+ |
HOXA9 | down-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255864 |
|
|
Homo sapiens |
Hematopoietic Stem Cell |
pmid |
sentence |
14701735 |
Here we demonstrate that MLL-ENL immortalizes cells mainly through inducing a reversible block on myeloid differentiation that is dependent on upregulation of Hoxa9 and Meis1 and that enforced expression of these two genes is sufficient to substitute for MLL-ENL function. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, ASXL1 in AML, DNMT3A in AML, Onco-fusion proteins in AML, MLL fusion protein in AML, AML_TRIPLETS, Triple mutant AML |
+ |
DPF2 | down-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261969 |
|
|
Homo sapiens |
Hematopoietic Stem Cell |
pmid |
sentence |
24332853 |
Here, DPF2 appears to be another important regulator of myeloid differentiation that can cooperate with PRMT4 to maintain the “stemness” of HSPCs. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
EP300 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-229780 |
|
|
Homo sapiens |
|
pmid |
sentence |
20660310 |
Switch to beta-catenin/p300-mediated gene expression is an essential first step in initiating normal cellular differentiation |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3 in AML |
+ |
TLR4 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261923 |
|
|
Homo sapiens |
Acute Myeloid Leukemia Cell |
pmid |
sentence |
28137827 |
S100A9 induces differentiation of acute myeloid leukemia cells through TLR4. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
SMAD5 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-242059 |
|
|
Mus musculus |
Ovarian Serous Carcinoma Cell |
pmid |
sentence |
23993924 |
Engagement of BMP4-mediated signaling in adult mouse ovary-derived OSCs cultured in vitro drives differentiation of these cells into IVD oocytes through Smad1/5/8 activation and transcriptional up-regulation of key meiosis-initiating genes. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
SPI1 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256372 |
|
|
Homo sapiens |
|
pmid |
sentence |
20861919 |
In the myeloid compartment, Gfi1 is part of a regulatory network that determines lineage fate decision between granulocyte and monocyte/macrophage development. In this compartment, Gfi1 antagonizes the function of the transcription factor Pu.1. Pu.1 promotes monocytic differentiation, whereas Gfi1 enhances granulocytic differentiation. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-249633 |
|
|
Mus musculus |
Myeloid Progenitor Cell |
pmid |
sentence |
12130514 |
The transcription factor PU.1 is required for normal blood cell development. PU.1 regulates the expression of a number of crucial myeloid genes, such as the macrophage colony-stimulating factor (M-CSF) receptor, the granulocyte colony-stimulating factor (G-CSF) receptor, and the granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor. Myeloid cells derived from PU.1(-/-) mice are blocked at the earliest stage of myeloid differentiation, similar to the blast cells that are the hallmark of human acute myeloid leukemia (AML). These facts led us to hypothesize that molecular abnormalities involving the PU.1 gene could contribute to the development of AML. |
|
Publications: |
2 |
Organism: |
Homo Sapiens, Mus Musculus |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, miRNA in AML, MLL fusion protein in AML, HaematopoiesisTranscriptionalControl, FLT3-ITD in AML |
+ |
NFATC1 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-270537 |
|
|
Homo sapiens |
B-lymphocyte |
pmid |
sentence |
11163226 |
In this study, the roles of NFATc1 and NFATc2 in T and B cells were examined. These results further characterize NFAT as a transcription factor family that plays a critical role in the regulation of lymphocyte effector differentiation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | B-cell activation |
+ |
AR | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251538 |
|
|
Homo sapiens |
|
pmid |
sentence |
15861399 |
AR homodimers recruit a panoply of factors including coactivators and mediator proteins whose enzymatic activities promote chromatin remodeling and transcriptional regulation of target genes leading to cell differentiation, survival, and proliferation |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Prostate Cancer |
+ |
PML-RARalpha | down-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255724 |
|
|
Homo sapiens |
|
pmid |
sentence |
20966922 |
APL cells closely resemble normal promyelocytes, a specific stage of the granulocytic differentiation pathway, suggesting that PML–RARα blocks the normal myeloid differentiation programme. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255723 |
|
|
Homo sapiens |
U-937 Cell |
pmid |
sentence |
8394219 |
We expressed the PML-RARa protein in U937 myeloid precursor cells and showed that they lost the capacity to differentiate under the action of different stimuli (vitamin Ds and transforming growth factor pl), acquired enhanced sensitivity to retinoic acid, and exhibited a higher growth rate consequent to diminished apoptotic cell death. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3 in AML, Onco-fusion proteins in AML |
