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Showing 1-30 of 123 results for "MAB1622" within Papers
Biomarker evidence for mild central nervous system injury after surgically-induced circulation arrest.
Siman, R; Roberts, VL; McNeil, E; Dang, A; Bavaria, JE; Ramchandren, S; McGarvey, M
Brain Research null
Christopher Schrecker et al.
Cancers, 13(14) (2021-07-25)
Colorectal cancer (CRC) is a leading cause of cancer-related morbidity and mortality. In a cohort of 189 patients with CRC, we recently showed that expression of the cytoskeletal scaffolding protein non-erythroid spectrin αII (SPTAN1) was lower in advanced metastatic tumours.
Stefania Marsili et al.
PloS one, 10(2), e0115723-e0115723 (2015-02-20)
To examine the occurrence of endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) following acute light damage in the naturally-occurring canine model of RHO-adRP (T4R RHO dog). The left eyes of T4R RHO dogs were briefly light-exposed and
Askar M Akimzhanov et al.
Cell calcium, 53(2), 152-158 (2012-11-06)
An important role in the regulation of apoptotic calcium release is played by the ubiquitously expressed family of inositol 1,4,5-trisphosphate receptor (IP(3)R) channels. One model for IP(3)R activation during apoptosis is cleavage by the apoptotic protease caspase 3. Here we
Fangliang Zhang et al.
The Journal of cell biology, 197(6), 819-836 (2012-06-06)
Talin is a large scaffolding molecule that plays a major role in integrin-dependent cell-matrix adhesion. A role for talin in cell-cell attachment through cadherin has never been demonstrated, however. Here, we identify a novel calpain-dependent proteolytic cleavage of talin that
Nikolai Klymiuk et al.
Human molecular genetics, 22(21), 4368-4382 (2013-06-21)
Duchenne muscular dystrophy (DMD) is caused by mutations in the X-linked dystrophin (DMD) gene. The absence of dystrophin protein leads to progressive muscle weakness and wasting, disability and death. To establish a tailored large animal model of DMD, we deleted
Taro Saito et al.
Journal of neurochemistry, 102(1), 133-140 (2007-05-18)
Dysregulation of cyclin-dependent kinase 5 (Cdk5) by cleavage of its activator p35 to p25 by calpain is involved in the neuronal cell death observed in neurodegenerative disorders, including Alzheimer's disease. However, it is not yet clear how p25/Cdk5 induces cell
Dong-Dong Ren et al.
Developmental dynamics : an official publication of the American Association of Anatomists, 242(12), 1454-1465 (2013-09-03)
Planar cell polarity (PCP) signaling regulates the coordinated polarization of cells and is required for the normal development and function of many tissues. Previous studies have identified conserved PCP genes, such as Van Gogh-like 2 (Vangl2) and Prickle (Pk), in
Jordi Pedragosa et al.
Experimental neurology, 346, 113865-113865 (2021-09-22)
Leukocyte infiltration and blood-brain barrier breakdown contribute to secondary brain damage after traumatic brain injury (TBI). TBI induces neuroimmune responses triggering pathogenic complement activation through different pathways, including the lectin pathway. We investigated mechanisms underlying mannose-binding lectin (MBL)-mediated brain damage
Alexander Andersohn et al.
Frontiers in cell and developmental biology, 7, 198-198 (2019-10-18)
Chronic ER stress occurs when protein misfolding in the Endoplasmic reticulum (ER) lumen remains unresolved despite activation of the unfolded protein response. We have shown that traumatic injury such as a severe burn leads to chronic ER stress in vivo
M Curcio et al.
Cell death & disease, 6, e1645-e1645 (2015-02-13)
The glial cell line-derived neurotrophic factor (GDNF) has an important role in neuronal survival through binding to the GFRα1 (GDNF family receptor alpha-1) receptor and activation of the receptor tyrosine kinase Ret. Transient brain ischemia alters the expression of the
Nicholas T Hertz et al.
Neuron, 103(3), 412-422 (2019-06-22)
Selective synaptic and axonal degeneration are critical aspects of both brain development and neurodegenerative disease. Inhibition of caspase signaling in neurons is a potential therapeutic strategy for neurodegenerative disease, but no neuron-specific modulators of caspase signaling have been described. Using
Alexandre Briguet et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 22(12), 4190-4200 (2008-08-30)
Dystrophin deficiency is the underlying molecular cause of progressive muscle weakness observed in Duchenne muscular dystrophy (DMD). Loss of functional dystrophin leads to elevated levels of intracellular Ca(2+), a key step in the cellular pathology of DMD. The cysteine protease
Mark A Rudolf et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 40(20), 3915-3932 (2020-04-29)
Loss of sensory hair cells causes permanent hearing and balance deficits in humans and other mammals, but for nonmammals such deficits are temporary. Nonmammals recover hearing and balance sensitivity after supporting cells proliferate and differentiate into replacement hair cells. Evidence
Zhongwei Qu et al.
Journal of neurochemistry, 143(3), 282-293 (2017-09-14)
The expression of transient receptor potential canonical 6 (TRPC6) in central nervous system (CNS) is important for neuronal functions and certain neural disorders. However, the regulatory mechanism of TRPC6 expression in neurons is still obscure. In this study, we show
M Deshmukh et al.
