Involvement of PI3K activation in TCR/CD3-dependent HIF-1α protein expression. Involvement of PI3K activation in TCR/CD3-dependent HIF-1α protein expression.

Slides:



Advertisements
Similar presentations
From: Regulation of Cdc42 Expression and Signaling Is Critical for Promoting Corneal Epithelial Wound Healing Invest. Ophthalmol. Vis. Sci ;54(8):
Advertisements

NK cells inhibited the expansion and function of ILC2s in vitro via IFN-γ. NK cells inhibited the expansion and function of ILC2s in vitro via IFN-γ. ILC2s.
Rab11-FIP3 silencing impairs T cell activation events.
Rab11-FIP3 silencing upregulates TCR-CD3 cell surface expression in an Lck-dependent manner. Rab11-FIP3 silencing upregulates TCR-CD3 cell surface expression.
Anti-CD40 and CpG induce activation of T cells in draining lymph nodes
Inhibition of PDGFR-β downstream signaling events by flavones.
CD44 ligation on peripheral blood polymorphonuclear cells induces interleukin-6 production by Giuseppe Sconocchia, Laura Campagnano, Domenico Adorno, Angela.
Volume 9, Issue 5, Pages (November 1998)
A novel TNFR1-triggered apoptosis pathway mediated by class IA PI3Ks in neutrophils by Barbara Geering, Ursina Gurzeler, Elena Federzoni, Thomas Kaufmann,
Constitutively activated phosphatidylinositol-3 kinase (PI-3K) is involved in the defect of apoptosis in B-CLL: association with protein kinase Cδ by Ingo.
TGF-β1 induces ILK activity in renal tubular epithelial cells.
Agonist-induced aggregation of Chinese hamster ovary cells coexpressing the human receptors for fibrinogen (integrin αIIbβ3) and the platelet-activating.
Small-molecule inhibitor QLT-0267 suppresses ILK activity and inhibits its downstream signaling. Small-molecule inhibitor QLT-0267 suppresses ILK activity.
Telomerase regulation in HTLV-I infection
Hyperphosphorylation of autoantigenic targets of paraproteins is due to inactivation of PP2A by Klaus-Dieter Preuss, Michael Pfreundschuh, Natalie Fadle,
Cell-surface CD74 initiates a signaling cascade leading to cell proliferation and survival by Diana Starlets, Yael Gore, Inbal Binsky, Michal Haran, Nurit.
Semaphorin-3A is expressed by tumor cells and alters T-cell signal transduction and function by Alfonso Catalano, Paola Caprari, Simona Moretti, Monica.
Expression and regulation of MD-2s.
The inhibition of PI3K and Akt in human T cells selectively inhibits the proliferation of human Tregs compared with Tconvs in a dose-dependent manner.
pIRS1(S636/639) IRS1 actin PF Supplemental Figure S1
FAS1 domain protein inhibits association of αvβ3 integrin with VEGFR-2 and attenuates VEGF165-induced VEGFR-2 phosphorylation. FAS1 domain protein inhibits.
The absence of ADCC by nivolumab in vitro.
The K594ScFv-SEA-D227A fusion protein targets CTL to lyse EA
NM-3 induces p21 levels and down-regulation of Cdk2 activity.
IL-10 upregulates IgG4 production by CD27+ B cells.
Germline PIK3CA and AKT1 Mutations in Cowden and Cowden-like Syndromes
Rapamycin inhibits TCR/CD3 engagement-dependent HIF-1α protein expression. Rapamycin inhibits TCR/CD3 engagement-dependent HIF-1α protein expression. Human.
The selective PI3K inhibitor A66 suppresses PIP3 accumulation, AKT phosphorylation at Thr308, and YAP/TAZ–regulated gene expression in PDAC cells. The.
p38 MAPK activation is required for phosphorylation of Akt at Ser473.
Volume 32, Issue 2, Pages (February 2010)
Vehicle Akti 0’ 2’ 5’ 10’ 0’ 2’ 5’ 10’ AktT308 β-actin GSK3βS9 β-actin
Transfection of stable β-catenin (S33Y) increased nuclear β-catenin and phosphorylated Akt expression (A) and reduced the promoting effect of HG on caspase-3.
Location, morphology and gene expression of skin CD8α+MHC II+ cells.
ADCC by T lymphocytes after transfection.
IL-6 neutralization results in induction of CD161+ FOXP3+ CD127– Tregs in EC–CD4+ T cell cocultures. IL-6 neutralization results in induction of CD161+
IL-6 neutralization reduces T cell-mediated injury in human artery allografts. IL-6 neutralization reduces T cell-mediated injury in human artery allografts.
Fig. 6. Effect of SAHA and ML on histone acetylation, BAX, and p21CDKN1A expression.PANC-1 and BxPC-3 cells were incubated for 48 hours with 5 µM.
