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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

SFFV proviral integration 1

PU.1, Spi-1
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, V1a, GATA-1, HAD, FATE
Papers using PU.1 antibodies
Signals for stress erythropoiesis are integrated via an erythropoietin receptor-phosphotyrosine-343-Stat5 axis.
Blagosklonny Mikhail V., In PLoS ONE, 2005
... spi-1-transgenic proerythroblastic cell lines (633, ...
Papers on PU.1
PU.1-Silenced Dendritic Cells Induce Mixed Chimerism and Alleviate Intestinal Transplant Rejection in Rats via a Th1 to Th2 Shift.
Li et al., Nanjing, China. In Cell Physiol Biochem, Feb 2016
Here, we demonstrate that in rat intestinal transplantation, PU.1-silenced dendritic cells (DCs) plus bone marrow (BM) cell transfusion results in mixed chimerism, and we investigate the mechanisms responsible for the effects of mixed chimerism rejection.
Reprogramming of human peripheral blood monocytes to erythroid lineage by blocking of the PU-1 gene expression.
Ebrahimi et al., Tehrān, Iran. In Ann Hematol, Feb 2016
To demonstrate whether PU.1 suppression induces monocyte lineage conversion into red blood cells, a combination of three PU.1-specific siRNAs was implemented to knock down PU.1 gene expression and generate the balance in favor of GATA-1 expression to induce erythroid differentiation.
The transcriptional regulator network of human inflammatory macrophages is defined by open chromatin.
Schultze et al., Bonn, Germany. In Cell Res, Feb 2016
UNASSIGNED: Differentiation of inflammatory macrophages from monocytes is characterized by an orderly integration of epigenetic and transcriptional regulatory mechanisms guided by lineage-determining transcription factors such as PU.1.
Interferon regulatory factor 8 and the regulation of neutrophil, monocyte, and dendritic cell production.
Goodridge et al., Los Angeles, United States. In Curr Opin Hematol, Jan 2016
Recent studies have shown that it collaborates with PU.1 to promote monocyte gene expression (in part via induction of Krüppel-like factor-4), associates with Batf3 to induce CD8α conventional dendritic cell differentiation via autoregulation of its own expression, and restricts neutrophil gene expression by disrupting the binding of c/EBPα to target genes.
High frequency of T helper type 9 cells in Chinese patients with allergic rhinitis.
Hong et al., Chongqing, China. In Asian Pac J Allergy Immunol, Dec 2015
METHODS: Th9 cells and related factors were assessed by measuring levels of interleukin-9 (IL-9), PU.1, interferon-regulatory factor 4 (IRF4), and numbers of Th9 cells.
Early enhancer establishment and regulatory locus complexity shape transcriptional programs in hematopoietic differentiation.
Leslie et al., New York City, United States. In Nat Genet, Nov 2015
Our method suggests a new mechanistic role for PU.1 at transition peaks during B cell specification and can be used to correct assignments of enhancers to genes.
Minimal PU.1 reduction induces a preleukemic state and promotes development of acute myeloid leukemia.
Steidl et al., United States. In Nat Med, Oct 2015
Although loss or near-complete loss of the hematopoietic transcription factor PU.1 induces acute myeloid leukemia (AML) in mice, a similar degree of PU.1 impairment is exceedingly rare in human AML; yet, moderate PU.1 inhibition is common in AML patients.
Population Variation and Genetic Control of Modular Chromatin Architecture in Humans.
Dermitzakis et al., Lausanne, Switzerland. In Cell, Sep 2015
Chromatin state variation at gene regulatory elements is abundant across individuals, yet we understand little about the genetic basis of this variability.
RORC1 Regulates Tumor-Promoting "Emergency" Granulo-Monocytopoiesis.
