نتایج جستجو برای: bet analysis

تعداد نتایج: 2831125  

Journal: :American journal of clinical pathology 2003
David M Dorfman Peter van den Elzen Andrew P Weng Aliakbar Shahsafaei Laurie H Glimcher

We studied T-bet expression in 91 cases of peripheral T-cell lymphoma (PTCL) by immunostaining and found expression in 42 cases (46%), including all 5 lymphoepithelioid lymphoma cases and 12 (86%) of 14 angioimmunoblastic lymphoma cases, but only 9 (25%) of 36 anaplastic large cell lymphoma cases. Expression of T-bet in PTCL correlates with expression of other markers of Th1 T-cell differentiat...

Journal: :ChemMedChem 2016
Natalie H Theodoulou Nicholas C O Tomkinson Rab K Prinjha Philip G Humphreys

The bromodomain and extra terminal (BET) family of bromodomains have been the focus of extensive research, leading to the development of many potent, selective chemical probes and recent clinical assets. The profound biology associated with BET bromodomain inhibition has provided a convincing rationale for targeting bromodomains for the treatment of disease. However, the BET family represents j...

Journal: :Molecular medicine reports 2014
Yuan Xue Yong Yang Zhaoliang Su Prince Amoatt Barnie Dong Zheng Yun Zhang Yan Xu Shengjun Wang Huaxi Xu

Th1 and Th17 cells are involved in the pathogenesis of rheumatoid arthritis (RA). T-bet, a Th1-specific transcription factor, appears to drive the maturation of Th1 and IFN-γ secretion. In the present study, we established the T-bet shRNA recombinant plasmid (p-T-shRNA) and explored its possible anti-inflammatory effect in a collagen-induced arthritis (CIA) model by local injection of plasmid v...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2003
Geanncarlo Lugo-Villarino Roberto Maldonado-Lopez Richard Possemato Cristina Penaranda Laurie H Glimcher

IFN-gamma is well known as the signature cytokine of CD4+ T helper 1, CD8+, and natural killer cells, but recent studies demonstrate that antigen-presenting cells, in particular dendritic cells (DCs), are another potent source for this proinflammatory cytokine. T-bet, a transcription factor that controls IFN-gamma expression in CD4+ T cells, was reported recently to be expressed in human monocy...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2009
Richard G Jenner Michael J Townsend Ian Jackson Kaiming Sun Russell D Bouwman Richard A Young Laurie H Glimcher Graham M Lord

Upon detection of antigen, CD4(+) T helper (Th) cells can differentiate into a number of effector types that tailor the immune response to different pathogens. Alternative Th1 and Th2 cell fates are specified by the transcription factors T-bet and GATA-3, respectively. Only a handful of target genes are known for these two factors and because of this, the mechanism through which T-bet and GATA-...

Journal: :The journal of physical chemistry. B 2005
P Ravi S Dai K C Tam

A well-defined poly(2-(dimethylamino)ethyl methacrylate) (PDMAEMA-b-C60) was synthesized using the atom transfer radical polymerization (ATRP) technique and betainized with 1,3-sulfobetaine to yield a Bet-PDMAEMA-b-C60. The solution properties were then studied by light transmittance, viscometric, 1H NMR laser light scattering, and transmission electron macroscopic techniques. It was found that...

Journal: :Hypertension 2013
Ali Abdalvand Jude S Morton Stephane L Bourque Anita L Quon Sandra T Davidge

Preeclampsia is a leading cause of maternal and fetal morbidity/mortality; however, the pathophysiological mechanisms are unclear. Vascular endothelial dysfunction in preeclampsia has been partially attributed to changes in endothelin-1 (ET-1). Several enzymes, including matrix metalloproteinases (MMPs; particularly MMP-2), cleave the inactive precursor big ET-1 (bET-1) to active ET-1. Notably,...

2014

Preeclampsia is a leading cause of maternal and fetal morbidity/ mortality; however, the pathophysiological mechanisms are poorly understood. Vascular endothelial dysfunction in preeclampsia has been partially attributed to changes in endothelin-1 (ET-1). Several enzymes, including matrix metalloproteinases (MMPs, particularly MMP-2), cleave the inactive precursor bigET-1 (bET-1) to active ET-1...

2014

Preeclampsia is a leading cause of maternal and fetal morbidity/ mortality; however, the pathophysiological mechanisms are poorly understood. Vascular endothelial dysfunction in preeclampsia has been partially attributed to changes in endothelin-1 (ET-1). Several enzymes, including matrix metalloproteinases (MMPs, particularly MMP-2), cleave the inactive precursor bigET-1 (bET-1) to active ET-1...

2014

Preeclampsia is a leading cause of maternal and fetal morbidity/ mortality; however, the pathophysiological mechanisms are poorly understood. Vascular endothelial dysfunction in preeclampsia has been partially attributed to changes in endothelin-1 (ET-1). Several enzymes, including matrix metalloproteinases (MMPs, particularly MMP-2), cleave the inactive precursor bigET-1 (bET-1) to active ET-1...

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