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Human Polyclonal SPI1 Primary Antibody pour ELISA, WB - ABIN314238
Harendza, Lovett, Stahl: The hematopoietic transcription factor PU.1 represses gelatinase A transcription in glomerular mesangial cells. dans The Journal of biological chemistry 2000
Show all 2 Pubmed References
Human Polyclonal SPI1 Primary Antibody pour WB - ABIN4240538
McDevit, Nikolajczyk: Changes in immunoglobulin-nucleoprotein complex structure mapped by chromatin immunoprecipitation. dans Molecular immunology 2006
Human Polyclonal SPI1 Primary Antibody pour FACS - ABIN4895271
Talotta, Berzi, Doria, Batticciotto, Ditto, Atzeni, Sarzi-Puttini, Trabattoni: The Immunogenicity of Branded and Biosimilar Infliximab in Rheumatoid Arthritis According to Th9-Related Responses. dans International journal of molecular sciences 2017
Human Monoclonal SPI1 Primary Antibody pour FACS, ELISA - ABIN3072909
Xu, Wang, Wang, Wu, Zhao, Zhu, Qiu, Xue, Shao, Guo, Li: PU.1 can regulate the ZNF300 promoter in APL-derived promyelocytes HL-60. dans Leukemia research 2010
These results bring indirect evidence that leukemia develops from cells which have bypassed Spi1-induced senescence. Overall, our results reveal senescence as a Spi1-induced anti-proliferative mechanism that may be a safeguard against the development of acute myeloid leukemia (Montrer BCL11A Anticorps).
In contrast, expression of Spi1/PU.1 in a Fli1 (Montrer FLI1 Anticorps) producing erythroleukemia cell line in which fli1 (Montrer FLI1 Anticorps) is activated, resulted in increased proliferation through activation of growth promoting proteins MAPK (Montrer MAPK1 Anticorps), AKT (Montrer AKT1 Anticorps), cMYC (Montrer MYC Anticorps) and JAK2 (Montrer JAK2 Anticorps)
Data show that protein phosphatase-1 (Montrer PPP1CB Anticorps) alpha (PP1alpha (Montrer PPP1CA Anticorps)) is required to maintain checkpoint kinase 1 (CHK1 (Montrer CHEK1 Anticorps)) in a dephosphorylated state and for the accelerated replication fork progression in Spi1/PU.1 transcription factor-overexpressing cells.
PU.1 supports TRAIL-induced cell death by inhibiting RelA (Montrer NFkBP65 Anticorps)-mediated cell survival and inducing DR5 (Montrer TNFRSF10B Anticorps) expression.
PU.1 and IL-9 (Montrer IL9 Anticorps) may play a role in AD pathogenesis and relate to disease severity and clinical eruption types.
PU.1-induced apoptosis in myeloma cells is associated with IRF4 (Montrer IRF4 Anticorps) downregulation and subsequent IRF7 (Montrer IRF7 Anticorps) upregulation.
Most cases of histiocytic sarcoma expressed histiocytic markers CD68 (Montrer CD68 Anticorps) (6 of 7 cases), CD163 (Montrer CD163 Anticorps) (5 of 5 cases), and PU.1 (3 of 4 cases).
findings highlight a unique role of SPI1 fusions in high-risk pediatric T cell acute lymphoblastic leukemia
expression of an essential mediator of neutrophil terminal differentiation, the ets transcription factor PU.1, was significantly decreased in Hbb(th3/+) neutrophils in beta-thalassemia
RUNX1 (Montrer RUNX1 Anticorps) overexpression induced partial DNA demethylation at SPI1 proximal promoter.
The analysis points to a critical role for Hoxa9 (Montrer HOXA9 Anticorps) and PU.1 in distal regulation of c-myb (Montrer MYB Anticorps) expression in murine myeloid cells during iL-6 (Montrer IL6 Anticorps)-induced cell differentiation.
