Lemur Tail (former tyrosine) Kinases (LMTKs) comprise a novel family of regulated serine/threonine specific kinases with three structurally and evolutionary related members. LMTKs exercise a confusing variety of cytosolic functions in cell signalling and membrane trafficking. Moreover, LMTK2 and LMTK3 also reside in the nucleus where they participate in gene transcription/regulation. As a consequence, LMTKs impact cell proliferation and apoptosis, cell growth and differentiation, as well as cell migration. All these fundamental cell behaviours can turn awry, most prominently during neuropathologies and tumour biogenesis. In cancer cells, LMTK levels are often correlated with poor overall prognosis and therapy outcome, not least owned to acquired drug resistance. In brain tissue, LMTKs are highly expressed and have been linked to neuronal and glia cell differentiation and cell homeostasis. For one member of the LMTK-family (LMTK2) a role in cystic fibrosis has been identified. Due to their role in fundamental cell processes, altered LMTK physiology may also warrant a hitherto unappreciated role in other diseases, and expose them as potential valuable drug targets.

On the backdrop of a compendium of LMTK cell functions, I hypothesize that the primary role of LMTKs may dwell within the endocytic cargo recycling and/or nuclear receptor transport pathways.

狐猴尾巴（前酪氨酸）激酶 (LMTK) 包含一个新型的调节丝氨酸/苏氨酸特异性激酶家族，具有三个结构和进化相关的成员。LMTKs 在细胞信号传导和膜运输中行使各种令人困惑的胞质功能。此外，LMTK2 和 LMTK3 也存在于细胞核中，它们参与基因转录/调控。因此，LMTK 会影响细胞增殖和凋亡、细胞生长和分化以及细胞迁移。所有这些基本的细胞行为都可能出错，尤其是在神经病理学和肿瘤生物发生期间。在癌细胞中，LMTK 水平通常与较差的整体预后和治疗结果相关，尤其是与获得性耐药有关。在脑组织中，LMTKs 高度表达，并与神经元和神经胶质细胞分化和细胞稳态有关。对于 LMTK 家族 (LMTK2) 的一个成员，已确定其在囊性纤维化中的作用。由于它们在基本细胞过程中的作用，改变的 LMTK 生理学也可能在其他疾病中发挥迄今为止未被重视的作用，并将它们暴露为潜在的有价值的药物靶点。

在 LMTK 细胞功能概要的背景下，我假设 LMTK 的主要作用可能存在于内吞货物再循环和/或核受体转运途径中。