Laboratory of Molecular Medicine, Medical Research Institute, Saga Medical Center KOSEIKAN, Saga 840-8571, Japan.
Research Institute for Clinical Oncology, Saitama Cancer Center, Saitama 362-0806, Japan.
Cells. 2023 Mar 6;12(5):819. doi: 10.3390/cells12050819.
CD133, also called prominin-1, is widely known as a cancer stem cell marker, and its high expression correlates with a poor prognosis in many cancers. CD133 was originally discovered as a plasma membranous protein in stem/progenitor cells. It is now known that Src family kinases phosphorylate the C-terminal of CD133. However, when Src kinase activity is low, CD133 is not phosphorylated by Src and is preferentially downregulated into cells through endocytosis. Endosomal CD133 then associates with HDAC6, thereby recruiting it to the centrosome via dynein motors. Thus, CD133 protein is now known to localize to the centrosome as endosomes as well as to the plasma membrane. More recently, a mechanism to explain the involvement of CD133 endosomes in asymmetric cell division was reported. Here, we would like to introduce the relationship between autophagy regulation and asymmetric cell division mediated by CD133 endosomes.
CD133，也称为 prominin-1，广泛被认为是癌症干细胞标志物，其高表达与许多癌症的不良预后相关。CD133 最初被发现是干细胞/祖细胞中的一种质膜蛋白。现在已知 Src 家族激酶磷酸化 CD133 的 C 末端。然而，当 Src 激酶活性较低时，CD133 不会被 Src 磷酸化，而是通过内吞作用优先下调到细胞内。内体 CD133 随后与 HDAC6 结合，从而通过动力蛋白将其招募到中心体。因此，CD133 蛋白现在已知既可以作为内体定位到中心体，也可以作为质膜定位到中心体。最近，报道了一种解释 CD133 内体参与不对称细胞分裂的机制。在这里，我们将介绍自噬调节与 CD133 内体介导的不对称细胞分裂之间的关系。
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