IRF4 expression regulates the sensitivity of CD8+ T cells to IL-2, IL-15, and IL-7. IRF4 expression regulates the sensitivity of CD8+ T cells to IL-2,
Fibronectin-induced integrin-mediated PDGFR-β tyrosine phosphorylation
SYK activity is required for anti-IgM–induced CD86 expression.
The CD28 Signaling Pathway Regulates Glucose Metabolism
MK-8628 modulates transcriptional signatures of activated T lymphocytes. MK-8628 modulates transcriptional signatures of activated T lymphocytes. Gene.
MK-8628 suppresses T lymphocyte proliferation.
Adipose tissue dysfunction induces increased liver HIF-1α expression
Exosome-mediated inhibition of T cells is reversible.
Active MT1-MMP is recycled to the cell surface in HT1080 cells.
Class 1 phosphatidylinositol 3-kinase (PI3K) p85 subunit dominant negative adenovirus regulates Pax2 and GAPDH abundance in NRK-52E cells. Class 1 phosphatidylinositol.
eNOS regulated IR-induced NO generation and EGFR signal activation.
CD16 uses additional pathways for killing.
In vivo localization of Iff2, Iff3 (Iff9), Iff5, Iff6, Iff8, and Dcw1 proteins. In vivo localization of Iff2, Iff3 (Iff9), Iff5, Iff6, Iff8, and Dcw1 proteins.
GA blocks HIF activity and reduces HIF target expression.
B7-H1–induced reverse signals in myeloma cells.
DGKζ and Cbl-b deficient T Cells have enhanced ERK1/2 and IκBα phosphorylation. DGKζ and Cbl-b deficient T Cells have enhanced ERK1/2 and IκBα phosphorylation.
B7-1 and PD-1 compete for binding to PD-L1.
Flow cytometric analysis of T cell activation.
Effect of anti-CYP3A and anti-CYP2C antibodies on the disappearance of MPA in human liver microsomes (GHL24). Effect of anti-CYP3A and anti-CYP2C antibodies.
Down-regulation of the erbB-2 receptor by trastuzumab decreases Akt kinase activation but not MAPK activation. Down-regulation of the erbB-2 receptor by.
Experimental metastasis inhibition by primary tumors is mediated by NK cells and IFNγ. Experimental metastasis inhibition by primary tumors is mediated.
Expression of dominant-negative RasN17 completely suppresses Ras activation in Rh1 cells. Expression of dominant-negative RasN17 completely suppresses.
Activation of Vγ9 T cells by three distinct stimuli is CD277 dependent
Expression of B7-H1, B7-DC, and PD-1 on B cells.
WP1066 induces caspase-dependent apoptosis.
The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. Serum-starved.
Enhanced expression of Cap43 gene by nickel in breast cancer cell lines. Enhanced expression of Cap43 gene by nickel in breast cancer cell lines. Expression.
BCR/ABL expression, tyrosine phosphorylation, and signaling in dasatinib- and imatinib-resistant cell lines and the ubiquitin inhibitor lactacystin modifies.
Effect of bevacizumab on the proliferation of A2780 cells.
e a b c d unstimulated +fMLP T308P-Akt S473P-Akt Akt (min)
Analysis of absolute CD4+ cytokine+ cell numbers pre- and post-ART.
LDL cholesterol inhibits Vγ9Vδ2 T-cell activation and cytokine production. LDL cholesterol inhibits Vγ9Vδ2 T-cell activation and cytokine production. Preexpanded.
Effect of SFN on the total activity and protein expression of HDACs in JB6 P+ cells. Effect of SFN on the total activity and protein expression of HDACs.
Presentation transcript:

Involvement of PI3K activation in TCR/CD3-dependent HIF-1α protein expression. Involvement of PI3K activation in TCR/CD3-dependent HIF-1α protein expression. A, Immunoblots for HIF-1α. Human peripheral blood T cells were incubated for 12 h in the absence or presence of 10 μM GF109203X (GX), 100 nM wortmannin (Wort), and immobilized anti-CD3 Ab (CD3). HIF-1α and β-actin proteins were detected in immunoblots as described in Materials and Methods. B, Akt phosphorylation. Human peripheral blood T cells were incubated for 12 h in the absence or presence of immobilized anti-CD3 mAb (CD3) under 21 or 1% oxygen concentration for 12 h. Thr308-phosphorylated form and total Akt protein was detected in immunoblots. Hiroshi Nakamura et al. J Immunol 2005;174:7592-7599 Copyright © 2005 by The American Association of Immunologists