AK5

Last update 08 May 2025

Basic Info

Synonyms

adenylate kinase 5, Adenylate kinase isoenzyme 5, AK 5

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Introduction

Nucleoside monophosphate (NMP) kinase that catalyzes the reversible transfer of the terminal phosphate group between nucleoside triphosphates and monophosphates. Active on AMP and dAMP with ATP as a donor. When GTP is used as phosphate donor, the enzyme phosphorylates AMP, CMP, and to a small extent dCMP. Also displays broad nucleoside diphosphate kinase activity.

100 Clinical Results associated with AK5

100 Translational Medicine associated with AK5

0 Patents (Medical) associated with AK5

Literatures (Medical) associated with AK5

01 Dec 2025·Molecular Biology Reports

Single-cell sequencing reveals that AK5 inhibits apoptosis in AD oligodendrocytes by regulating the AMPK signaling pathway

Article

Author: Chen, Jibing ; Luo, Ning ; Jiang, Yuanjing ; Tong, Wangxia ; Zhang, Jiatong ; Yang, Shiyun ; Zhou, Xinmei ; Chen, Bolun

BACKGROUNDNeuroinflammation and abnormal energy metabolism have been shown to significantly contribute to the progression of Alzheimer's disease (AD). Adenylate kinase 5 (AK5), an enzyme predominantly expressed in the brain regulates ATP metabolism, has an unclear role in energy metabolism and neuroinflammation in AD.METHODSThe AD datasets were derived from the GEO public database to analyze the expression levels of AK5 in AD and normal samples and to assess the relationship between AK5 expression and the clinical characteristics of AD patients. Functional enrichment analysis was employed to investigate the effects of changes in AK5 expression on energy metabolism and immunoinflammation in AD, as well as the underlying mechanisms. Moreover, the influence of AK5 expression variations on oligodendrocyte development was assessed, and the predicted outcomes were validated through cellular experiments.RESULTSBioinformatic analysis revealed that AK5 was lowly expressed in AD olfactory lobe tissues, accompanied by increased immunoinflammation and apoptosis. Increased expression of AK5 was associated with the activation of AMPK signaling, enhanced oxidative phosphorylation, and overall stimulation of energy metabolism. In oligodendrocytes treated with Aβ1-42, overexpression of AK5 resulted in elevated levels of P-AMPK, SIRT1, and BCL-2 proteins, while reducing the levels of BAX, CASPASE-3, and NF-κB proteins. This modulation activated AMPK signaling, thereby inhibiting neuroinflammation and apoptosis. In contrast, low levels of AK5 expression during early differentiation triggered inflammatory responses and increased apoptosis in oligodendrocytes.CONCLUSIONAK5 inhibits AD oligodendrocyte apoptosis by activating the AMPK signaling pathway.

01 Apr 2025·Journal of Neurology

Exploring autoantigens in autoimmune limbic encephalitis using phage immunoprecipitation sequencing

Article

Author: McKeon, Andrew ; Karsten, Carley ; Losada, Vaniolky ; Gilligan, Michael ; Mills, John R ; Zekeridou, Anastasia ; Dubey, Divyanshu ; Knight, Andrew M ; Pittock, Sean J ; Kherbek, Haidara ; LaFrance-Corey, Reghann G ; Dasari, Surendra ; Paramasivan, Naveen K ; Thakolwiboon, Smathorn

