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. 2021 Oct 25;35(1):360–378. doi: 10.1007/s13577-021-00636-7

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — Regulatory role of USP30-AS1 mediates ANKRD13A upregulating to induce HLA-I internalization. A Survival analysis between AML patients with low and high expression of ANKRD13A. B Co-immunoprecipitation was used to identify interaction between HLA-I and ANKRD13A or SUP30-AS1 in AML cells, including knockdown and overexpression. C FISH analysis of the location of HLA-I (green) in the cytomembrane of AML cells across knockdown and overexpression treatments. D Protein expressions of HLA-I were measured in AML cells transfected with recombinant plasmids, including knockdown and overexpression. Significant differences are indicated by *p < 0.05, n = 3