Identification of the transcription factor MAZ as a regulator of erythropoiesis
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Identification of the transcription factor MAZ as a regulator of erythropoiesis. / Deen, Darya; Butter, Falk; Daniels, Deborah E; Ferrer-Vicens, Ivan; Ferguson, Daniel C J; Holland, Michelle L; Samara, Vasiliki; Sloane-Stanley, Jacqueline A; Ayyub, Helena; Mann, Matthias; Frayne, Jan; Garrick, David; Vernimmen, Douglas.
In: Blood advances, Vol. 5, No. 15, 10.08.2021, p. 3002-3015.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Identification of the transcription factor MAZ as a regulator of erythropoiesis
AU - Deen, Darya
AU - Butter, Falk
AU - Daniels, Deborah E
AU - Ferrer-Vicens, Ivan
AU - Ferguson, Daniel C J
AU - Holland, Michelle L
AU - Samara, Vasiliki
AU - Sloane-Stanley, Jacqueline A
AU - Ayyub, Helena
AU - Mann, Matthias
AU - Frayne, Jan
AU - Garrick, David
AU - Vernimmen, Douglas
N1 - © 2021 by The American Society of Hematology.
PY - 2021/8/10
Y1 - 2021/8/10
N2 - Erythropoiesis requires a combination of ubiquitous and tissue-specific transcription factors (TFs). Here, through DNA affinity purification followed by mass spectrometry, we have identified the widely expressed protein MAZ (Myc-associated zinc finger) as a TF that binds to the promoter of the erythroid-specific human α-globin gene. Genome-wide mapping in primary human erythroid cells revealed that MAZ also occupies active promoters as well as GATA1-bound enhancer elements of key erythroid genes. Consistent with an important role during erythropoiesis, knockdown of MAZ reduces α-globin expression in K562 cells and impairs differentiation in primary human erythroid cells. Genetic variants in the MAZ locus are associated with changes in clinically important human erythroid traits. Taken together, these findings reveal the zinc-finger TF MAZ to be a previously unrecognized regulator of the erythroid differentiation program.
AB - Erythropoiesis requires a combination of ubiquitous and tissue-specific transcription factors (TFs). Here, through DNA affinity purification followed by mass spectrometry, we have identified the widely expressed protein MAZ (Myc-associated zinc finger) as a TF that binds to the promoter of the erythroid-specific human α-globin gene. Genome-wide mapping in primary human erythroid cells revealed that MAZ also occupies active promoters as well as GATA1-bound enhancer elements of key erythroid genes. Consistent with an important role during erythropoiesis, knockdown of MAZ reduces α-globin expression in K562 cells and impairs differentiation in primary human erythroid cells. Genetic variants in the MAZ locus are associated with changes in clinically important human erythroid traits. Taken together, these findings reveal the zinc-finger TF MAZ to be a previously unrecognized regulator of the erythroid differentiation program.
KW - DNA-Binding Proteins/genetics
KW - Erythroid Cells/metabolism
KW - Erythropoiesis/genetics
KW - Gene Expression Regulation
KW - Humans
KW - K562 Cells
KW - Promoter Regions, Genetic
KW - Transcription Factors/genetics
U2 - 10.1182/bloodadvances.2021004609
DO - 10.1182/bloodadvances.2021004609
M3 - Journal article
C2 - 34351390
VL - 5
SP - 3002
EP - 3015
JO - Blood advances
JF - Blood advances
SN - 2473-9529
IS - 15
ER -
ID: 276701164