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1 cells and an excess of immature cells called promyelocytes.
2 psin G stored in the azurophilic granules of promyelocytes.
3 he normal gene expression pattern of primary promyelocytes.
4 was remarkably similar to that of wild-type promyelocytes.
5 ing RARalpha-PLZF and PLZF-RARalpha in their promyelocytes.
6 at highest levels in cells representative of promyelocytes.
7 t 2 days, corresponding to the appearance of promyelocytes.
8 e stably expressed in undifferentiated HL-60 promyelocytes.
9 rlichia-infected equine neutrophils or HL-60 promyelocytes.
10 e WBC differential showed 64% blasts and 24% promyelocytes.
12 rogenitor cell line, with characteristics of promyelocytes able to differentiate into granulocytes.
14 ll culture to monitor the oxidative burst of promyelocytes and in vivo to image lung inflammation.
15 sed proliferating myeloid precursors such as promyelocytes and myelocytes, only mature monocytes and
16 reduced endogenous PU.1 mRNA levels in HL60 promyelocytes, and decreased Sfpi1 mRNA levels were also
18 erminal granulocytic differentiation of MPRO promyelocytes, and this differentiation is associated wi
19 epsilon mRNA is markedly enhanced as the NB4 promyelocytes are induced by retinoids to differentiate
20 cer of terminal differentiation of malignant promyelocytes, but its effects on more primitive hematop
21 cer of terminal differentiation of malignant promyelocytes, but its effects on more primitive hematop
23 a, PKCbeta, PKCbetaI, and PKCbetaII on HL-60 promyelocyte cell differentiation and proliferation were
25 onstructed from the murine RA-inducible MPRO promyelocyte cell line to identify immediate-early genes
28 o)) myeloid cells, including myeloblasts and promyelocytes, constitutively expressed the beta-chain o
29 s of ELANE point mutations was the result of promyelocyte death and differentiation arrest, and was a
30 expression in HL-60 and NB4 myeloblasts and promyelocytes decreased their proliferative capacity.
31 ythroid, myeloid, and lymphoid [EML]-derived promyelocytes) derived from EML-ic/ic cells, a myeloid m
32 ned the expression profiles of normal murine promyelocyte-enriched samples, nontransformed murine pro
33 ation and deficient functional maturation of promyelocytes (erythroid, myeloid, and lymphoid [EML]-de
35 cyte-enriched samples, nontransformed murine promyelocytes expressing human promyelocytic leukemia-re
36 d that IFN-gammaR-deficient CDllb(lo)Gr1(lo) promyelocytes from E. muris-infected mice exhibited sign
37 GATA-1 and GATA-2 was detected in eosinophil promyelocyte HL-60 clone 15 cells in response to biochem
40 genic mice and leukemic animals had abundant promyelocytes in the bone marrow, only leukemic mice exh
41 tent EML cells but not in the committed MPRO promyelocytes, indicating that differences in HDAC-conta
43 length human C/EBP-epsilon was cloned from a promyelocyte-late myeloblast-derived lambda gt11 library
45 a fraction of the Mre11 complex was bound to promyelocyte leukemia protein bodies in undamaged cells.
46 mphoma (Baf3), differentiation of the murine promyelocyte line 32D, and activation of MAP kinase in C
47 leukemias, especially those that were at the promyelocyte (M3) and myeloblast (M2) stages of developm
48 results in a clinical remission by inducing promyelocyte maturation, a significant number of patient
49 = .009), the percentage of blood blasts plus promyelocytes (median 29% v 8.5%; P = .03), and the abso
53 ish the requirement for C/EBPepsilon for the promyelocyte-myelocyte transition in myeloid differentia
54 4(-)MPO(++)) cell population, which includes promyelocytes, myelocytes and metamyelocytes; mean (+/-
55 ressed primarily in myeloid cells, including promyelocytes, myelomonocytes, and their differentiated
56 RA is indeed expressed at high levels in the promyelocytes of Ctsg-PML-RARA mice and alters the trans
59 mRNA levels were observed in myeloblasts and promyelocytes, similar to myeloperoxidase, a marker of a
63 o cause APML in an animal model, we used the promyelocyte-specific targeting sequences of the human c
64 iptionally activated at the beginning of the promyelocyte stage and are transcriptionally repressed a
65 racteristic myeloid maturation arrest at the promyelocyte stage and demonstrated an increased AMP/ADP
71 CYBB is transcriptionally inactive until the promyelocyte stage of myelopoiesis, and in mature phagoc
72 opmentally regulated pattern, peaking at the promyelocyte stage, or in cell model systems, appearing
82 R had greater percentages of myeloblasts and promyelocytes than controls (53% +/- 13% versus 3% +/- 2
83 pment, resulting an accumulation of leukemic promyelocytes that are often highly sensitive to retinoi
85 gin is a committed myeloid precursor (e.g. a promyelocyte) versus an hematopoietic stem/progenitor ce
86 n of EML cells that increased in EML-derived promyelocytes, whereas cells lacking Lbr exhibited compl
87 nal granulocytic differentiation of the MPRO promyelocytes while potentiating interleukin-3 (IL-3)-in
88 rentiation, is severely impaired in leukemic promyelocytes with the t(11;17) translocation compared w
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