腺苷激酶（ADK）是一种关键的代谢酶，属于嘌呤代谢酶家族，主要负责催化腺苷（adenosine）的磷酸化反应，将其转化为腺苷一磷酸（AMP），同时消耗ATP。这一反应在维持细胞内腺苷水平平衡中至关重要，而腺苷是一种重要的信号分子，参与多种生理过程，如神经传递、血管舒张、免疫调节和能量代谢。ADK主要表达于肝脏、大脑和肌肉等组织，尤其在脑内的高表达对调节腺苷的神经抑制作用具有关键影响。ADK的功能异常或突变可能导致腺苷代谢紊乱，进而影响其介导的信号通路。例如，ADK功能丧失突变会导致细胞内腺苷积累，过度激活腺苷受体（如A1和A2A受体），可能引发癫痫、睡眠障碍或神经保护效应减弱；而ADK过表达则会降低腺苷水平，可能导致神经兴奋性增高、炎症反应加剧或心血管功能异常。研究表明，ADK与多种疾病相关，如癫痫、缺血性脑损伤、某些癌症和炎症性疾病。在癫痫中，ADK的上调会减少腺苷的抗惊厥作用；而在脑缺血时，抑制ADK可增加腺苷水平，发挥神经保护作用。此外，ADK在肿瘤代谢重编程中也可能发挥作用，因为癌细胞常依赖嘌呤代谢支持其快速增殖。ADK属于嘌呤代谢酶家族，该家族成员通常参与嘌呤核苷酸的合成与回收，维持细胞内嘌呤库的稳定。家族成员包括腺苷脱氨酶（ADA）、嘌呤核苷磷酸化酶（PNP）等，它们共同调控嘌呤代谢通路，影响细胞增殖、能量供应和信号转导。ADK表达的异常（过高或过低）会干扰腺苷依赖的生理过程，例如过表达可能导致神经兴奋毒性或促炎状态，而表达降低则可能增强腺苷的抑制性效应，如镇静、抗炎或心脏保护作用。因此，ADK是代谢和疾病治疗研究的重要靶点之一。

该基??因能催化伽玛磷酸从ATP转移至腺苷，从而用作两个外腺苷的浓度和细胞内腺嘌呤核苷酸的调节剂的酶。腺苷对心血管，神经，呼吸道，和免疫系统和酶的抑制剂广泛影响可以发挥提高血管内腺苷浓度并用作抗炎剂的重要的药理学作用。已发现该基因编码不同亚型的多个抄本变形。 [由RefSeq的，2011年1月提供]

Adenosine kinase (ADK) is a critical metabolic enzyme within the purine metabolism family that catalyzes the ATP-dependent phosphorylation of adenosine to adenosine monophosphate (AMP), thereby serving as a primary mechanism for regulating intracellular adenosine homeostasis. As adenosine is a potent signaling molecule involved in neurotransmission, vasodilation, immune modulation, and energy metabolism, ADK activity is essential for fine-tuning these physiological processes, particularly in tissues with high expression levels such as the liver, brain, and skeletal muscle. In the central nervous system, ADK-mediated clearance of adenosine is crucial for modulating neuroinhibitory signaling; consequently, loss-of-function mutations lead to adenosine accumulation and excessive activation of adenosine receptors (such as A1 and A2A), which can result in altered sleep patterns, reduced neuroprotection, or paradoxical effects on seizure thresholds, whereas overexpression lowers adenosine levels, potentially increasing neuronal excitability, exacerbating inflammatory responses, and disrupting cardiovascular function. This regulatory role positions ADK as a significant target in various pathological contexts, including epilepsy, where its upregulation diminishes the anticonvulsant effects of adenosine, and ischemic brain injury, where its inhibition enhances adenosine-mediated neuroprotection. Furthermore, given that cancer cells often rely on purine salvage pathways to support rapid proliferation, ADK may contribute to tumor metabolic reprogramming, and its dysregulation is implicated in inflammatory diseases and cardiac disorders. As a key component of the purine nucleotide recycling network alongside enzymes like adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP), ADK maintains cellular purine pool stability, linking metabolic flux to critical signaling outcomes such as neuroexcitotoxicity, inflammation, and cardiac protection, thereby establishing it as a promising therapeutic target for metabolic and neurological diseases.

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