Cell death and differentiation, 7(3), 250-261 (2000-04-04)
To examine whether multiple pathways of cell death exist in sympathetic neurons, we studied the cell death pathway induced by staurosporine (STS) in sympathetic neurons and compared it with the well-characterized NGF deprivation-induced death pathway. Increasing concentrations of STS were
Anne Korwitz et al.
The Journal of cell biology, 212(2), 157-166 (2016-01-20)
Proteolytic cleavage of the dynamin-like guanosine triphosphatase OPA1 in mitochondria is emerging as a central regulatory hub that determines mitochondrial morphology under stress and in disease. Stress-induced OPA1 processing by OMA1 triggersmitochondrial fragmentation, which is associated with mitophagy and apoptosis
Allopregnanolone prevents dieldrin-induced NMDA receptor internalization and neurotoxicity by preserving GABA(A) receptor function.
Briz, V; Parkash, J; Sanchez-Redondo, S; Prevot, V; Su?ol, C
Endocrinology null
Jing-Jing Zhou et al.
Experimental neurology, 332, 113391-113391 (2020-07-01)
Volume-regulated anion channels (VRACs) are critically involved in regulating cell volume, and leucine-rich repeat-containing protein 8A (LRRC8A, SWELL1) is an obligatory subunit of VRACs. Cell swelling occurs early after brain ischemia, but it is unclear whether neuronal LRRC8a contributes to
B Thivichon-Prince et al.
Journal of dental research, 88(10), 910-915 (2009-09-29)
A primary cilium, a sensory organelle present in almost every vertebrate cell, is regularly described in odontoblasts, projecting from the surfaces of the cells. Based on the hypothesis that the primary cilium is crucial both for dentin formation and possibly
Jonasz J Weber et al.
Human molecular genetics, 29(6), 892-906 (2020-01-22)
Proteolytic fragmentation of polyglutamine-expanded ataxin-3 is a concomitant and modifier of the molecular pathogenesis of Machado-Joseph disease (MJD), the most common autosomal dominant cerebellar ataxia. Calpains, a group of calcium-dependent cysteine proteases, are important mediators of ataxin-3 cleavage and implicated
Shao-Xia Chen et al.
Journal of neurochemistry, 145(2), 154-169 (2018-02-10)
Previous work from our laboratory showed that motor nerve injury by lumbar 5 ventral root transection (L5-VRT) led to interleukin-6 (IL-6) over-expression in bilateral spinal cord, and that intrathecal administration of IL-6 neutralizing antibody delayed the induction of mechanical allodynia
Kristen E DeDominicis et al.
Frontiers in neurology, 9, 490-490 (2018-07-20)
Treatments to improve outcomes following severe traumatic brain injury (TBI) are limited but may benefit from understanding subacute-chronic brain protein profiles and identifying biomarkers suitable for use in this time. Acute alterations in the well-known TBI biomarkers glial fibrillary acidic
Beatrice D'Orsi et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 32(5), 1847-1858 (2012-02-04)
Excitotoxicity resulting from excessive Ca(2+) influx through glutamate receptors contributes to neuronal injury after stroke, trauma, and seizures. Increased cytosolic Ca(2+) levels activate a family of calcium-dependent proteases with papain-like activity, the calpains. Here we investigated the role of calpain
Kaori Sugiyama et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 37(36), 8830-8844 (2017-08-20)
Glutamate-mediated excitotoxicity induces neuronal death by altering various intracellular signaling pathways and is implicated as a common pathogenic pathway in many neurodegenerative diseases. In the case of motor neuron disease, there is significant evidence to suggest that the overactivation of
Sohila Zadran et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 30(3), 1086-1095 (2010-01-22)
Calpain is a calcium-dependent protease that plays a significant role in synaptic plasticity, cell motility, and neurodegeneration. Two major calpain isoforms are present in brain, with mu-calpain (calpain1) requiring micromolar calcium concentrations for activation and m-calpain (calpain2) needing millimolar concentrations.
Li Wan et al.
Frontiers in molecular neuroscience, 11, 287-287 (2018-09-07)
Potassium chloride co-transporter 2 (KCC2), a major chloride transporter that maintains GABAA receptor inhibition in mature mammalian neurons, is down-regulated in the hippocampus during epileptogenesis. Impaired KCC2 function accelerates or facilitates seizure onset. Calpain, with two main subtypes of m-
Hermann C Altmeppen et al.
eLife, 4 (2015-02-06)
The prion protein (PrP(C)) is highly expressed in the nervous system and critically involved in prion diseases where it misfolds into pathogenic PrP(Sc). Moreover, it has been suggested as a receptor mediating neurotoxicity in common neurodegenerative proteinopathies such as Alzheimer's
Guo-Ying Yang et al.
The Journal of biological chemistry, 286(8), 6566-6576 (2010-12-24)
Axon development involves spatial-temporal cytoskeletal reorganization. However, how the cytoskeleton remodeling is modulated by extracellular cues is unclear. Here, we report a role of Wnt/Ca(2+) signaling in regulating actin and growth cone dynamics. We found that treatment of cultured cortical
T Lovekamp-Swan et al.
Neuroscience, 148(3), 644-652 (2007-08-21)
Soy phytoestrogens have been proposed as an alternative to estrogen replacement therapy and have demonstrated potential neuroprotective effects in the brain. We have shown that a high soy diet significantly reduces infarct size following permanent middle cerebral artery occlusion (MCAO).
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