The mechanism of action for TRIO, CHKA and BMX lies between the AT1R and EGFR. (A) Our hypothesis is that TRIO, CHKA and BMX lie between the activated.

Slides:

Advertisements

Similar presentations

Midbrain electrosensory neurons respond to envelopes.

Advertisements

From: Phosphatase-Mediated Crosstalk Control of ERK and p38 MAPK Signaling in Corneal Epithelial Cells Invest. Ophthalmol. Vis. Sci ;47(12):

Fig. 5. Prip silencing enhances the co-localization of GABARAP with insulin vesicles and β-tubulin.Co-localization of GABARAP (green) with insulin (red)

Recruitment of PH-Akt-GFP to the leading edge of the cell during chemotaxis. Recruitment of PH-Akt-GFP to the leading edge of the cell during chemotaxis.

RNAi screen for host factors involved in L. monocytogenes dissemination. RNAi screen for host factors involved in L. monocytogenes dissemination. (A) Images.

Fig. 5. Effect of MPO on surface elasticity of human platelets

A highly conserved six-amino-acid region in the C-terminal CT domain of MARCH8 is responsible for its ability to downregulate TfR. A highly conserved six-amino-acid.

Fig. 2. p85β regulates cell adhesion

Specific inhibition of Ras, but not Rac, inhibits EGF-stimulated protrusion. Specific inhibition of Ras, but not Rac, inhibits EGF-stimulated protrusion.

Fig. 3. Read-outs of mTORC1 (P-S6(S235/236)) and mTORC2 (P-Akt(S473)) in wtPC12 and PC12-27 cells.(A,B) wtPC12 and PC12-27 cells were treated for 48 hr.

Fig. 1. Loss of PC following INT depletion

The trafficking of VSVG–GFP to pre‐Golgi structures is impaired by depletion of GMAP‐210.The trafficking of VSVG–GFP to pre‐Golgi structures is impaired.

TWEAK downregulates SIRT3 in cultured tubular cells and this is prevented by crotonate. TWEAK downregulates SIRT3 in cultured tubular cells and this is.

Proteins associated with PfSec13.

Fig. 3. Coilin levels correlate with altered nascent U2 snRNA, hTR and rRNA levels.RNA isolated from HeLa or WI-38 cells following RNAi targeting coilin.

Fig. 5. Receptor tyrosine kinase activation in response to growth factor stimulation. Receptor tyrosine kinase activation in response to growth factor.

FAK tyrosine phosphorylation is unaffected by loss of LAR activity.

Illustration of the hypothetical relationships among metabolic level, the intraspecific scaling exponent b and cell size. Illustration of the hypothetical.

Fig. 3. Rnd proteins induce stronger responses in subconfluent endothelial cells.HUVECs were transfected with Rnd1, Rnd2, Rnd3 or GFP-encoding plasmids.

Tamoxifen injections in αMHC-MerCreMer mice induce a loxP-independent DNA damage response, leading to myocardial dysfunction and death. Tamoxifen injections.

Fig. 4. Co-immunostaining of nocodazole or ASNase treated RPE-1 cells with anti-hASNS and anti-alpha tubulin showed defect in both mitotic spindle formation.

Overview of possible mechanisms by which activin can contribute to tumorigenesis. Overview of possible mechanisms by which activin can contribute to tumorigenesis.

TWEAK increases histone crotonylation in kidney tubular cells.

Fig. 4. Elevated levels of tRNAiMet promote migration and invasion of melanoma cells. Elevated levels of tRNAiMet promote migration and invasion of melanoma.

ArfGAP1 expression alters GBF1 recruitment to Golgi membranes.

Example of a putative bridging fiber.

Fig. 1. Loss of PC following INT depletion

SBF-SEM of mitotic spindles.

HEK293 cells transfected with ABCG2-K86M display no transport activity

The SIM domain of RAD51 is required for HR

MMP16 upregulation during myofibroblast differentiation

AT1R–EGFR transactivation occurs in HMEC-LST-AT1R cells.

Expression of active Rho partially rescues Erk1/2 activation and peripheral FA phenotype in RIAM-knockdown cells. Expression of active Rho partially rescues.

Synergistic WNT1 and WNT7B signaling is downstream of LRP6 phosphorylation and β-catenin stabilization. Synergistic WNT1 and WNT7B signaling is downstream.

Functions of AP-1 subunits in various cellular processes and disease.

miR-145 regulates embryo attachment.

Stimulation of cells with FFAR4 agonist.

The expression of two forms of N-cadherin.

Effect of the siRNA-mediated knockdown of endogenous MARCH8 on the expression levels of MARCH8 substrates, TfR and CD98, in HepG2 cells. Effect of the.

miR-145 overexpression reduces IGF1-coated bead attachment.

