Fig. 3. β-AR signaling induces IL-6 in NSCLC cells via activation of PKC and CREB. β-AR signaling induces IL-6 in NSCLC cells via activation of PKC and.

Slides:



Advertisements
Similar presentations
From: Protective Effect of a GLP-1 Analog on Ischemia-Reperfusion Induced Blood–Retinal Barrier Breakdown and Inflammation Invest. Ophthalmol. Vis. Sci..
Advertisements

Fig. 2. Effects of AZD4785 on proliferation and MAPK pathway signaling in KRAS mutant and wild-type cancer cells in vitro. Effects of AZD4785 on proliferation.
Fig. 7. Downstream effects of α-synuclein on mitochondria.
Fig. 1. IL-6 is associated with resistance to EGFR TKIs and is induced by stress hormones. IL-6 is associated with resistance to EGFR TKIs and is induced.
Differentiation of AZD4785 from MAPK pathway inhibitors in vitro
Fig. 3. Cytokines trigger proliferation and block differentiation of perivascular adipocytes. Cytokines trigger proliferation and block differentiation.
Transfer of miR-223 during neutrophil-epithelial cell interactions
A FOXO3a-BIM cascade mediates sensitivity to PARP and MEK inhibition
Fig. 2. Pharmacologic inhibition of ALK impairs STING activation.
Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.
Fig. 8. Gene and protein changes in ALK-dependent STING pathways in human sepsis. Gene and protein changes in ALK-dependent STING pathways in human sepsis.
β-ARs signal cooperatively with mutant EGFR and inactivate LKB1
Fig. 5 Maraba induces antitumor T cell immunity.
Fig. 4. Biomechanical properties of treated tibiae.
Fig. 4. Functional annotation of VUS in EGFR.
Analysis of brain and spinal cord of treated Gaa−/− mice and controls
Fig. 3. Frequencies of amino acids at critical PGT121 and contact sites in the SHIV-SF162P3 challenge stock. Frequencies of amino acids at critical.
Fig. 2 Maraba treatment results in complete responses in the window of opportunity setting. Maraba treatment results in complete responses in the window.
PVSRIPO-mediated APC activation occurs in immunosuppressive conditions
Fig. 6. Increased efficacy of immunotherapy in lymphangiogenic B16 melanomas depends on CCR7 signaling before therapy and local activation and expansion.
Fig. 3 TLR8 signaling induces CXCL4 and IFN-α secretion by SSc PDCs.
Bio-AMS enhances the activity of rifampicin and ethambutol in vitro
Fig. 8. Therapeutic effects of the transplantation of hiPSC-EPO–producing cells on renal anemia in adenine-treated mice. Therapeutic effects of the transplantation.
Fig. 4 CXCL4 potentiates TLR8-mediated activation of SSc pDCs.
Fig. 5. Stimulation of EPO expression and secretion under hypoxic culture conditions. Stimulation of EPO expression and secretion under hypoxic culture.
Identification of bioactive compounds modulating STING activation
Fig. 7 Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors. Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors.
Fig. 4. MATE1 transcription in RCC.
Fig. 7 pDCs are critical for the maintenance of skin fibrosis and for the presence of CXCL4 in the skin. pDCs are critical for the maintenance of skin.
Fig. 6. Apoptotic MSCs exert in vivo immunosuppression in a TH2-type inflammation model in the absence of cytotoxic cells. Apoptotic MSCs exert in vivo.
Fig. 4. Actin polymerization rhythms are required for circadian regulation of adhesion and wound-healing efficacy by fibroblasts. Actin polymerization.
Representative CT and PET/CT images of three patients with NSCLCs
Fig. 4 DMF enhances VSVΔ51 therapeutic efficacy in syngeneic and xenograft tumor models. DMF enhances VSVΔ51 therapeutic efficacy in syngeneic and xenograft.
Fig. 5 EGFR mutation status of patients with NSCLC, detected by histological examination and ARMS PCR. EGFR mutation status of patients with NSCLC, detected.
Fig. 1. mGlu7 expression is reduced in RTT autopsy samples.
Fig. 3. Recovery of AVP-deficient rats from anemia induced by sublethal irradiation. Recovery of AVP-deficient rats from anemia induced by sublethal irradiation.
Fig. 3. The effects of DCA on hemodynamic and functional end points and their association with genetic factors (variants of the SIRT3 and UCP2 genes) that.
Fig. 5 CXCL4 potentiates TLR9-mediated activation but has minimal effect on TLR7-mediated activation of pDCs purified from SSc or HDs. CXCL4 potentiates.
Fig. 2 Fas controls IL-1RA–sEV secretion in murine MSCs.
Fig. 7 Improvement of clinical score and axon pathology by nasal IL-4 treatment during chronic EAE. Improvement of clinical score and axon pathology by.
Fig. 7. Therapeutic effects of hiPSC-EPO protein on renal anemia in adenine-treated mice. Therapeutic effects of hiPSC-EPO protein on renal anemia in adenine-treated.
Fig. 8 SQLE inhibitor terbinafine suppresses NAFLD-HCC growth in vitro and in vivo. SQLE inhibitor terbinafine suppresses NAFLD-HCC growth in vitro and.
Fig. 7 CSPG4-high GBMs show more microglia than CSPG4-low GBMs and express TNFα. CSPG4-high GBMs show more microglia than CSPG4-low GBMs and express TNFα.
Fig. 5. Nutlin-3 treatment rescues the proliferation and differentiation of NPCs in vitro. Nutlin-3 treatment rescues the proliferation and differentiation.
Fig. 4 TNF-α up-regulates Fas/Fap-1 expression to promote IL-1RA–sEV release in murine MSCs. TNF-α up-regulates Fas/Fap-1 expression to promote IL-1RA–sEV.
STING activation induces inhibition of the mTORC1 pathway.
Fig. 1. β-APP overexpression or exposure to inflammatory mediators induces sIBM-like pathology in cultured rat myocytes that is abrogated by arimoclomol.
Human HFpEF is associated with impaired cardiac myofibril relaxation
Fig. 2 In vitro and preclinical study with 18F-MPG.
Fig. 2. Exposure of both TCR and CAR antigens diminishes efficacy of CAR8 but not CAR4 cells. Exposure of both TCR and CAR antigens diminishes efficacy.
Fig. 1. In vivo fates of patient-derived AML cells defined by mutational profile. In vivo fates of patient-derived AML cells defined by mutational profile.
Fig. 5. Induction of apoptosis via enhanced BCL-2 dependence in FLT3-ITD+ AML cells with diverse coexisting somatic mutations by in vivo kinase inhibition.
Fig. 5 DMN-Tre labeling is selective for live mycobacteria.
Fig. 6 DMF inhibits NF-κB translocation upon infection.
Fig. 7. Scale-up of AAV vector–mediated liver gene transfer of secretable GAA to nonhuman primates. Scale-up of AAV vector–mediated liver gene transfer.
Fig. 1 LB100 and LB102 specifically inhibit PP2A phosphatase activity and the growth of BCR-ABL+ cells. LB100 and LB102 specifically inhibit PP2A phosphatase.
CSF1 secretion by melanoma cells is induced by CTL-derived cytokines
Fig. 4 ALRN-6924 inhibits cellular proliferation and clonogenic capacity, and induces cell cycle arrest and apoptosis in AML cell lines. ALRN-6924 inhibits.
Fig. 2. BET inhibition enhances PARPi-induced DNA damage.
Fig. 3. Phenotypic characterization of FM2.5.
TGFBRAP1 plays a critical role in CHIT1 augmentation of TGF-β1 signaling and TGFβR expression. TGFBRAP1 plays a critical role in CHIT1 augmentation of.
Fig. 2. CD treatment facilitates regression of murine atherosclerosis.
Differentiation of AZD4785 from MAPK pathway inhibitors in vitro
Fig. 2. Spontaneous inflammasome activation by pyrin S242R.
IL-6 inhibits insulin-induced formation of p85/IRS-1 complexes.
Fig. 3. Effects of Tec on IL-1β-induced apoptosis in chondrocytes.
Fig. 1 AVPR1A is regulated by the AR coactivator VAV3 and AR-V7 and is increased in advanced human PC. AVPR1A is regulated by the AR coactivator VAV3 and.
ATF4 overexpression preserves parkin protein levels after treatment with dopaminergic neuronal toxins. ATF4 overexpression preserves parkin protein levels.
Aβ-mediated Ras-MAPK signaling and Cyclin D1 expression in B103 cells are dependent on APP expression and can be reversed with MEK or Ras inhibition. Aβ-mediated.
TGFβ1/Smad3 signaling suppresses IFNγ production via an E4BP4-dependent mechanism in NK-92 cells. TGFβ1/Smad3 signaling suppresses IFNγ production via.
Presentation transcript:

