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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 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
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
these results suggest that attenuating PU.1 may be a valid therapeutic approach to limit microglial-mediated inflammatory responses in Alzheimer's disease
PU.1 3'UTR attenuates TNFalphainduced proliferation and cytokine release of RAFLS by acting as a ceRNA for FOXO3 to regulate miR155 activity.
Inhibition of endogenous miR-155 in B cells of rheumatoid arthritis patients restores PU.1 and reduces production of antibodies.
PU.1 binds to OX40L promoter in dendritic cells.
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.
In contrast, expression of Spi1/PU.1 in a Fli1 producing erythroleukemia cell line in which fli1 is activated, resulted in increased proliferation through activation of growth promoting proteins MAPK, AKT, cMYC and JAK2
Data show that protein phosphatase-1 alpha (PP1alpha) is required to maintain checkpoint kinase 1 (CHK1) in a dephosphorylated state and for the accelerated replication fork progression in Spi1/PU.1 transcription factor-overexpressing cells.
the results indicate that PU.1 may be a critical factor for the innate defense against A. fumigatus, and may therefore be a potential target for the prophylaxis and treatment of IPA.
PU.1 supports TRAIL-induced cell death by inhibiting RelA-mediated cell survival and inducing DR5 expression.
PU.1 directly activates the expression of HOTAIRM1 through binding to the regulatory region of HOTAIRM1 during granulocytic differentiation.
PU.1 and IL-9 may play a role in AD pathogenesis and relate to disease severity and clinical eruption types.
PU.1 has a role in tumor suppression in PEL and its down-regulation is associated with PEL development.
PU.1-induced apoptosis in myeloma cells is associated with IRF4 downregulation and subsequent IRF7 upregulation.
Most cases of histiocytic sarcoma expressed histiocytic markers CD68 (6 of 7 cases), CD163 (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
Alzheimer's disease heritability was enriched within the PU.1 cistrome, implicating a myeloid PU.1 target gene network in AD.
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 overexpression induced partial DNA demethylation at SPI1 proximal promoter.
This study demonstrated the novel role of PU.1 in the immune response to A. fumigatus through upregulation of Dectin-1 expression and its translocation to the nucleus in A. fumigatus-stimulated THP-1 cells.
PU.1 is an important modulator of VDR signaling in monocytes.
Results show that PU.1 selects the sites that it will occupy in changing chromatin contexts, and that its binding at certain classes of sites does control early T-cell gene expression. At non-promoter sites, PU.1 binding criteria is more stringent than at promoters, and PU.1 is also more effective as a transcriptional regulator at nonpromoter sites where local chromatin accessibility depended on the presence of PU.1.
EVI1 overexpression reprograms hematopoiesis via upregulation of Spi1 transcription
PU.1 mediates allergic responses in mast cells. PU.1 directly binds to Syk promoter.
Mice lacking both PU.1 and SpiB in mature B cells do not generate germinal centers and high-affinity antibody after protein immunization. PU.1 and SpiB double-deficient B cells have a survival defect after engagement of CD40 or Toll-like receptors (TLR), despite paradoxically enhanced plasma cell differentiation.
PU.1 can bind directly to the most-proximal Ets motif, which is essential for the transcriptional function of the mouse OX40L promoter in dendritic cells.
PU.1 suppresses Sirt1 translation via transcriptional promotion of miR-34a/-29c.
The analysis points to a critical role for Hoxa9 and PU.1 in distal regulation of c-myb expression in murine myeloid cells during iL-6-induced cell differentiation.
Data suggest that site-specifically bound PU.1 dimers occupy an extended DNA interface downstream from 5prime-GGAA-3prime core consensus relative to its 1:1 counterpart, thus explaining apparent site size requirement for sequential dimerization of PU.1.
PU.1 levels affected the expression of mouse orthologs of many Alzheimer's diseas risk genes and the phagocytic activity of mouse microglial cells
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 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 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 homologs, PU.1 and Ets-1, to DNA sites harboring a hemi- and fully methylated CpG dinucleotide, were measured.
this study shows that the generation of central nervous system macrophages relies on the transcription factor PU.1
this study shows that PU.1 functions as a positive regulator of CD11c gene expression by directly binding to the Itgax promoter and through transactivation of the Irf4 gene
Here we demonstrate that the transcription factors SPI1 (PU.1) and HOXC13 synergistically regulate Zfp521 expression, and identify the regions of the Zfp521 promoter required for this transcriptional activity. We also show that SPI1 and HOXC13 activate Zfp521 in a dose-dependent manner.
Authors report that PU.1 serves as a critical regulator of alternatively activated macrophage(AAM) polarization and promotes the pathological progress of asthmatic airway inflammation.
findings suggest that Gata1 & 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 expression via direct binding to the NFATc1 promoter
GATA1 and PU.1 bind in vitro and in vivo the proximal promoter region of the RPS19 gene which is frequently mutated in Diamond-Blackfan Anemia.
Data show that Spi1 is a downstream target of histone demethylase Jmjd3 (Jmjd3) during myelopoiesis.
The vertical and paralleled Pu.1/Spi-b regulatory networks control the development of rostral blood island and ventral wall of dorsal aorta-borne macrophages by regulating Irf8.
eaf1 has a role in suppressing foxo3b expression to modulate transcriptional activity of gata1 and spi1 in primitive hematopoiesis
Our results indicate that Kzp is a critical transcriptional factor for the expression of gata2 and pu.1 to modulate primitive hematopoiesis.
Runx1 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 modulates the erythroid versus myeloid fate outcomes from HSCs by differentially controlling the levels of gata1 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 LPM.
the promoter of this gene has been isolated and characterized
PU.1 determines myelo-erythroid progenitor cell fate in zebrfish
Knockdown of the myeloid transcription factor gene pu.1 resulted in complete loss of primitive macrophage development, with effects on granulocyte development only with maximal knockdown.
antisense lncRNA blocking PU.1 translation promotes adipogenesis in porcine preadipocytes
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