本文为转化医学网原创，转载请注明出处作者：Rainbow 导读：肝细胞癌（HCC）是肝癌最常见的亚型，约占所有肝癌病例的75%。 3月27日，贵州医科大学左石、陈腾祥共同通讯在期刊《Cell Death Discovery》上在线发表题为“NAP1L1 regulates BIRC2 ubiquitination modification via E3 ubiquitin ligase UBR4 and hence determines hepatocellular carcinoma progression”的研究论文，研究结果为开发靶向NAP1L1治疗肝细胞癌的药物提供了新的理论依据。 https://www.nature.com/articles/s41420-024-01927-2 研究背景 01 原发性肝癌是全球第七大常见肿瘤，也是癌症相关死亡的第二大原因，其发病率逐年增加。肝细胞癌（HCC）是肝癌最常见的亚型，约占所有肝癌病例的75%。肝细胞癌（HCC）的进展与肿瘤细胞的凋亡逃逸密切相关，这促进了癌细胞的长期存活和异常增殖，是多药耐药发展的重要机制。激活或恢复肿瘤细胞凋亡是治疗肿瘤的有效策略。肿瘤细胞的凋亡逃逸涉及多条信号通路和表观遗传修饰，包括关键蛋白的翻译后调控。泛素化在泛素-蛋白酶体系统中是重要的翻译后修饰，负责调控与凋亡相关蛋白的降解和周转。 NAP1L1是核小体组装蛋白1样蛋白家族的成员，具有高度保守的中心结构域、一个晶体结构域和两个N端结构域。它主要分布在细胞质中，其次分布在细胞核中。几项研究表明，NAP1L1是潜在的促肿瘤因子，参与了恶性肿瘤（如肝细胞癌、结直肠癌和乳腺癌）的发展进程。阐明NAP1L1对肝细胞癌细胞不同恶性特征的影响可能有助于理解NAP1L1的生理功能。 BIRC2通过与肿瘤坏死因子受体相关因子结合来抑制细胞凋亡，并已被确定为肿瘤细胞异常增殖、多药耐药和免疫逃逸的关键驱动因素。BIRC2介导的细胞凋亡逃避在HCC的发生中起关键作用。泛素化的失调与BIRC2的异常降解和癌细胞的凋亡逃逸有关。研究BIRC2稳定在HCC进展中的作用对于了解HCC细胞凋亡逃逸机制非常重要。研究发现 02 之前已经证实，NAP1L1的异常高表达通过募集HDGF来调节c-Jun的功能，增强了CCND1的表达，并促进了HCC细胞的增殖。在这项研究中，研究人员发现NAP1L1不影响HCC细胞的迁移和侵袭能力，而是通过E3泛素连接酶UBR4影响BIRC2蛋白的稳定性，调节细胞凋亡的发生并决定HCC的进展。总之，这项研究揭示了一种新的机制，NAP1L1通过UBR4影响BIRC2的泛素化，并调节细胞凋亡以确定HCC的进展。该机制代表了靶向NAP1L1治疗以NAP1L1或BIRC2高表达为特征的HCC的有前景的策略。研究结论 03 综上所述，研究结果为开发靶向NAP1L1治疗肝细胞癌的药物提供了新的理论依据。参考资料： https://www.nature.com/articles/s41420-024-01927-2 注：本文旨在介绍医学研究进展，不能作为治疗方案参考。如需获得健康指导，请至正规医院就诊。热门·直播/活动 🕓 上海｜06月14日-16日 ▶ 第六届上海国际癌症大会将于6月14-16日在上海举办，学科交叉，共同推进肿瘤研究与诊治多模态！ 🕓 北京｜09月20日-21日 ▶ 第五届单细胞技术应用研讨会暨空间组学前沿研讨会欢迎您的参与！点击对应文字查看详情

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