Nuclear calcium signaling drives nuclear actin polymerization in T cells. Nuclear calcium signaling drives nuclear actin polymerization in T cells. (A)

Slides:

Advertisements

Similar presentations

Immunologic responses after the MN-mediated cancer immunotherapy.

Advertisements

Cytotoxicity of MSP samples to normal and cancer cell lines.

Nuclear Arp3 mediates formation of TCR-induced nuclear actin filaments

Increased movement of GPR55 KO cells in association with epithelial cells. Increased movement of GPR55 KO cells in association with epithelial cells. (A)

CD169+ macrophages mediate Lm translocation to the splenic T cell zones. CD169+ macrophages mediate Lm translocation to the splenic T cell zones. (A) Confocal.

Comparative analysis of the nuclear F-actin networks in A3

TCR signaling induces nuclear actin polymerization.

Inhibition of macropinocytosis activates the TFEB-TRPML1 axis.

Human PBMC-derived MERS-CoV–specific T cells are multifunctional.

Cytosolic entry of Lm required for CD8α+ DC recruitment.

Arp2/3-mediated formation of nuclear actin networks is essential for CD4+ T cell effector functions. Arp2/3-mediated formation of nuclear actin networks.

Characterization of the light-responsive transdermal MNs.

Mammary cell proliferation is inhibited when LAD1 is depleted.

Murine gingival MSCs and skin MSCs produce and secrete IL-1RA–EV

Ag governs CTL behavior at islets but is not required for their accumulation in large numbers. Ag governs CTL behavior at islets but is not required for.

Immune cell recruitment after the NIR-boosted and MN-mediated cancer immunotherapy. Immune cell recruitment after the NIR-boosted and MN-mediated cancer.

NCMs regulate T cell survival in TLOs via PD-L1.

PD-L1 expression is maintained on NCMs under inflammatory conditions and PD-L1+NCMs are found in TLOs. PD-L1 expression is maintained on NCMs under inflammatory.

Fig. 1 ZIKV RNA in blood and tissues.

LIMK1 inhibition protects against Aβ-induced neuronal hyperexcitability. LIMK1 inhibition protects against Aβ-induced neuronal hyperexcitability. (A) Representative.

Fig. 4 Labeling of Msmeg with DMN-Tre is fast and specific and depends on Ag85A function. Labeling of Msmeg with DMN-Tre is fast and specific and depends.

Cell viability tests. Cell viability tests. SEM images of (A) MC3T3-E1 cells and (B) MSCs on days 1, 3, and 5 of culture. (C) Survival rates of MC3T3-E1.

CD169+ macrophages mediate the transport of bacteria to T cell zones by trans-infecting CD8α+ DCs. CD169+ macrophages mediate the transport of bacteria.

Evaluation of multidonor class Ig sequences obtained from H5N1 and H7N9 vaccinated donors. Evaluation of multidonor class Ig sequences obtained from H5N1.

Microrobots with different cell-carrying capacities under different grid lengths (lg) and burr lengths (lb). Microrobots with different cell-carrying capacities.

CD4+CLA+CD103+ T cells in skin and blood are clonally related.

Vaccine MN confer protective innate and adaptive immunity.

Inhibition of CDK9 by UNC drives MYC loss.

Optimization of a MYC degradation screen.

Shared phenotype of CD4+CLA+CD103+ T cells from human blood and skin.

MYC degradation screen identifies a compound that stabilizes MYC protein. MYC degradation screen identifies a compound that stabilizes MYC protein. (A)

Memory-biased TCRs induce weaker TCR signals than effector-biased TCRs in vitro. Memory-biased TCRs induce weaker TCR signals than effector-biased TCRs.

Fig. 2 FcRL1 deficiency impairs antigen binding–induced calcium mobilization and the in vitro proliferation of primary B cells. FcRL1 deficiency impairs.

Fig. 1 Bioinspired design of AAD for promoting wound contraction.

Fig. 5 Conceptual diagram of the impact of acid deposition on calcium cycling and subsequent plant water use. Conceptual diagram of the impact of acid.

Fig. 2 ODN enhances EV transfer between cells expressing TLR9.

S-Affs colocalize with SUMO in mammalian cells.

Sensitivity analysis of cellular responses to perturbation of the DNA damage response signaling in the presence of chemotherapies. Sensitivity analysis.

Fig. 6 WPS imaging of different chemical components in living cells.

Galloping-like gait with the design of a two-legged robot.

Fig. 3 Hydrostatic pressure induces intracellular calcium increase via TRPM7 activation. Hydrostatic pressure induces intracellular calcium increase via.

Calcium release through TRPML1 controls myosin IIA retrograde flow at the rear of LPS-DCs. Calcium release through TRPML1 controls myosin IIA retrograde.

GSDMD localizes to the plasma membrane and is processed during NET formation. GSDMD localizes to the plasma membrane and is processed during NET formation.

Fig. 3 Prophylactic or therapeutic use of DECON protects from herpes infections in vitro. Prophylactic or therapeutic use of DECON protects from herpes.

Fig. 4 Effects of morphogen priming of engineered mesenchymal condensations on in vitro chondrogenic lineage specification at the time of implantation.

Initial testing and characterization of cAMPr in ES cells.