Peroxisome speeds were slower in patient and control cells.

Downregulation of caveolin-1 by si-RNA in NIH3T3 cells increased survivin expression. Downregulation of caveolin-1 by si-RNA in NIH3T3 cells increased.

Fig. 6. RhoB is required for Rnd3-induced stress fibre formation

Biphasic increase of PI(4,5)P2 level in LPS-stimulated cells.

Clustering of CD14 in the plane of the plasma membrane of LPS-stimulated cells. Clustering of CD14 in the plane of the plasma membrane of LPS-stimulated.

Table 1. Measurement of ring diameters of proteins localizing in ring-like patterns around centrioles.Consideration of the size of IgG (about 8 nm) raises.

Effect of PDGF-BB on mesenchymal mesonephric cell migration.

Suppression of SNX2 or the joint suppression of SNX2 and SNX1 has no gross affect on EGF or transferrin receptor sorting. Suppression of SNX2 or the joint.

The number of neurons presenting crosstalk from cAMP to the ERK1/2 cascade increases with age. The number of neurons presenting crosstalk from cAMP to.

WT MARCH8, but not the CS mutant, specifically ubiquitinates and downregulates TfR. WT MARCH8, but not the CS mutant, specifically ubiquitinates and downregulates.

FAK is required for LPA-mediated induction of trailing-edge retraction and the restoration of normal morphology. FAK is required for LPA-mediated induction.

BCL-3 regulates expression of stemness-associated Wnt targets.

BCL-3 does not mediate β-catenin activity through promoting nuclear translocation or altering levels of LEF1. BCL-3 does not mediate β-catenin activity.

CD151-knockdown cells show an aberrant spreading response to PMA

Effect of siRNA transfection on colony formation by Renca cells.

Membrane integration of the model constructs depends on protein sequence, not codon usage. Membrane integration of the model constructs depends on protein.

Telomere cohesion is established in S phase in cohesin-ring-depleted cells. Telomere cohesion is established in S phase in cohesin-ring-depleted cells.

The impact of FIH-1 on ASPP2 protein interactions.

Role of Src and PTP-PEST in upregulation of tyrosine phosphorylation of paxillin and FAK. (A) Mock and D11 cells were pre-incubated with PP2 or PP3 (10 µM,

Extracellular BMP modulators have different effects on endothelial cell sprouting in the tube formation assay. Extracellular BMP modulators have different.

GPR124 is the receptor for WNT7B responsible for synergistic signaling

Tsg protein stimulates endothelial cell migration, proliferation and collagen gel spheroid sprouting. Tsg protein stimulates endothelial cell migration,

Loss of Drp1 induces replication stress-mediated genome instability.

The dynamics of Akt activation in cultured human keratinocytes.

Phenotype of S. pombe cells in the presence of B21P2 or LMB

TRIM17 and Beclin 1 colocalize with the anti-autophagy factor Mcl-1.

Effect of ERα Ub-binding ability on E2-induced receptor transcriptional activity. Effect of ERα Ub-binding ability on E2-induced receptor transcriptional.

Schematics of mechanisms behind compartmentalization of RBPs on microtubules. Schematics of mechanisms behind compartmentalization of RBPs on microtubules.

OPCML-associated RTK modulation affects downstream signaling.

Double knockdown of HER2/EGFR abolishes HPSE nucleolar localization in 231BR3 cells. Double knockdown of HER2/EGFR abolishes HPSE nucleolar localization.

Presentation transcript:

The mechanism of action for TRIO, CHKA and BMX lies between the AT1R and EGFR. (A) Our hypothesis is that TRIO, CHKA and BMX lie between the activated AT1R and EGFR and thus modulate the AT1R–EGFR transactivation response. The mechanism of action for TRIO, CHKA and BMX lies between the AT1R and EGFR. (A) Our hypothesis is that TRIO, CHKA and BMX lie between the activated AT1R and EGFR and thus modulate the AT1R–EGFR transactivation response. A proposed model for this theory is illustrated. (B) HMEC-LST-AT1R cells were transfected with siGFP, siTRIO, siCHKA or siBMX SMARTpool siRNAs for 72 hours and stimulated with either AngII (100 nM) or EGF ligand (0.5 ng/ml) for 10 minutes. Knockdown of TRIO (B), BMX (C) or CHKA (D) did not alter the response of the cells to 0.5 ng/ml EGF ligand. Data are representative of three independent experiments. Amee J. George et al. J Cell Sci 2013;126:5377-5390 © 2013. Published by The Company of Biologists Ltd