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Showing 1-30 of 63 results for "M6690" within Papers
Jonasz Jeremiasz Weber et al.
Neuropharmacology, 133, 94-106 (2018-01-23)
Deciphering the molecular pathology of Huntington disease is of particular importance, not only for a better understanding of this neurodegenerative disease, but also to identify potential therapeutic targets. The polyglutamine-expanded disease protein huntingtin was shown to undergo proteolysis, which results
Ming Zhou et al.
Brain research, 1500, 19-27 (2013-01-23)
α-Synuclein (α-syn) and oxidative stress play pivotal roles in the pathogenesis of Parkinson's disease (PD). However, the mechanisms underlying the interaction between α-syn and oxidative stress remain poorly understood. The present study provides evidence to suggest that the nuclear translocation
Gernot Walko et al.
PLoS genetics, 7(12), e1002396-e1002396 (2011-12-07)
Autosomal recessive mutations in the cytolinker protein plectin account for the multisystem disorders epidermolysis bullosa simplex (EBS) associated with muscular dystrophy (EBS-MD), pyloric atresia (EBS-PA), and congenital myasthenia (EBS-CMS). In contrast, a dominant missense mutation leads to the disease EBS-Ogna
Kelli G Sharp et al.
Experimental neurology, 257, 186-204 (2014-04-22)
As part of the NIH "Facilities of Research Excellence-Spinal Cord Injury" project to support independent replication, we repeated key parts of a study reporting robust engraftment of neural stem cells (NSCs) treated with growth factors after complete spinal cord transection
Wen-Feng Cai et al.
Cardiovascular research, 94(2), 333-341 (2012-03-14)
Junctin and triadin are calsequestrin-binding proteins that regulate sarcoplasmic reticulum (SR) Ca(2+) release by interacting with the ryanodine receptor. The levels of these proteins are significantly down-regulated in failing human hearts. However, the significance of such decreases is currently unknown.
Zhifeng Liu et al.
Experimental & molecular medicine, 52(4), 702-712 (2020-04-30)
To explore the role of calpain and its signaling pathway in lipopolysaccharide (LPS)-induced acute kidney injury (AKI), animal models of endotoxemia were established by administration of LPS to mice with endothelial-specific Capn4 knockout (TEK/Capn4-/-), mice with calpastatin (an endogenous calpain
Philip R Williams et al.
Nature communications, 5, 5683-5683 (2014-12-17)
Therapeutic strategies for spinal cord injury (SCI) commonly focus on regenerating disconnected axons. An alternative approach would be to maintain continuity of damaged axons, especially after contusion. The viability of such neuropreservative strategies depends on the degree to which initially
Zijing Sheng et al.
The Journal of clinical investigation, 122(12), 4344-4361 (2012-11-13)
8-Oxoguanine (8-oxoG), a common DNA lesion caused by reactive oxygen species, is associated with carcinogenesis and neurodegeneration. Although the mechanism by which 8-oxoG causes carcinogenesis is well understood, the mechanism by which it causes neurodegeneration is unknown. Here, we report
Vítor Ennes-Vidal et al.
PloS one, 6(4), e18371-e18371 (2011-04-13)
Trypanosoma cruzi is the etiological agent of Chagas' disease. During the parasite life cycle, many molecules are involved in the differentiation process and infectivity. Peptidases are relevant for crucial steps of T. cruzi life cycle; as such, it is conceivable
Wen-Yan Wang et al.
Experimental and therapeutic medicine, 25(5), 196-196 (2023-04-24)
Cerebral ischemia-reperfusion injury (CIRI) is associated with a poor neurological prognosis in patients who have experienced cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). The aim of the current study was to investigate the potential role of a calpain inhibitor in
Lorelei B Silverman-Gavrila et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 33(5), 1975-1990 (2013-02-01)
Low-frequency depression (LFD) of transmitter release occurs at phasic synapses with stimulation at 0.2 Hz in both isolated crayfish (Procambarus clarkii) neuromuscular junction (NMJ) preparations and in intact animals. LFD is regulated by presynaptic activity of the Ca(2+)-dependent phosphatase calcineurin
Himakarnika Alluri et al.
The Journal of biological chemistry, 291(53), 26958-26969 (2016-11-23)
Blood-brain barrier (BBB) breakdown and the associated microvascular hyperpermeability followed by brain edema are hallmark features of several brain pathologies, including traumatic brain injuries (TBI). Recent studies indicate that pro-inflammatory cytokine interleukin-1β (IL-1β) that is up-regulated following traumatic injuries also
Sachiko Murase
International journal of molecular sciences, 16(7), 15659-15669 (2015-07-18)
Excitatory/inhibitory imbalances are implicated in many neurological disorders. Previously, we showed that chronically elevated network activity induces vulnerability in neurons due to loss of signal transducer and activator of transcription 3 (STAT3) signaling in response to the impairment of the
Martin Puskarjov et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 32(33), 11356-11364 (2012-08-17)
The K-Cl cotransporter KCC2 plays a crucial role in neuronal chloride regulation. In mature central neurons, KCC2 is responsible for the low intracellular Cl(-) concentration ([Cl(-)](i)) that forms the basis for hyperpolarizing GABA(A) receptor-mediated responses. Fast changes in KCC2 function
Xiaoping Li et al.
BMC cardiovascular disorders, 13, 8-8 (2013-02-22)
Recent studies have demonstrated that myocardial calpain triggers caspase-3 activation and myocardial apoptosis in models of sepsis, whereas the inhibition of calpain activity down-regulates myocardial caspase-3 activation and apoptosis. However, the mechanism underlying this pathological process is unclear. Therefore, in
Stephanie N Thompson et al.
