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Trichostatin A Induces Transforming Growth Factor β Type II Receptor Promoter Activity and Acetylation of Sp1 by Recruitment of PCAF/p300 to a Sp1·NF-Y Complex*
TLDR
Results showed that TSA treatment of pancreatic cancer cells leads to transcriptional activation of the TβRII promoter through modulation of the components of a Sp1·NF-Y·p300·PCAF·HDAC-1 multiprotein complex. Expand
Interferon Consensus Sequence Binding Protein (ICSBP) Decreases β-Catenin Activity in Myeloid Cells by Repressing GAS2 Transcription
TLDR
These studies have identified a Gas2/calpain-dependent mechanism by which ICSBP influences β-catenin activity in myeloid leukemia. Expand
The Interferon Consensus Sequence-binding Protein (ICSBP/IRF8) Represses PTPN13 Gene Transcription in Differentiating Myeloid Cells*
TLDR
It is found that ICSBP influenced Fas-induced apoptosis in a Fap-1-dependent manner, and the interaction increased during myeloid differentiation and was regulated by phosphorylation of conserved tyrosine residues in the interferon regulatory factor domain of I CSBP. Expand
PU.1, Interferon Regulatory Factor (IRF) 2, and the Interferon Consensus Sequence-binding Protein (ICSBP/IRF8) Cooperate to Activate NF1 Transcription in Differentiating Myeloid Cells*
TLDR
This study found that ICSBP/IRF8 cooperates with PU.1 and interferon regulatory factor 2 to activate a composite ets/ IRF-cis element in the NF1 promoter, and identifies a tumor-suppressor function for the “oncogenic” transcription factor, IRF2.1. Expand
Constitutive activation of SHP2 in mice cooperates with ICSBP deficiency to accelerate progression to acute myeloid leukemia.
TLDR
It was found that constitutive activation of SHP2 protein tyrosine phosphatase synergized with ICSBP haploinsufficiency to facilitate cytokine-induced myeloproliferation, apoptosis resistance, and rapid progression to AML in a murine bone marrow transplantation model. Expand
Leukemia-Associated, Constitutively Active Mutants of SHP2 Protein Tyrosine Phosphatase Inhibit NF1 Transcriptional Activation by the Interferon Consensus Sequence Binding Protein
TLDR
The studies suggest that leukemia-associated ICSBP deficiency cooperates with leukemia- associated activating mutants of SHP2-PTP to contribute to the proliferative phenotype in myeloid malignancies. Expand
HoxA10 Activates Transcription of the Gene Encoding Mitogen-activated Protein Kinase Phosphatase 2 (Mkp2) in Myeloid Cells*
TLDR
This work identifies a mechanism by which overexpressed HoxA10 contributes to inappropriate cell survival during myelopoiesis and identifies the DUSP4 gene, which encodes mitogen-activated protein kinase phosphatase 2 (Mkp2), as a Hox a10 target gene. Expand
Increased Fanconi C expression contributes to the emergency granulopoiesis response.
TLDR
It is found that IRF8 (also known as ICSBP), an interferon regulatory transcription factor that activates phagocyte effector genes during the innate immune response, activates the gene encoding Fanconi C (Fancc) in murine myeloid progenitor cells, which contributes to genomic stability during emergency granulopoiesis. Expand
Constitutively Active SHP2 Cooperates with HoxA10 Overexpression to Induce Acute Myeloid Leukemia*
TLDR
It is hypothesized that constitutive SHP2 activation synergizes with HoxA10 overexpression to accelerate progression to AML and contribute to understanding biochemical aspects of disease progression in myeloid malignancy. Expand
Activation of SHP2 Protein-tyrosine Phosphatase Increases HoxA10-induced Repression of the Genes Encoding gp91PHOX and p67PHOX*
TLDR
HoxA10 is a substrate for a constitutively active mutant form of SHP2 in both undifferentiated and differentiating myeloid cells, which suggests that these mutations could cooperate, leading to decreasedMyeloid-specific gene transcription and functional differentiation block in myeloids cells with both defects. Expand
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