These studies reveal an important role for PU.1 in the regulation of Igkappa transcription and rearrangement and a requirement for PU.1 and Spi-B (Montrer SPIB Anticorps) in B cell development.
expression of an essential mediator of neutrophil terminal differentiation, the ets transcription factor PU.1, was significantly decreased in Hbb(th3/+) neutrophils in a model of beta-thalassemia
Moreover, the expression of a cell proliferation marker Ki67 (Montrer MKI67 Anticorps) was significantly decreased in tumors from the mice not taking doxycycline, compared with that of tumors from the mice continuously taking doxycycline. The present data strongly suggest that PU.1 functions as a tumor suppressor of myeloma cells in vivo.
the affinities of two sequence-divergent ETS (Montrer ETS1 Anticorps) homologs, PU.1 and Ets-1 (Montrer ETS1 Anticorps), to DNA sites harboring a hemi- and fully methylated CpG dinucleotide, were measured.
this study shows that PU.1 functions as a positive regulator of CD11c (Montrer ITGAX Anticorps) gene expression by directly binding to the Itgax (Montrer ITGAX Anticorps) promoter and through transactivation of the Irf4 (Montrer IRF4 Anticorps) gene
Here we demonstrate that the transcription factors SPI1 (PU.1) and HOXC13 synergistically regulate Zfp521 (Montrer ZNF521 Anticorps) expression, and identify the regions of the Zfp521 (Montrer ZNF521 Anticorps) promoter required for this transcriptional activity. We also show that SPI1 and HOXC13 activate Zfp521 (Montrer ZNF521 Anticorps) in a dose-dependent manner.
findings suggest that Gata1 (Montrer GATA1 Anticorps) & PU.1 transcription factors are only executing and reinforcing lineage choice once made. These results challenge the current prevailing model of early myeloid lineage choice
involved in osteoclast development by transactivating NFATc1 (Montrer NFATC1 Anticorps) expression via direct binding to the NFATc1 (Montrer NFATC1 Anticorps) promoter
GATA1 (Montrer GATA1 Anticorps) and PU.1 bind in vitro and in vivo the proximal promoter region of the RPS19 (Montrer RPS19 Anticorps) gene which is frequently mutated in Diamond-Blackfan Anemia.
Data show that Spi1 is a downstream target of histone demethylase (Montrer MBD2 Anticorps) Jmjd3 (Jmjd3 (Montrer Kdm6b Anticorps)) during myelopoiesis.
The vertical and paralleled Pu.1/Spi-b (Montrer SPIB Anticorps) regulatory networks control the development of rostral blood island and ventral wall of dorsal aorta-borne macrophages by regulating Irf8 (Montrer IRF8 Anticorps).
eaf1 (Montrer EAF1 Anticorps) has a role in suppressing foxo3b expression to modulate transcriptional activity of gata1 (Montrer GATA1 Anticorps) and spi1 in primitive hematopoiesis
Our results indicate that Kzp (Montrer ANPEP Anticorps) is a critical transcriptional factor for the expression of gata2 and pu.1 to modulate primitive hematopoiesis.
Runx1 (Montrer RUNX1 Anticorps) is induced by high Pu.1 level and in turn transrepresses pu.1 expression, thus constituting a negative feedback loop that fashions a favorable Pu.1 level required for balanced fate commitment to neutrophils versus macrophages.
The authors show that tif1gamma (Montrer TRIM33 Anticorps) modulates the erythroid versus myeloid fate outcomes from HSCs by differentially controlling the levels of gata1 (Montrer GATA1 Anticorps) and pu.1.
found a gene group downregulated on spi1 knockdown,containing all 5 previously identified Spi1-dependent genes as well as a large set of novel immune-related genes
In zebrafish, spi1 marks a rostral population of LPM cells committed to a myeloid fate anatomically separated from and developmentally independent of erythroid commitment in the caudal (Montrer CAD Anticorps) LPM.
This gene encodes an ETS-domain transcription factor that activates gene expression during myeloid and B-lymphoid cell development. The nuclear protein binds to a purine-rich sequence known as the PU-box found near the promoters of target genes, and regulates their expression in coordination with other transcription factors and cofactors. The protein can also regulate alternative splicing of target genes. Multiple transcript variants encoding different isoforms have been found for this gene.
31 kDa transforming protein
, 31 kDa-transforming protein
, SPI-1 proto-oncogene
, hematopoietic transcription factor PU.1
, spleen focus forming virus (SFFV) proviral integration oncogene spi1
, transcription factor PU.1
, SFFV proviral integration 1 protein
, SFFV proviral integration 1
, spleen focus forming virus proviral integration oncogene spi1
, transcription factor spi1
, Spi-1/PU.1 transcription factor
, LOW QUALITY PROTEIN: transcription factor PU.1
, spleen focus forming virus (SFFV) proviral integration oncogene