Tregs preferentially regulate TH2 cytokines in skin.

The channel-kinase TRPM7 regulates antigen gathering and internalization in B cells by Mithunah Krishnamoorthy, Laabiah Wasim, Fathima Hifza Mohamed Buhari,

Fig. 4 Enzyme activity of PE-ProK/Pt tuned by changing temperature or NIR light. Enzyme activity of PE-ProK/Pt tuned by changing temperature or NIR light.

Chronic Treg reduction exacerbates bleomycin-induced skin fibrosis.

UNC drives MYC protein loss.

IFN treatment of human midgestation villous explants induces syncytial knot formation. IFN treatment of human midgestation villous explants induces syncytial.

Fig. 6 MSC encapsulation in vitro within PdBT cross-linked gels.

Fig. 2 BX795 is nontoxic to HCE cells at therapeutic concentration.

Expansion of omental FRCs and FALC remodeling after intraperitoneal exposure to bacterial antigen. Expansion of omental FRCs and FALC remodeling after.

NE cleaves and activates GSDMD.

IL-9–expressing TH cells are highly enriched in CCR4+/CCR8+ effector memory TH cells. IL-9–expressing THcells are highly enriched in CCR4+/CCR8+effector.

Acute circadian disruption alters ILC3 cytokine secretion.

REV-ERBα deficiency reduces frequency and number of NKp46+ ILC3s.

Fig. 5 Reconstitution of the dormant state using fetal ovaries.

GSDMD is required for nuclear expansion during NETosis.

Fig. 2 Polymer-mediated optical activation of TRPV1 stimulates proliferation in ECFCs. Polymer-mediated optical activation of TRPV1 stimulates proliferation.

Fig. 4 Light-induced TRPV1 activation promotes in vitro tubulogenesis in ECFC cultures. Light-induced TRPV1 activation promotes in vitro tubulogenesis.

Fig. 3 Gene expression analysis in 48-plex drug treatment experiments.

Fig. 3 Neuroblast-induced morphological dynamics of reactive astrocytes involve the inhibition of Cdc42-regulated actin polymerization. Neuroblast-induced.

Fig. 2 hTERT induces expression of heat shock protein genes through HSF1 and interacts with Hsp70-1. hTERT induces expression of heat shock protein genes.

Fig. 3 Three small molecules inhibit the transport of CCR5 and do not affect transport of CCR1 or CXCR4. Three small molecules inhibit the transport of.

Fig. 1 Differential anterograde transport of CCR5 and TNF.

The neuropod cells. The neuropod cells. (Top left) Neuropod cells synapse with sensory neurons in the small intestine, as shown in a confocal microscopy.

Fig. 3 4n hybrids undergo bipolar and tripolar mitosis.

Presentation transcript:

Nuclear calcium signaling drives nuclear actin polymerization in T cells. Nuclear calcium signaling drives nuclear actin polymerization in T cells. (A) Live-cell imaging of Ca2+ release (top, X-Rhod-1 AM) and nuclear actin polymerization (bottom) in Jurkat NLA cells upon contact with a TCR-stimulatory surface. Shown are still images at the indicated time after exposure to the stimulatory surface (see also movie S4). (B) Quantification of Ca2+ release triggered upon contact with a TCR-stimulatory surface in cells analyzed as in (A). Depicted are means ± SD of total and nuclear Ca2+ levels from eight cells analyzed. FC, fold change. (C) Single-cell analysis over 20 min after activation. Occurrence of actin polymerization at the PM (red) or the nucleus (green) as well as Ca2+ release (yellow) is shown. (D to G) Visualization of Ca2+ release and nuclear actin polymerization upon PMA/Iono stimulation in A3.01 NLA cells. (D and E) Stills of live-cell imaging movies of Ca2+ release of the same cell before (t = 0 s) and after (t = 44 s) stimulation with PMA/Iono. Dashed circles indicate the position of the nucleus. (F and G) Quantification of Ca2+ release (means ± SD from at least six cells each; intensities normalized to the frame before stimulation). Cells were treated with DMSO (D and F) or the Ca2+ chelator BAPTA-AM (E and G). (H) Relative occurrence of nuclear actin filaments in A3.01 NLA cells after treatment with the indicated stimuli and small-molecule inhibitors of Ca2+ signaling (means ± SD from three experiments with at least 30 cells evaluated each per condition). (I and J) Inhibition of nuclear CaM impairs the formation of nuclear F-actin filaments. Representative micrographs (I) and quantification of occurrence of nuclear or PM F-actin (means ± SD of three experiments with 30 cells evaluated each per condition) (J). A3.01 NLA (nuclear F-actin) or Jurkat NLA (F-actin ring) cells transiently expressing mCherry or the nuclear CaM inhibitor CaMBP4.mCherry were analyzed 58 s or 5 min after activation of a TCR-stimulatory surface, respectively. Asterisks indicate mCherry-positive cells. Statistical significance relative to the PMA/Iono (H) or mCherry (J) control was assessed by one-way analysis of variance (ANOVA) or one-sample t test, respectively. Scale bars, 5 μm. Arrowheads indicate examples of nuclear F-actin filaments. N. Tsopoulidis et al. Sci. Immunol. 2019;4:eaav1987 Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works