+ |
LEF1 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-229770 |
|
|
Homo sapiens |
|
pmid |
sentence |
17081971 |
The interaction of beta-catenin with the N terminus of tcf/lef transiently converts it into an activator, translating the Wnt signal into the transient transcription of Tcf target genes. The Wnt pathway has distinct transcriptional outputs, which are determined by the identity of the responding cell, and range from cell proliferation and survival to the terminal differentiation of postmitotic cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | WNT Signaling |
+ |
PAX7 | down-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255367 |
|
|
|
|
pmid |
sentence |
15501225 |
We found that ectopic expression of Pax-7 prevented myogenic differentiation and the induction of myogenin protein. |
|
Publications: |
1 |
Tissue: |
Skeletal Muscle |
Pathways: | Acute Myeloid Leukemia, miRNA in AML |
+ |
GATA4 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-265480 |
|
|
Homo sapiens |
Embryonic Stem Cell |
pmid |
sentence |
32376282 |
HYDIN promotes expression of Gata4 in cardiomyocyte differentiation. HYDIN functions as a positive regulator of human cardiomyocyte differentiation and promotes expression of cardiac contractile genes in hESC cells. This is mediated through GATA4, a critical transcription factor in heart development. Cardiac-specific Hydin knockdown in vivo leads to Gata4 downregulation and enhanced atrial septal defect (ASD) risk in mice. GATA4 is a fundamental TF in embryonic heart development and cardiac differentiation, and reduction in GATA4 function results in a diverse range of CHDs |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MYCL | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259202 |
|
|
Mus musculus |
|
pmid |
sentence |
7882978 |
These observations indicate that continued late-stage expression of L-myc affected differentiation processes directly, rather than indirectly through deregulated growth control, whereas constitutive c-myc expression inhibited proliferative arrest, but did not appear to disturb differentiation. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Tissue: |
Lens Fiber |
+ |
SF3B1 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256004 |
|
|
Homo sapiens |
K-562 Cell, HEL Cell |
pmid |
sentence |
25428262 |
Taken together, these data show that SF3B1 knockdown results in inhibition of cell growth, induction of cell cycle arrest and impairment of erythroid differentiation in myeloid cell lines.[…]SF3B1 knockdown compared with the scramble control, suggesting that normal SF3B1 function is required for erythroid differentiation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ITGAM | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255662 |
|
|
Homo sapiens |
|
pmid |
sentence |
12393465 |
CD11b, another marker for differentiation, was also less expressed in patients with t(8;21) in comparison to patients without t(8;21) |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CARM1 | down-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261968 |
|
|
Homo sapiens |
Hematopoietic Stem Cell |
pmid |
sentence |
24332853 |
PRMT4 blocks myeloid differentiation of human hematopoietic stem/progenitor cells While PRMT4 promotes differentiation in several biological systems including T cell, adipocyte and muscle development, it blocks differentiation in the hematopoietic system, allowing HSPCs to maintain stemness. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CCR1 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254369 |
|
|
Homo sapiens |
|
pmid |
sentence |
25230753 |
CCL3, an eosinophil precursor-produced chemokine that signals through CCR1, promotes terminal differentiation of CCR1-positive eosinophil precursors in the absence of IL-5, highlighting an autocrine loop capable of sustaining eosinophil differentiation |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CBFbeta-MYH11 | down-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255736 |
|
|
Homo sapiens |
|
pmid |
sentence |
29958106 |
In adult hematopoiesis, allelic CBFβ-SMMHC expression alters hematopoietic stem cell (HSC) differentiation, with clonal expansion of the short-term HSCs and pre-leukemic myeloid progenitor cells |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, KIT in AML |
+ |
BCOR | down-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256010 |
|
|
Mus musculus |
Bone Marrow Cell |
pmid |
sentence |
26847029 |
Our results strongly suggest that BCOR plays an indispensable role in hematopoiesis by inhibiting myeloid cell proliferation and differentiation and offer a mechanistic explanation for how BCOR regulates gene expression such as Hox genes. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
+ |
ETV2 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256009 |
|
|
Mus musculus |
Embryonic Stem Cell |
pmid |
