1.Effects of SUMOylation on the subcellular localization and function of DAXX.
Ling LI ; Juan WEN ; Qin-Hui TUO ; Duan-Fang LIAO
Acta Physiologica Sinica 2013;65(1):89-95
Death domain-associated protein (DAXX) as a multifunctional nuclear protein widely resides in nucleolus, nucleoplasm, chromatin, promyelocytic leukaemia nuclear bodies (PML-NBs) and cytoplasm. It plays significant roles in transcriptional regulation, apoptosis, cell cycle and other biological activities. Small ubiquitin-like modifier (SUMO) is required for SUMOylation which is a highly conserved post-translational modification in a wide variety of cellular processes. Numerous studies demonstrated that SUMOylation has a great effect on the subcellular localization and functional regulation of DAXX. This review will provide a summary for SUMOylation of DAXX.
Adaptor Proteins, Signal Transducing
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physiology
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Gene Expression Regulation
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Humans
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Nuclear Proteins
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physiology
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Sumoylation
2.The Relationship between ASXL2 and ZBTB7A Gene Mutations and Prognosis in Patients with Acute Myeloid Leukemia.
Journal of Experimental Hematology 2021;29(2):450-455
OBJECTIVE:
To investigate the relationship between acute myeloid leukemia (AML) patients ASXL2, ZBTB7A gene mutations and the prognosis.
METHODS:
42 AML Patients treated in our hospital from January 2014 to January 2016 were selected and ASXL2 and ZBTB7A genes of their bone marrow samples were sequenced, the genetic characteristics and prognosis of core-binding factor-AML(CBF-AML) patients with ASXL2 and ZBTB7A mutations were analyzed.
RESULTS:
ASXL2 (33.3%) and ZBTB7A (9.5%) mutations were found in t (8; 21) AML patients. Compared with wild-type, patients with ASXL2 mutations showed significantly higher white blood cell count at diagnosis [(9.49±1.85)×10
CONCLUSION
ASXL2 and ZBTB7A mutations are frequently found in t (8; 21) AML patients. The mutation of ASXL2 and ZBTB7A genes shows no significant effect on the prognosis of AML patients.
Cell Line, Tumor
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DNA-Binding Proteins/genetics*
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Humans
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Leukemia, Myeloid, Acute/genetics*
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Mutation
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Oncogene Proteins, Fusion/genetics*
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Prognosis
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Repressor Proteins/genetics*
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Transcription Factors/genetics*