Fig. 3. β-AR signaling induces IL-6 in NSCLC cells via activation of PKC and CREB. β-AR signaling induces IL-6 in NSCLC cells via activation of PKC and CREB. (A) HCC827 and HCC4006 cells were treated with NE with or without Ro31-8220 (5 μM). LKB1S428 and p-CREBS133 were quantified by Western blotting, and (B) IL-6 was quantified by ELISA (*P ≤ 0.01; one-way ANOVA). Data are means ± SD. Representative data from two independent experiments performed in triplicate. (C) HCC827 cells were treated with a PKC inhibitor peptide and then stimulated with NE. LKB1S428 and p-CREBS133 were quantified by Western blotting. (D) LKB1 was stably overexpressed in HCC827 cells. After treatment with NE, IL-6 secretion was evaluated by ELISA. *P = 0.009; by two-tailed Student’s t test. Data are means ± SD. (E) NSCLC cells harboring EGFR-activating mutations (HCC827, HCC4006, H1650, and PC9) or wild-type EGFR (H460 and A549) were stimulated with NE, and p-CREBS133 was quantified by Western blotting. (F) HCC8227 and HCC4006 cells were treated with NE alone or in the presence of the CREBBP inhibitor SGC-CBP30 (1 μM), and IL-6 production was evaluated by ELISA. *P ≤ 0.01; one-way ANOVA. Data are means ± SEM. Monique B. Nilsson et al., Sci Transl Med 2017;9:eaao4307 Published by AAAS