Sica et al., Milano, Italy. In Cancer Cell, Sep 2015
RORC1 orchestrates myelopoiesis by suppressing negative (Socs3 and Bcl3) and promoting positive (C/EBPβ) regulators of granulopoiesis, as well as the key transcriptional mediators of myeloid progenitor commitment and differentiation to the monocytic/macrophage lineage (IRF8 and PU.1).
Microglia recapitulate a hematopoietic master regulator network in the aging human frontal cortex.
Ponting et al., Oxford, United Kingdom. In Neurobiol Aging, Aug 2015
We identified a subnetwork of transcription factors, including RUNX1, IRF8, PU.1, and TAL1, which are master regulators (MRs) for the age-dependent microglia module.
Positive and negative regulators of the metallothionein gene (review).
Takahashi, Sagamihara, Japan. In Mol Med Report, Jul 2015
Previous studies from the group of the present review have revealed that the hematopoietic master transcription factor, PU.1, directly represses the expression levels of MT genes through its epigenetic activities, and upregulation of MT results in the potent inhibition of myeloid differentiation.
Batf3 maintains autoactivation of Irf8 for commitment of a CD8α(+) conventional DC clonogenic progenitor.
Murphy et al., Saint Louis, United States. In Nat Immunol, Jul 2015
Irf8 expression in CDPs required prior autoactivation of Irf8 that was dependent on the transcription factor PU.1.
RUNX1-Evi-1 fusion gene inhibited differentiation and apoptosis in myelopoiesis: an in vivo study.
Zhong et al., Shanghai, China. In Bmc Cancer, 2014
Early stage of myelopoiesis was flourishing with the high expression of pu.1, but it was inhibited along with the low expression of mpo.
Different pathways of macrophage activation and polarization.
Myśliwska et al., Gdańsk, Poland. In Postepy Hig Med Dosw (online), 2014
Mediators of M1 macrophage TLR-dependent polarization include transcription factors such as NF-κB, AP-1, PU.1, CCAAT/enhancer-binding protein α (C/EBP-α), STAT1 as well as interferon regulatory factor 5 (IRF5), while the transcription factors which promote M2 activation include IRF4, C/EBP-β, Krüppel-like factor 4 (KLF4), STAT6 and PPARγ receptor.
What makes Xanthomonas albilineans unique amongst xanthomonads?
Cociancich et al., Montpellier, France. In Front Plant Sci, 2014
Xanthomonas albilineans causes leaf scald, a lethal disease of sugarcane.
Macrophage dectin-1 expression is controlled by leukotriene B4 via a GM-CSF/PU.1 axis.
Peters-Golden et al., Ann Arbor, United States. In J Immunol, 2012
Leukotriene B4-enhanced expression of transcription factor PU.1 controls dectin-1 expression in macrophages.
Down-regulation of hematopoiesis master regulator PU.1 via aberrant methylation in chronic myeloid leukemia.
Ma et al., Shanghai, China. In Int J Hematol, 2012
These data suggest that aberrant methylation of PU.1 may play a role in CML pathogenesis, and may therefore serve as a useful biomarker and potential target for demethylating drugs.
Runx1 regulates embryonic myeloid fate choice in zebrafish through a negative feedback loop inhibiting Pu.1 expression.
Wen et al., Hong Kong, Hong Kong. In Blood, 2012
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.
PU.1 is linking the glycolytic enzyme HK3 in neutrophil differentiation and survival of APL cells.
Tschan et al., Bern, Switzerland. In Blood, 2012
HK3 is: (1) directly activated by PU.1, (2) repressed by PML-RARA, and (3) functionally involved in neutrophil differentiation and cell viability of acute promyelocytic leukemia cells.
DNA binding regulates the self-association of the ETS domain of PU.1 in a sequence-dependent manner.
Poon, Pullman, United States. In Biochemistry, 2012
The structural and thermodynamic data supported a model in which DNA binding dissociates a PU.1 ETS dimer to a 1:1 protein-DNA complex followed by, at higher concentrations, an asymmetric 2:1 complex.
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