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Autophagy as a regulatory component of erythropoiesis
#MMPMID25689426
Zhang J
; Wu K
; Xiao X
; Liao J
; Hu Q
; Chen H
; Liu J
; An X
Int J Mol Sci
2015[Feb]; 16
(2
): 4083-94
PMID25689426
show ga
Autophagy is a process that leads to the degradation of unnecessary or
dysfunctional cellular components and long-lived protein aggregates.
Erythropoiesis is a branch of hematopoietic differentiation by which mature red
blood cells (RBCs) are generated from multi-potential hematopoietic stem cells
(HSCs). Autophagy plays a critical role in the elimination of mitochondria,
ribosomes and other organelles during erythroid terminal differentiation. Here,
the modulators of autophagy that regulate erythroid differentiation were
summarized, including autophagy-related (Atg) genes, the B-cell lymphoma 2
(Bcl-2) family member Bcl-2/adenovirus E1B 19 kDa interacting protein 3-like
(Nix/Binp3L), transcription factors globin transcription factor 1 (GATA1) and
forkhead box O3 (FoxO3), intermediary factor KRAB-associated protein1 (KAP1), and
other modulators, such as focal adhesion kinase family-interacting protein of
200-kDa (FIP200), Ca2+ and 15-lipoxygenase. Understanding the modulators of
autophagy in erythropoiesis will benefit the autophagy research field and
facilitate the prevention and treatment of autophagy-related red blood cell
disorders.
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