OBJECTIVESTo describe the use of high-throughput whole-human proteome phage immunoprecipitation sequencing (PhIP-Seq) in identifying potential antigens for antibody-negative autoimmune limbic encephalitis (ALE).METHODSWe used PhIP-Seq to analyze cerebrospinal fluid (CSF) from patients with antibody-negative ALE evaluated in our lab with detailed clinical records available (2008-2023). Identified autoantigens were validated using recombinant protein-based assay.RESULTSOf the 18 CSF samples from patients with ALE, 1 sample showed neuronal PAS domain protein 4 (NPAS4) as the putative autoantigen with the highest enrichment score. Patient presented with cognitive decline, gait dysfunction and unique MRI brain findings revealing asymmetric involvement of the medial temporal lobes with extension to the insular cortex and anterior temporal lobes. No malignancy was detected, and although the patient was initiated on immunotherapy, follow-up evaluation was limited. Another sample with very similar clinical and MRI brain findings, who developed ALE following COVID-19 infection, was referred for evaluation for neural-specific autoantibodies, and PhIP-Seq identified NPAS4 as the putative autoantigen. In both these samples, NPAS4-IgG was confirmed by cell-based assay (CBA) and enzyme-linked immunosorbent assay (ELISA). To assess the specificity of the NPAS4 autoantigen, a large cohort of disease (CSF, n = 49, serum, n = 220) and healthy controls (serum, n = 90) were tested by ELISA which were also negative. In addition, three samples had a high enrichment score for adenylate kinase 5 (AK5), an autoantigen associated with ALE. These patients also displayed a unique immunosignature that included AK5-IgG, which is distinct from NPAS4-IgG ALE or antibody-negative ALE. All three AK5-IgG seropositive cases presented with subacute memory loss, with MRI/PET brain florid showing medial temporal lobe involvement. No malignancy was detected in any of the three patients and immunotherapy led to improvement in one.CONCLUSIONOur study demonstrates the utility of high-throughput PhIP-Seq in identifying potential autoantigens in antibody-negative ALE. The identification of NPAS4 as a putative antigen and identification of additional AK5-IgG-positive cases, underscores the potential of PhIP-Seq as a powerful tool in autoimmune disease research.

22 Jan 2025·Current Pharmaceutical Biotechnology

Integrative Bioinformatics and Experimental Validation Reveal the Mechanistic Action of Patchouli Alcohol in Prostate Cancer Treatment

Article

Author: Zhao, Juan ; Cai, Jian ; Zhai, Songhui

Introduction:Prostate cancer is an androgen-dependent malignancy, and the use of androgen deprivation therapies frequently results in treatment resistance, relapse, and the development of aggressive castration-resistant tumors. Patchouli alcohol, a tricyclic sesquiterpene derived from Pogostemon cablin of the Labiatae family, has demonstrated potential in modulating inflammatory responses and tumor progression. This study aimed to investigate the mechanisms through which patchouli alcohol influences inflammatory pathways associated with prostate cancer using bioinformatics and experimental validation.Methods:Differentially Expressed Genes (DEGs) were identified from the GSE46602 dataset, containing 36 prostate cancer and 14 normal prostate biopsy samples, using the GEO2R tool (adjusted P < 0.05). Functional annotation was performed using GO and KEGG databases, while PPI networks were constructed via STRING and Cytoscape. Key hub genes were identified. To validate the bioinformatics findings, qPCR and Western blotting were employed to confirm the differential expression of selected hub genes in DU145 prostate cancer cells treated with patchouli oil.Results:Bioinformatic analysis revealed 71 DEGs, including 35 upregulated and 36 downregulated genes. Thirteen hub genes were identified (DCK, APRT, ADK, KCNK9, ADSL, PKM, KCNK3, S100A10, ENTPD2, PKLR, ARHGEF38, TPK1, and AK5), which were enriched in pathways, such as MAPK, PI3K-Akt, Ras, and Rap1. Experimental validation confirmed the upregulation of DCK, APRT, KCNK9, ADSL, PKM, S100A10, ENTPD2, PKLR, ARHGEF38, and AK5, and the downregulation of ADK, KCNK3, and TPK1 at both the mRNA and protein levels.Conclusion:Patchouli alcohol appears to influence multiple hub genes associated with prostate cancer progression through its modulation of key cellular signaling and metabolic pathways. These findings support its potential role as a therapeutic agent for prostate cancer.

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AK5

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