sentence |
24583263 |
Using the embryoid body differentiation system, we demonstrate that co-expression of Gata2 augments the activity of Etv2 in promoting endothelial and hematopoietic lineage differentiation. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
hsa-mir-223 | up-regulates
|
Differentiation |
0.4 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255763 |
|
|
Homo sapiens |
|
pmid |
sentence |
24708856 |
We found overexpression of miR-155 led to increase in cJUN, FOS and TRIB2, and decrease in MEIS1, GFI1, cMYC and JARID2. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, miRNA in AML |
+ |
CEBPB | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250572 |
|
|
|
|
pmid |
sentence |
16319681 |
The transcription factor C/EBPalpha controls differentiation and proliferation in normal granulopoiesis in a stage-specific manner. Loss of C/EBPalpha function in myeloid cells in vitro and in vivo leads to a block to myeloid differentiation similar to that which is observed in malignant cells from patients with acute myeloid leukemia. The finding of C/EBPalpha alterations in subgroups of acute myeloid leukemia patients suggests a direct link between critically decreased C/EBPalpha function and the development of the disorder. |
|
Publications: |
1 |
Pathways: | Acute Myeloid Leukemia, miRNA in AML |
+ |
S100A9 | down-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261932 |
|
|
Mus musculus |
Myeloid Progenitor Cell |
pmid |
sentence |
18809714 |
We report here that up-regulation of S100A9 in myeloid precursors in cancer inhibits DC and macrophage differentiation and induces accumulation of MDSCs. This may represent a universal molecular mechanism of tumor-induced abnormalities in myeloid cells in cancer, directly linking inflammation and immune suppression. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
Core Binding Factor complex | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255740 |
|
|
Mus musculus |
|
pmid |
sentence |
19813271 |
The core binding factor (CBF), consisting of a Runx protein and the CBFβ protein, is a transcription factor complex that is essential for emergence of the hematopoietic stem cell (HSC) from an endothelial cell stage. The hematopoietic defects observed in either Runx1 or CBFβ knockout mice underscore the necessity of this complex for definitive hematopoiesis. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | AML1-ETO in AML |
+ |
ERK1/2 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254355 |
|
|
Homo sapiens |
|
pmid |
sentence |
19819937 |
In addition to the JAK2–STAT5 pathway, the Ras GTPase–extracellular signal-regulated kinase (Ras–ERK) pathway has also been implicated in signaling of IL-5 and is important for IL-5-dependent cell survival, proliferation and differentiation of eosinophils. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3 in AML, KIT in AML, AML_TRIPLETS, B-cell activation, FLT3-ITD in AML, Triple mutant AML, NPM1_new |
+ |
MYOD1 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255417 |
|
|
Homo sapiens |
|
pmid |
sentence |
16275751 |
Together, these results support the notion that Myf5 functions toward myoblast proliferation, whereas MyoD prepares myoblasts for efficient differentiation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Skeletal Muscle |
Pathways: | NOTCH Signaling |
+ |
RUNX1 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-249631 |
|
|
Homo sapiens |
|
pmid |
sentence |
19334039 |
AML1/RUNX1 mutants play a central role in the pathogenesis of MDS/AML. Both AML1 mutants are initiating factors for MDS-genesis by inhibiting differentiation of hematopoietic stem cells, and Ni-type mutant requires acquisition of proliferation ability. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3 in AML, Onco-fusion proteins in AML, KIT in AML, miRNA in AML, MLL fusion protein in AML, HaematopoiesisTranscriptionalControl, NPM1_new |
+ |
CAMTA1 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259100 |
|
|
Homo sapiens |
SH-EP Cell |
pmid |
sentence |
21385898 |
Our findings define properties of CAMTA1 in growth suppression and neuronal differentiation that support its assignment as a 1p36 tumor suppressor gene in neuroblastoma. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
NFATC2 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-270538 |
|
|
Homo sapiens |
B-lymphocyte |
pmid |
sentence |
11163226 |
In this study, the roles of NFATc1 and NFATc2 in T and B cells were examined. These results further characterize NFAT as a transcription factor family that plays a critical role in the regulation of lymphocyte effector differentiation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | B-cell activation |
+ |
DNMT3A | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255714 |
|
|
Homo sapiens |
|
pmid |
sentence |
27639498 |
