The Kank (kidney or KN motif and ankyrin repeat domain-containing) family of proteins has been described as essential for crosstalk between actin and microtubules. Kank1, 2, 3 and 4 arose by gene duplication and diversification and share conserved structural domains. KANK proteins are localised mainly to the plasma membrane in focal adhesions, indirectly affecting RhoA and Rac1 thus regulating actin cytoskeleton. In addition, Kank proteins are part of the cortical microtubule stabilisation complex regulating microtubules. Most of the data have been collected for Kank1 protein whose expression promotes apoptosis and cell-cycle arrest while Kank3 was identified as hypoxia-inducible proapoptotic target of p53. A discrepancy in Kanks role in regulation of cell migration and sensitivity to antitumour drugs has been observed in different cell models. Since expression of Kank1 and 3 correlate positively with tumour progression and patient outcome, at least in some tumour types, they are candidates for tumour suppressors.

Kank（包含肾脏或 KN 基序和锚蛋白重复结构域）蛋白家族被描述为肌动蛋白和微管之间串扰所必需的。 Kank1、2、3 和 4 由基因复制和多样化产生，并共享保守的结构域。 KANK 蛋白主要定位于粘着斑的质膜，间接影响 RhoA 和 Rac1，从而调节肌动蛋白细胞骨架。此外，Kank 蛋白是调节微管的皮质微管稳定复合物的一部分。大多数数据都是针对 Kank1 蛋白收集的，其表达促进细胞凋亡和细胞周期停滞，而 Kank3 被确定为 p53 缺氧诱导的促凋亡靶标。在不同的细胞模型中观察到 Kanks 在调节细胞迁移和抗肿瘤药物敏感性方面的作用存在差异。由于 Kank1 和 3 的表达与肿瘤进展和患者结果呈正相关，至少在某些肿瘤类型中，因此它们是肿瘤抑制因子的候选者。