ANP32E

Last update 08 May 2025

Basic Info

Synonyms

Acidic leucine-rich nuclear phosphoprotein 32 family member E, acidic nuclear phosphoprotein 32 family member E, ANP32E

+ [4]

Introduction

Histone chaperone that specifically mediates the genome-wide removal of histone H2A.Z/H2AZ1 from the nucleosome: removes H2A.Z/H2AZ1 from its normal sites of deposition, especially from enhancer and insulator regions. Not involved in deposition of H2A.Z/H2AZ1 in the nucleosome. May stabilize the evicted H2A.Z/H2AZ1-H2B dimer, thus shifting the equilibrium towards dissociation and the off-chromatin state (PubMed:24463511). Inhibits activity of protein phosphatase 2A (PP2A). Does not inhibit protein phosphatase 1. May play a role in cerebellar development and synaptogenesis.

100 Clinical Results associated with ANP32E

100 Translational Medicine associated with ANP32E

0 Patents (Medical) associated with ANP32E

Literatures (Medical) associated with ANP32E

01 Jan 2025·International Immunopharmacology

ANP32E promotes esophageal cancer progression and paclitaxel resistance via P53/SLC7A11 axis-regulated ferroptosis

Article

Author: Huang, Zhi-Qun ; Li, Bo-Xin ; Du, Run-Lei ; Chen, Fei-Shan ; Zhu, Hang-Jia ; Zhang, Xiao-Dong ; Li, Le ; Liu, Yi ; Sun, Li-Ying ; Zhang, Jian-Feng ; Chen, Yong-Shun ; Cai, Yu-Xin ; Ke, Shao-Bo

Esophageal cancer (EC) is associated with high mortality rates and widespread resistance to chemotherapeutic agents, like paclitaxel (PTX), posing a significant global public health challenge. ANP32E is a member of the acidic nuclear phosphoprotein 32 family, its specific biological functions and mechanisms in EC remain unclear. Through bioinformatics analysis and clinical tissue sample studies, we observed a marked upregulation of ANP32E expression in EC tissues. Utilizing ANP32E knock-out EC cell models and xenograft experiments in nude mice, we demonstrated that the absence of ANP32E significantly inhibits tumor progression and migration, whereas its overexpression exacerbates tumor growth. Transcriptomic sequencing (RNA-seq) further revealed activation of the ferroptosis pathway in ANP32E deficient cells, which was confirmed through experiments showing enhanced ferroptosis that could be reversed by the ferroptosis inhibitor ferrostatin-1. At the molecular level, ANP32E regulates EC progression and ferroptosis via the p53/SLC7A11 axis. ANP32E depletion resulted in increased p53 expression level, while inhibition of p53 partially restored the suppressed cell proliferation and increased ferroptosis in ANP32E-depleted cells. Additionally, knocking out ANP32E significantly enhanced EC cell sensitivity to PTX, Combining PTX with the ferroptosis inducer erastin was more effective in inhibiting tumor growth. In vivo, we confirmed the synergistic effect of ANP32E knock-out combined with PTX demonstrating superior tumor suppressing. Overall, our findings suggest that ANP32E regulates EC progression and ferroptosis through the p53/SLC7A11 axis, offering a potential molecular target for overcoming PTX resistance in EC treatment.

01 Jan 2025·Iranian journal of basic medical sciences

Bioinformatics analysis identifies dysregulation of miR-548F-3p and its hub gene in triple-negative breast cancer.

Article

Author: Salimi, Mahdieh ; Behroozi, Samira ; Allahyari Fard, Najaf

ObjectivesTriple-negative breast cancer (TNBC), which affects 15-20% of cases, lacks targeted therapies and poses challenges in treatment. MicroRNAs (miRNAs) are potential biomarkers and therapeutic targets in breast cancer. To unravel its unique regulatory role, this study focused on miRNA microarray analysis, particularly miR-548F-3p, in TNBC samples.Materials and MethodsUsing the GSE76275 dataset, gene expression profiles were analyzed using the Affymetrix Human Genome U133 Plus 2.0 Array. Differentially expressed genes (DEGs) were identified using robust preprocessing. Weighted gene co-expression network analysis (WGCNA) explored gene modules and identified hub genes co-expressed with miR-548F-3p. Functional enrichment and protein-protein interaction (PPI) network analyses were conducted. Survival analysis was used to assess the prognostic impact of the identified genes.ResultsThe study found 224 up-regulated DEGs, with miR-548F-3p exhibiting significant down-regulation. MultimiR identified 400 genes that were targeted by miR-548F-3p. WGCNA revealed a blue co-expression module, with 356 genes targeted by miR-548F-3p. A Venn diagram identified common genes, including VANGL2, BRCC3, ANP32E, and ANLN. Functional enrichment highlighted crucial pathways in TNBC pathogenesis, including mitotic spindle organization, spindle assembly checkpoint signaling, cell cycle, and amino acid (serine) metabolism. PPI network analysis identified hub genes, including FOXM1, KIF23, and CDC20. VANGL2, BRCC3, ANP32E, and ANLN were significantly associated with patient outcomes in survival analysis.ConclusionThis analysis highlighted TNBC's molecular landscape, emphasizing miR-548F-3p's regulatory role. The identified genes, VANGL2, BRCC3, ANP32E, and ANLN, offer insights into TNBC pathogenesis and potential therapeutic targets, laying the foundation for understanding their clinical implications in the intricate landscape of TNBC.

04 Oct 2024·Science Advances

Cell type–specific epigenetic priming of gene expression in nucleus accumbens by cocaine

Article

Author: Mews, Philipp ; Garcia, Benjamin A. ; Ryan, Meagan ; Browne, Caleb J. ; Reyes, Abner A. ; Ramakrishnan, Aarthi ; Nestler, Eric J. ; Estill, Molly ; Kronman, Hope ; Shen, Li ; Van der Zee, Yentl ; Gurung, Ashik ; Sidoli, Simone ; Futamura, Rita

A hallmark of addiction is the ability of drugs of abuse to trigger relapse after periods of prolonged abstinence. Here, we describe an epigenetic mechanism whereby chronic cocaine exposure causes lasting chromatin and downstream transcriptional modifications in the nucleus accumbens (NAc), a critical brain region controlling motivation. We link prolonged withdrawal from cocaine to the depletion of the histone variant H2A.Z, coupled with increased genome accessibility and latent priming of gene transcription, in D1 dopamine receptor–expressing medium spiny neurons (D1 MSNs) that relate to aberrant gene expression upon drug relapse. The histone chaperone ANP32E removes H2A.Z from chromatin, and we demonstrate that D1 MSN–selective Anp32e knockdown prevents cocaine-induced H2A.Z depletion and blocks cocaine’s rewarding actions. By contrast, very different effects of cocaine exposure, withdrawal, and relapse were found for D2 MSNs. These findings establish histone variant exchange as an important mechanism and clinical target engaged by drugs of abuse to corrupt brain function and behavior.

Analysis

Perform a panoramic analysis of this field.

view full example data

AI Agents Built for Biopharma Breakthroughs

Accelerate discovery. Empower decisions. Transform outcomes.

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

ANP32E

Basic Info

Related

Analysis