miR-155 impairs TGF-β1–mediated RB activation in DLBCL

Slides:



Advertisements
Similar presentations
Supplementary Figure 1. MiR-30a binding sites in NOTCH1 and NOTCH2 3’UTRs. The miR-30a binding site in NOTCH1 (nucleotides of the human 3’UTR.
Advertisements

PP1 and PP2A inhibitors rescue α-SMA expression and Akt phosphorylation from the inhibitory effects of TSA. After serum starvation, NHLFs were pretreated.
Takehiko Wada, Jeffrey W. Pippin, Yoshio Terada, Stuart J. Shankland 
Fig. 5. The measurement of phosphorylation of p53 level in N2A cells under high glucose condition and agmatine treatment. (A, B) p53 phosphorylation levels.
Pro-inflammatory stimulation of meniscus cells increases production of matrix metalloproteinases and additional catabolic factors involved in osteoarthritis.
Rab11-FIP3 silencing impairs T cell activation events.
by Nathalie Magnus, Delphine Garnier, and Janusz Rak
by Yunping Lin, Lauren Brown, David W. Hedley, Dwayne L
Antiangiogenic antithrombin down-regulates the expression of the proangiogenic heparan sulfate proteoglycan, perlecan, in endothelial cells by Weiqing.
Multiple myeloma cells catalyze hepatocyte growth factor (HGF) activation by secreting the serine protease HGF-activator by Esther P.M. Tjin, Patrick W.B.
The lymphoma-associated NPM-ALK oncogene elicits a p16INK4a/pRb-dependent tumor-suppressive pathway by Paola Martinelli, Paola Bonetti, Cristina Sironi,
The TCL1 oncoprotein inhibits activation-induced cell death by impairing PKCθ and ERK pathways by Gilles Despouy, Marjorie Joiner, Emilie Le Toriellec,
Genetic alterations in the PI3K–PTEN–AKT pathway detected during disease progression and their functional impacts. Genetic alterations in the PI3K–PTEN–AKT.
FAM49B controls T cell activation by regulating cytoskeleton remodeling. FAM49B controls T cell activation by regulating cytoskeleton remodeling. (A) J.FAM49B.
TGF-β1 induces ILK activity in renal tubular epithelial cells.
by Fan Dong, and Andrew C. Larner
by Katsushi Miura, and Donald W. MacGlashan
A. D. B. C. - ΔNP63α - β-Actin IMEC - SUM MDA-MB IMEC
Angiopoietins can directly activate endothelial cells and neutrophils to promote proinflammatory responses by Caroline Lemieux, Ricardo Maliba, Judith.
Small-molecule inhibitor QLT-0267 suppresses ILK activity and inhibits its downstream signaling. Small-molecule inhibitor QLT-0267 suppresses ILK activity.
Signal transducer and activator of transcription 6 is frequently activated in Hodgkin and Reed-Sternberg cells of Hodgkin lymphoma by Brian F. Skinnider,
2-Methoxyestradiol causes functional repression of transforming growth factor β3 signaling by ameliorating Smad and non-Smad signaling pathways in immortalized.
Constitutive STAT6 activation in primary mediastinal large B-cell lymphoma by Chrystelle Guiter, Isabelle Dusanter-Fourt, Christiane Copie-Bergman, Marie-Laure.
Volume 66, Issue 5, Pages (November 2004)
a b MCF-7 TR2 MCF-7 TR2 (Fold change) MTT Assay , (Fold change)
IN-1130, a novel transforming growth factor-β type I receptor kinase (ALK5) inhibitor, suppresses renal fibrosis in obstructive nephropathy  J.-A. Moon,
Human osteoarthritic chondrocytes are impaired in matrix metalloproteinase-13 inhibition by IFN-γ due to reduced IFN-γ receptor levels  R. Ahmad, M. El.
Supplementary Figure S2
Semaphorin-3A is expressed by tumor cells and alters T-cell signal transduction and function by Alfonso Catalano, Paola Caprari, Simona Moretti, Monica.
Pro-inflammatory stimulation of meniscus cells increases production of matrix metalloproteinases and additional catabolic factors involved in osteoarthritis.
CaMKII inhibition in human primary and pluripotent stem cell-derived chondrocytes modulates effects of TGFβ and BMP through SMAD signaling  B. Saitta,
Andreea M. Bujor, Jaspreet Pannu, Shizhong Bu, Edwin A. Smith, Robin C
The ΔrlmA mutant strain has impaired CWI pathway activation.
Volume 64, Issue 2, Pages (August 2003)
Yongli Bai, Chun Yang, Kathrin Hu, Chris Elly, Yun-Cai Liu 
MiR-34a contributes to megakaryocytic differentiation of K562 cells independently of p53 by Francisco Navarro, David Gutman, Eti Meire, Mario Cáceres,
Volume 84, Issue 2, Pages (August 2013)
Cellular localization of the “writers” and “erasers” in U2OS-G3BP1 cells. Cellular localization of the “writers” and “erasers” in U2OS-G3BP1 cells. (A)
Upregulation of Tenascin-C Expression by IL-13 in Human Dermal Fibroblasts via the Phosphoinositide 3-kinase/Akt and the Protein Kinase C Signaling Pathways 
Analysis of GFP expression in gfp loss-of-function mutants.
Supplementary Materials DNMT1-shRNA’ DNMT1-shRNA control DNMT1 DNMT3a
Inhibition of the Epidermal Growth Factor Receptor Suppresses Telomerase Activity in HSC-1 Human Cutaneous Squamous Cell Carcinoma Cells  Arief Budiyanto,
The role of SRC-C3G-RAP1 signaling in transformation induced by CRKL
Dimethylfumarate Specifically Inhibits the Mitogen and Stress-Activated Kinases 1 and 2 (MSK1/2): Possible Role for its Anti-Psoriatic Effect  Borbala.
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.
Volume 70, Issue 5, Pages (September 2006)
Alterations to TNFR1 signaling and complex formation in the absence of TRADD. (A–C) ERK, JNK, and IκB. traddWT/WT and traddKO/KO MEFs (A) and BM-Macs (B)
The effects of laminarin, PMA and zymosan on PKC phosphorylation.
Fig. 2. Histone H3 phosphorylation appears at prometaphase upon C4 treatment.(A) Western blots were realized on cells synchronized at mitotic entry in.
MiR-200c/141 overexpression in LS-8 cells induces E-cad expression and cell-cell adhesion. miR-200c/141 overexpression in LS-8 cells induces E-cad expression.
Time-dependent phosphorylation profile of p38-MAPK and JNKs in samples from gills of Mytilus galloprovincialis specimens subjected to hyperthermia (30°C).
miR-29 Inhibits Bleomycin-induced Pulmonary Fibrosis in Mice
USP2a regulates MYC expression through the MDM2–p53 axis.
(fold of TGF-β1 response)
PER is a substrate of CK1α.
Viral induction and targeted inhibition of galectin-1 in EBV+ posttransplant lymphoproliferative disorders by Jing Ouyang, Przemyslaw Juszczynski, Scott.
Morphologic changes induced in immortalized human podocytes after treatment with TGF-β1 (10 ng/mL, right) for 3 days when compared with control cells (left),
The dynamics of Akt activation in cultured human keratinocytes.
OPCML-associated RTK modulation affects downstream signaling.
The alterations of GSK-3 activity after pharmacological manipulation.
Variation in dUTPase expression in cell lines.
by Abigail M. Druck Shudofsky, and Chou-Zen Giam
Relationship of PMBL to Hodgkin lymphoma.
Heterozygous Mutations in MAP3K7, Encoding TGF-β-Activated Kinase 1, Cause Cardiospondylocarpofacial Syndrome  Carine Le Goff, Curtis Rogers, Wilfried.
Effects of visfatin on the cell proliferation and phosphorylation of ERK, Akt, and GSK-3β proteins in HCC cells. Effects of visfatin on the cell proliferation.
Curcumin suppresses the expression of antiapoptotic proteins in multiple myeloma cells. Curcumin suppresses the expression of antiapoptotic proteins in.
MDM2 Protein Overexpression Inhibits Apoptosis of TF-1 Granulocyte-Macrophage Colony-Stimulating Factor–Dependent Acute Myeloblastic Leukemia Cells by.
Expression of dominant-negative RasN17 completely suppresses Ras activation in Rh1 cells. Expression of dominant-negative RasN17 completely suppresses.
by Dana S. Levy, Jason A. Kahana, and Rakesh Kumar
The adaptor protein Lad associates with the G protein β subunit and mediates chemokine-dependent T-cell migration by Dongsu Park, Inyoung Park, Deogwon.
Presentation transcript:

miR-155 impairs TGF-β1–mediated RB activation in DLBCL miR-155 impairs TGF-β1–mediated RB activation in DLBCL. Western blot analysis of hypo-pRB (left panels) or phospho-Ser780 residue (right panels) was performed in the DLBCL cell lines Ly7 (A), Ly18 (B), and DHL5 (C), genetically modified to express an empty ... miR-155 impairs TGF-β1–mediated RB activation in DLBCL. Western blot analysis of hypo-pRB (left panels) or phospho-Ser780 residue (right panels) was performed in the DLBCL cell lines Ly7 (A), Ly18 (B), and DHL5 (C), genetically modified to express an empty vector (MSCV) or miR-155. Upon TGF-β1 exposure (5 ng/mL), an increase in the abundance of hypo-pRB (active RB) is detected in the MSCV-expressing cell lines and, to a much lesser degree, in their isogenic counterparts expressing miR-155 (left panels). In agreement with this observation, the phosphorylation levels of RB’s Ser780 residue was markedly suppressed by TGF-β1 in MSCV-expressing cells, but not in their isogenic miR-155 counterparts (right panels). Immunoblotting for total RB confirms that miR-155 does not modify its expression level, and equal loading is also verified with β-actin or tubulin. The data shown in this figure were confirmed in 2 to 4 biological replicates. Daifeng Jiang, and Ricardo C. T. Aguiar Blood 2014;123:86-93 ©2014 by American Society of Hematology