Discovering What Makes STAT Signaling TYK in T-ALL

Fontán, Lorena; Melnick, Ari

doi:10.1158/2159-8290.cd-13-0123

Cited by 3 publications

(2 citation statements)

References 11 publications

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“…STAT3 responds to factors including IL-6, IL-10, and vascular endothelial growth factor and is involved in T-helper cell 17 (Th17) and Treg cell development and tumorigenesis (Lin et al, 2013;Nieminen et al, 2013). STAT4 and STAT6 control Th1 and Th2 cell differentiation in response to IL-12 and IL-4/13, respectively (Fontan and Melnick, 2013;Meisch et al, 2013;Singh et al, 2013). Due to the large involvement of STATs in a variety of cell processes, it is critical that their activity be tightly regulated.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-29a promotes apoptosis of monocytes by targeting STAT3 during sepsis

Song¹,

Wang²,

Geng³

2015

Genet. Mol. Res.

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ABSTRACT. Sepsis is a major cause of morbidity and mortality in critically ill patients. The sepsis syndrome results from a dysregulated inflammatory response to infection that leads to multiple-organ failure, but the underlying mechanisms remain poorly understood. More and more reports show that microRNAs (miRNAs) play an important role in sepsis. In the progression of this syndrome, cells change their behavior in response to cytokines stimulated by sepsis, such as interleukin-10 (IL-10). IL-10 can activate JAK2-STAT3 in the cells to protect them from damage. miR-29a is a potential miRNA directly targeting STAT3. In this study, we investigate the role of miR-29a in targeting STAT3 during sepsis. When cells were treated with IL-10, STAT3 was activated in monocytes, as determined using western blotting. It was verified that STAT3 was a new target gene of miR-29a. miR-29a could inhibit IL-10-induced cytokine release by targeting JAK-STAT3 in monocytes. In conclusion, this study demonstrates for the first time that miR-29a inhibits STAT3 in human monocytes during sepsis.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-29a promotes apoptosis of monocytes by targeting STAT3 during sepsis

Song¹,

Wang²,

Geng³

2015

Genet. Mol. Res.

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“…19 Since TYK2 mutations are so rare in T-ALL patients, the second explanation seems more likely. In general, given the high frequency of JAK1, JAK2, and JAK3 mutations, the very low frequency of TYK2 aberrations in the entire spectrum of hematologic malignancies is highly intriguing.…”

mentioning

confidence: 99%

Structural modeling of JAK1 mutations in T-cell acute lymphoblastic leukemia reveals a second contact site between pseudokinase and kinase domains

2016

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STAT1 Regulates MD-2 Expression in Monocytes of Sepsis via miR-30a

Wang

et al. 2014

Inflammation

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Sepsis is a major cause of morbidity and mortality in critically ill patients. MD-2 is a 25-kDa lipopolysaccharide (LPS)-binding protein that forms a heterodimer with TLR42, but its regulation in sepsis is not clear. This study aims to investigate the molecular mechanism of regulation of MD-2. Inflammation cytokines in monocytes were analyzed by real-time RT-PCR and ELISA, and it was found that IL-10 was elevated significantly in the monocytes with LPS treatment. And then, when the cells were treated with IL-10, STAT1 was activated in the monocytes using Western blotting. It was also found that STAT1 could enhance MD-2 expression on transcriptional and posttranscriptional levels. Finally, miR-30a was predicted to the molecule that may regulate STAT1 expression. It was verified that STAT1 was a new target gene of miR-30a. miR-30a could inhibit IL-10-induced cytokine release by targeting STAT1-MD-2 in monocytes. In conclusion, this study for the first time demonstrated that miR-30a inhibits MD-2 expression by targeting of STAT1 in human monocytes.

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Discovering What Makes STAT Signaling TYK in T-ALL

Cited by 3 publications

References 11 publications

MicroRNA-29a promotes apoptosis of monocytes by targeting STAT3 during sepsis

MicroRNA-29a promotes apoptosis of monocytes by targeting STAT3 during sepsis

Structural modeling of JAK1 mutations in T-cell acute lymphoblastic leukemia reveals a second contact site between pseudokinase and kinase domains

STAT1 Regulates MD-2 Expression in Monocytes of Sepsis via miR-30a

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