Hypoxia and expression of hypoxia-related proteins in acute myeloid leukemia

2011 ◽  
Vol 35 (5) ◽  
pp. 573-574 ◽  
Author(s):  
Michael Fiegl ◽  
Karsten Spiekermann
2009 ◽  
Vol 28 (1) ◽  
pp. 63-69
Author(s):  
S. Klymenko ◽  
I. Ilyenko ◽  
N. Golarnik ◽  
O. Maznichenko ◽  
A. Breier ◽  
...  

2017 ◽  
Vol Volume 10 ◽  
pp. 3635-3644 ◽  
Author(s):  
Hong Guo ◽  
Ting-juan Zhang ◽  
Xiang-mei Wen ◽  
Jing-dong Zhou ◽  
Ji-chun Ma ◽  
...  

2018 ◽  
Vol 19 (4) ◽  
pp. 299-309
Author(s):  
Alex José de Melo Silva

Abstract The family of Bcl-2 proteins is one of the most responsible for apoptosis pathway, that is a critical process to the maintenance of tissue homeostasis. Bcl-2 is an essential apoptotic regulator belonging to a family of functionally and structurally related proteins known as the Bcl-2 family. Some members of this family act as anti-apoptotic regulators, whereas others act in pro-apoptotic function. The relationship between the pro and anti-apoptotic proteins can regulate whether cells begin the apoptosis or remain its life cycle. Increasing of Bcl-2 expression has been found in some hematologic diseases, such as Acute Myeloid Leukemia (AML) and their effects on responsiveness to anticancer therapy have been recently described. Thus, this review aims to discuss apoptosis and the role of the Bcl-2 family of proteins in chemoresistance when overexpressed in patients committed with Acute Myeloid Leukemia submitted to chemotherapy treatment.


2022 ◽  
Vol 23 (1) ◽  
pp. 514
Author(s):  
Sang-Soo Park ◽  
Kwang-Hyun Baek

Acute myeloid leukemia (AML), the most common form of an acute leukemia, is a malignant disorder of stem cell precursors of the myeloid lineage. Ubiquitination is one of the post-translational modifications (PTMs), and the ubiquitin-like proteins (Ubls; SUMO, NEDD8, and ISG15) play a critical role in various cellular processes, including autophagy, cell-cycle control, DNA repair, signal transduction, and transcription. Also, the importance of Ubls in AML is increasing, with the growing research defining the effect of Ubls in AML. Numerous studies have actively reported that AML-related mutated proteins are linked to Ub and Ubls. The current review discusses the roles of proteins associated with protein ubiquitination, modifications by Ubls in AML, and substrates that can be applied for therapeutic targets in AML.


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