类型2的kalreticulin突变激活ATF6,以促进BCL-xL介导的存活在骨髓增殖性瘤中

Nicole S Arellano1,2, William L Heaton1, Mirielle C Nauman3

  • 1Division of Hematology and Hematological Malignancies, The University of Utah, Salt Lake City, UT.

Blood
|May 22, 2025
PubMed
概括

卡尔雷丘林 (CALR) 类型2突变激活了ATF6途径的展开蛋白质反应 (UPR) 由于失去了陪伴者功能. CALRins5细胞依赖ATF6生存,BCL-XL被确定为一个关键目标.

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