Results 101 to 110 of about 48,228 (282)

Mitochondria and Neuromast Tagging With Fluorescent Gallium‐Triapine Analogues: In Cellulo MP FLIM and Zebrafish Live Imaging

open access: yesAdvanced Science, EarlyView.
Fluorescent BODIPY‐conjugated thiosemicarbazone ligands and their Ga(III), In(III), and Fe(III) complexes, inspired by Triapine, are developed as theranostic agents. Multiphoton FLIM and confocal microscopy in cancer cells and zebrafish reveal real‐time uptake, mitochondrial localisation, and whilst spectroscopic assays indicated preserved complex ...
Megan J. Green   +15 more
wiley   +1 more source

PVNCRF Neurons Regulate Migraine‐Like Allodynia by Activating CRFR2 on Spinal Trigeminal Caudalis Glutamatergic Neurons

open access: yesAdvanced Science, EarlyView.
Paraventricular CRF neurons in the hypothalamus project to glutamatergic neurons of the spinal trigeminal caudal nucleus, enhancing neuronal activation and CRFR2 signaling. This pathway increases CRF release and excitatory drive, promoting central sensitization and migraine‐related behaviors. Targeting the PVN–SP5C circuit provides a potential strategy
Jiang Bian   +13 more
wiley   +1 more source

Development and Structural Characterization of UTE‐156, a Covalent Inhibitor of the VCP/p97 AAA+ ATPase

open access: yesAdvanced Science, EarlyView.
The AAA+ ATPase Valosin‐containing protein (VCP/p97) regulates protein homeostasis by unfolding ubiquitinated substrates. Here, we describe UTE‐156, a novel irreversible covalent inhibitor that modifies Cys522 in the D2 ATPase motor domain. Although its pharmacochemical limitations preclude immediate therapeutic use, UTE‐156 serves as a valuable ...
Daniela Tamayo‐Jaramillo   +8 more
wiley   +1 more source

Acid Sphingomyelinase Regulates the Localization and Trafficking of Palmitoylated Proteins [PDF]

open access: yes, 2019
In human, loss of Acid Sphingomeylinase (ASM/SMPD1) causes Niemann-Pick Disease, type A. ASM hydrolyzes sphingomyelins to produce ceramides but protein targets of ASM remain largely unclear. ...
Kim, Yongsoon   +7 more
core   +2 more sources

T Cell Exhaustion in Cancer Immunotherapy: Heterogeneity, Mechanisms, and Therapeutic Opportunities

open access: yesAdvanced Science, EarlyView.
T cell exhaustion limits immunotherapy efficacy. This article delineates its progression from stem‐like to terminally exhausted states, governed by persistent antigen, transcription factors, epigenetics, and metabolism. It maps the exhaustion landscape in the TME and proposes integrated reversal strategies, providing a translational roadmap to overcome
Yang Yu   +7 more
wiley   +1 more source

How Escherichia coli Circumvent Complement-Mediated Killing

open access: yesFrontiers in Immunology, 2017
Complement is a crucial arm of the innate immune response against invading bacterial pathogens, and one of its main functions is to recognize and destroy target cells.
Angela S. Barbosa   +2 more
doaj   +1 more source

Serum MASP-1 in complex with MBL activates endothelial cells. [PDF]

open access: yes, 2014
The complement system plays an important role in the induction of inflammation. In this study we demonstrate that the initiation complexes of the lectin pathway, consisting of mannose-binding lectin (MBL) and associated serine proteases (MASPs) elicit ...
Ambrus   +50 more
core   +1 more source

Endoplasmic Reticulum Geometry Dictates Neuronal Bursting via Calcium Store Refill Rates and Exposes Selective Neuronal Vulnerability

open access: yesAdvanced Science, EarlyView.
The ER's continuous tubular network is maintained by ER‐shaping proteins whose mutation or dysregulation contributes to neurodegenerative diseases. Here, we show that ER morphology sets the speed of Ca2+ store replenishment between firing events. Disrupting ER continuity slows intra‐ER Ca2+ redistribution from extracellular refill (SOCE) sites, driving
Valentina Davi   +13 more
wiley   +1 more source

Secreted phospholipases A2 in hereditary angioedema with C1-inhibitor deficiency [PDF]

open access: yes, 2018
BackgroundHereditary angioedema (HAE) caused by deficiency (type I) or dysfunction (type II) of the C1 inhibitor protein (C1-INH-HAE) is a disabling, potentially fatal condition characterized by recurrent episodes of swelling. We have recently found that
Andrea Zanichelli   +16 more
core   +3 more sources

Immune Checkpoint Inhibitors and Immunomodulators for Cancer Immunotherapy: Insights Into Resistance and Therapeutic Strategies

open access: yesAdvanced Science, EarlyView.
The schematic diagram illustrates the roles of novel immune checkpoints, immunomodulatory factors, cell death and multimodal technologies in cancer immunotherapy. Abstract Cancer immunotherapy has redefined cancer treatment. However, the molecular and cellular basis of immune evasion and therapeutic resistance remains incompletely understood.
Fangquan Chen   +7 more
wiley   +1 more source

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