Journal of neurotrauma, 27(12), 2233-2243 (2010-09-30)
The cytoskeletal and neuronal protective effects of early treatment with the blood-brain barrier- and cell-permeable calpain inhibitor MDL-28170 was examined in the controlled cortical impact (CCI) traumatic brain injury (TBI) model in male CF-1 mice. This was preceded by a
Brian V Lien et al.
Experimental neurology, 314, 46-57 (2019-01-18)
Neural stem cells (NSCs) can differentiate into both neurons and glia after transplantation into spinal cord injury (SCI) sites. The neuronal component of stem cell grafts has the potential to form functional synaptic relays across the lesion site. The glial
Sarah E Pease-Raissi et al.
Neuron, 96(2), 373-386 (2017-10-13)
Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating side effect of many cancer treatments. The hallmark of CIPN is degeneration of long axons required for transmission of sensory information; axonal degeneration causes impaired tactile sensation and persistent pain. Currently the molecular
Adrienne L Andres et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 33(43), 16945-16960 (2013-10-25)
The complex effects of stress on learning and memory are mediated, in part, by stress-induced changes in the composition and structure of excitatory synapses. In the hippocampus, the effects of stress involve several factors including glucocorticoids and the stress-released neuropeptide
Leiting Pan et al.
Advanced science (Weinheim, Baden-Wurttemberg, Germany), 6(18), 1900865-1900865 (2019-09-29)
The dynamic response of the cell to osmotic changes is critical to its physiology and is widely exploited for cell manipulation. Here, using three-dimensional stochastic optical reconstruction microscopy (3D-STORM), a super-resolution technique, the hypotonic stress-induced ultrastructural changes of the cytoskeleton
Wen-Yan Wang et al.
International immunopharmacology, 93, 107377-107377 (2021-02-01)
Cerebral ischemia-reperfusion injury (CIRI) is the leading cause of poor neurological prognosis after cardiopulmonary resuscitation (CPR). We previously reported that the extracellular signal-regulated kinase (ERK) activation mediates CIRI. Here, we explored the potential ERK/calpain-2 pathway role in CIRI using a
D Jantas et al.
Neurotoxicology, 32(6), 845-856 (2011-06-21)
The dysfunction of the proteasome system is implicated in the pathomechanism of several chronic neurodegenerative diseases. Lactacystin (LC), an irreversible proteasome inhibitor, induces cell death in primary cortical neurons, however, the molecular mechanisms of its neurotoxic action has been only
Marina G Yefimova et al.
International journal of molecular sciences, 22(23) (2021-12-11)
Visual deficit is one of the complications of Huntington disease (HD), a fatal neurological disorder caused by CAG trinucleotide expansions in the Huntingtin gene, leading to the production of mutant Huntingtin (mHTT) protein. Transgenic HD R6/1 mice expressing human HTT
Amy L Clark et al.
Scientific reports, 7(1), 5611-5611 (2017-07-19)
Pro-inflammatory cytokines are important mediators of islet inflammation, leading to beta cell death in type 1 diabetes. Although alterations in both endoplasmic reticulum (ER) and cytosolic free calcium levels are known to play a role in cytokine-mediated beta cell death
Jin Wei et al.
Cell, 184(1), 76-91 (2020-11-05)
Identification of host genes essential for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection may reveal novel therapeutic targets and inform our understanding of coronavirus disease 2019 (COVID-19) pathogenesis. Here we performed genome-wide CRISPR screens in Vero-E6 cells with SARS-CoV-2
Tianling Ou et al.
PLoS pathogens, 17(1), e1009212-e1009212 (2021-01-20)
Hydroxychloroquine, used to treat malaria and some autoimmune disorders, potently inhibits viral infection of SARS coronavirus (SARS-CoV-1) and SARS-CoV-2 in cell-culture studies. However, human clinical trials of hydroxychloroquine failed to establish its usefulness as treatment for COVID-19. This compound is
Qun Chen et al.
Biochemical and biophysical research communications, 415(4), 533-538 (2011-11-08)
Ubiquitous calpains (calpain I and II) are generally recognized as cytosolic proteins. Recently, mitochondrial localized calpain I (μ-calpain) has been identified. Activation of mito-μ-calpain cleaves apoptosis inducing factor (AIF), a flavoprotein located within the mitochondrial intermembrane space, in liver mitochondria
Jian-Ying Zhang et al.
PloS one, 7(12), e52270-e52270 (2013-01-04)
The Ca(2+) paradox represents a good model to study Ca(2+) overload injury in ischemic heart diseases. We and others have demonstrated that contracture and calpain are involved in the Ca(2+) paradox-induced injury. This study aimed to elucidate their roles in
Hasan A Ahmad et al.
American journal of respiratory cell and molecular biology, 47(3), 379-386 (2012-05-15)
Right heart failure from right ventricular (RV) pressure overload is a major cause of morbidity and mortality, but its mechanism is incompletely understood. We tested the hypothesis that right heart failure during 4 hours of RV pressure overload is associated
Marek Ma et al.
Journal of neurotrauma, 29(2), 445-451 (2011-11-15)
Traumatic axonal injury is characterized by early cytoskeletal proteolysis and disruption of axonal transport. Calpain inhibition has been shown to protect axons in rodent models of traumatic brain injury. However, in these models, both white and gray matter are injured
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