The DNA methyltransferase 3 genes (DNMT3A and DNMT3B) encode methyltransferases that catalyze the addition of a methyl group to the cytosine residue of CpG dinucleotide; therefore they play an essential role in DNA methylation and gene silencing regulatory processes. DNMT3A function is involved in hematopoietic stem cells (HSCs) renewal and myeloid differentiation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, Onco-fusion proteins in AML, miRNA in AML, AML_TRIPLETS, Triple mutant AML |
+ |
MEIS1 | down-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255865 |
|
|
Homo sapiens |
Hematopoietic Stem Cell |
pmid |
sentence |
14701735 |
Here we demonstrate that MLL-ENL immortalizes cells mainly through inducing a reversible block on myeloid differentiation that is dependent on upregulation of Hoxa9 and Meis1 and that enforced expression of these two genes is sufficient to substitute for MLL-ENL function. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, MLL fusion protein in AML, AML_TRIPLETS, Triple mutant AML |
+ |
SOX4 | down-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255676 |
|
|
Homo sapiens |
Leukemia Cell |
pmid |
sentence |
24183681 |
Collectively, our experiments identified the oncogene Sox4 as a factor mediating increased serial-replating ability and blocked differentiation of Cebpa-deficient progenitors. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, FLT3 in AML, AML_TRIPLETS, Triple mutant AML |
+ |
MN1 | down-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256016 |
|
|
Mus musculus |
|
pmid |
sentence |
17494859 |
MN1 is a unique oncogene in hematopoiesis that both promotes proliferation/self-renewal and blocks differentiation, and may become useful as a predictive marker in AML treatment. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
SMAD1 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255259 |
|
|
Mus musculus |
Ovarian Serous Carcinoma Cell |
pmid |
sentence |
23993924 |
Engagement of BMP4-mediated signaling in adult mouse ovary-derived OSCs cultured in vitro drives differentiation of these cells into IVD oocytes through Smad1/5/8 activation and transcriptional up-regulation of key meiosis-initiating genes. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
NOTCH1 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-241998 |
|
|
Homo sapiens |
|
pmid |
sentence |
18342499 |
Genetic ablation or activation of the pathway reveals that Notch signalling promotes differentiation of the hair follicle, sebaceous gland and interfollicular epidermal lineages |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, NOTCH Signaling |
+ |
CEBPA | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-249632 |
|
|
Homo sapiens |
Myeloid Progenitor Cell |
pmid |
sentence |
16319681 |
The transcription factor C/EBPalpha controls differentiation and proliferation in normal granulopoiesis in a stage-specific manner. Loss of C/EBPalpha function in myeloid cells in vitro and in vivo leads to a block to myeloid differentiation similar to that which is observed in malignant cells from patients with acute myeloid leukemia. The finding of C/EBPalpha alterations in subgroups of acute myeloid leukemia patients suggests a direct link between critically decreased C/EBPalpha function and the development of the disorder. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, FLT3 in AML, Onco-fusion proteins in AML, HaematopoiesisTranscriptionalControl, AML_TRIPLETS, FLT3-ITD in AML, Triple mutant AML, NPM1_new |
+ |
Polycomb repressive complex 2 | down-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-241910 |
|
|
Homo sapiens |
|
pmid |
sentence |
21248841 |
The importance of polycomb function for stem cells is best illustrated by various PcG-knockout mice. Deletion of any of the PRC2 members results in embryonic lethality. In vitro studies with ES cells demonstrated that cells lacking EED or Suz12 could not maintain their pluripotency and were prone to differentiation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MLLT11 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259201 |
|
|
Mus musculus |
OP-9 Cell |
pmid |
sentence |
21715312 |
Our results indicate that AF1q cooperates with the Notch signaling pathway to foster the emergence of BM prothymocytes and drive subsequent intrathymic specification toward the T-cell lineage. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
ETV6 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256017 |
|
|
Homo sapiens |
UT-7 Cell, B-lymphoblastoid Cell Line |
pmid |
sentence |
15958056 |
We thus conclude that TEL is also an accelerator for erythroid differentiation upon cytokine stimulation in human hematopoietic cells. We demonstrated in the present study that TEL accelerates erythroid differentiation induced by a physiological cytokine EPO in human leukemia cell line UT-7/GM. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, KIT in AML, AML_TRIPLETS, Triple mutant AML |
+ |
S100A9 | up-regulates
|
Differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261922 |
|
|
Homo sapiens |
Acute Myeloid Leukemia Cell |
pmid |
sentence |
28137827 |
S100A9 induces differentiation of acute myeloid leukemia cells through TLR4. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |