• Immune cells as Microglia, Astrocytes and neurons are liable for inflammatory reaction that activate and produce inflammatory mediators to clear cellular debris from the damage area. (omicsonline.org)
  • To see which brain cells carried which VPS26, Simoes cultured primary mouse neurons, astrocytes, microglia, and endothelial cells separately. (alzforum.org)
  • Importantly, Aβ and tau species are able to activate astrocytes and microglia, which release several proinflammatory cytokines, such as tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β), together with reactive oxygen (ROS) and nitrogen species (RNS), triggering neuroinflammation. (biomedcentral.com)
  • Microglia (and astrocytes , another type of glial cells) are distributed in large non-overlapping regions throughout the brain and spinal cord. (anti-agingfirewalls.com)
  • Secondly, astrocytes are activated, disrupting normal function and driving amyloid beta accumulation. (howwechangedourminds.com)
  • However, new methods of characterizing some of the dynamic actions and multiple phenoypes of microglia and astrocytes have emerged, and these, combined with observational data and genome-wide association studies, can characterize pathologic events earlier in the course of disease and redirect research toward a more productive and proactive path. (howwechangedourminds.com)
  • Jansen 2019) Since microglia and astrocytes are the primary producers of APOE, the protein with the strongest genetic link to AD, they are predicted to have a critical and complementary role in pathophysiology. (howwechangedourminds.com)
  • 2009) A Nurr1/CoREST pathway in microglia and astrocytes protects dopaminergic neurons from inflammation-induced death. (justia.com)
  • This protein has been identified as part of the enzymatic complex that cleaves amyloid-beta peptide from APP. (wikipedia.org)
  • Since alpha-secretase cleaves APP closer to the cell membrane than BACE1 does, it removes a fragment of the amyloid-β peptide. (pipelinedrugs.com)
  • APOE binds to cell-surface receptors to deliver lipids and to the hydrophobic amyloid-β peptide, regulating amyloid-β aggregations and clearances in the brain. (dovepress.com)
  • This behaviour is consistent with an apelin-bicelle binding process allowing significant peptide mobility, facilitating membrane-catalyzed GPCR encounter. (phoenixpeptide.com)
  • Tau protein is an integral part of microtubules in healthy neurons and support to nutrients, vesicles, mitochondria and chromosomes. (omicsonline.org)
  • It is a progressive, irreversible, and incurable neurodegenerative disorder that disrupts the synaptic communication between millions of neurons, resulting in neuronal death and functional loss due to the abnormal accumulation of two naturally occurring proteins, amyloid β (Aβ) and tau. (frontiersin.org)
  • In one, published December 28 last year, first author Sabrina Simoes and colleagues reported that neurons rely on vacuolar protein sorting ortholog 26b (VPS26b), a retromer component. (alzforum.org)
  • In the January 18 issue, Small, Beth Stevens at Boston Children's Hospital, and colleagues reported that knocking out a different retromer protein, VPS35, in hippocampal neurons in mice not only jammed neuronal endosome traffic but also caused microglia to assume shapes resembling those seen in AD. (alzforum.org)
  • Adding VPS35 back into the neurons restored both protein trafficking and microglial morphology. (alzforum.org)
  • Apolipoprotein E (APOE) is a lipid-transport protein abundantly expressed in most neurons in the central nervous system. (dovepress.com)
  • The amyloid precursor protein (APP) is a transmembrane glycoprotein expressed in several cells, including central nervous system neurons. (biomedcentral.com)
  • The microtubular protein tau is also essential in providing internal support and carrying nutrients to neurons. (biomedcentral.com)
  • [1] [2] Microglia are constantly scavenging the CNS for damaged neurons, plaques, and infectious agents. (anti-agingfirewalls.com)
  • Nurr1 continues to be expressed in adult mDA neurons, and the adult-onset deletion of the corresponding protein results in progressive loss of mDA neurons. (justia.com)
  • A subsequent study by Kovacs (1996) showed that PS1 and PS2 proteins are expressed in similar amounts, and in the same organelles as each other, in mammalian neuronal cells. (wikipedia.org)
  • In a cross-sectional study of 48 AD patients without diabetes, 20 cognitively normal diabetic patients, 16 patients with frontotemporal dementia, and 84 cognitively normal controls, researchers found that dysfunctionally phosphorylated insulin receptor substrate-1 (IRS-1), a neuronal protein, is detectable in blood using exosome-based technology and may be able to predict AD up to 10 years before the appearance of symptoms. (medscape.com)
  • The identification of dystrophic (senescent) microglia has created an ostensible conflict with prior work claiming a role for activated microglia and neuroinflammation during normal aging and in AD, and this has raised a basic question: does the brain's immune system become hyperactive (inflamed) or does it become weakened (senescent) in elderly and demented people, and what is the impact on neuronal function and cognition? (biomedcentral.com)
  • Both processes are damaging for microglia as they synergistically exhaust this essential cell population to the point where the brain's immune system is effete and unable to support neuronal function. (biomedcentral.com)
  • Similarly, marked modifications occur in the larger phosphoprotein clusters involving cytoskeleton and neuronal structures, membrane stabilization, and kinase regulation in the late elderly.Present findings may increase understanding of human brain proteostasis modifications in the elderly in the subpopulation of individuals not having AD neuropathological change and any other neurodegenerative change in any telencephalon region. (ibecbarcelona.eu)
  • Although different neuronal cell populations are affected across diverse neurodegenerative disorders, hallmark protein modifications is a common feature that supports the differential disease diagnosis and provides a mechanistic basis to gauge disease progression (Bossy-Wetzel et al. (maxwellmagneticmeds.co.za)
  • Here we show OS involvement in brain damage in a diabetic animal model that is at least partially mediated through an AD-pathology-independent mechanism apart from amyloid-β accumulation. (nature.com)
  • Alzheimer's disease (AD), the most common form of dementia, is characterized by the accumulation of amyloid β (Aβ) and hyperphosphorylated tau protein aggregates. (biomedcentral.com)
  • In AD, the propensity of neurotoxic proteins to form template or oligomers is higher and accelerates the conversion and aggregation of endogenous proteins, which eventually convert into fibrils ( Schaffert and Carter, 2020 ). (frontiersin.org)
  • Neuroinflammation and oxidative stress, mitochondrial dysfunction, dysregulation of the expression of histone deacetylases, and aggregation of pathogenic forms of proteins are among the most common and significant pathological features of neurodegenerative diseases. (actanaturae.ru)
  • Moreover, the transplantation of BMMSCs can decrease aberrant amyloid-beta peptides as well as tau aggregates, inhibit neuroinflammation, and stimulate synaptogenesis. (biomedcentral.com)
  • APOE is also involved in the formation of chylomicrons and VLDL and affects the activity of other lipid metabolism-associated proteins and enzymes, such as hepatic lipase and lipoprotein lipase. (dovepress.com)
  • Here, we examine interactions of the apelin-13 and -17 isoforms with isotropic zwitterionic and mixed zwitterionic-anionic lipid bicelles to test for hallmarks of membrane catalysis in a more physiological membrane-mimetic environment than a micelle. (phoenixpeptide.com)
  • Specifically, 3 areas of genetic correlation with AD-lipid regulation, immune regulation, and protein clearance-are promising areas of focus for targeted intervention. (howwechangedourminds.com)
  • Microglia, mobile throughout the CNS and tight regulators of lipid and lipoprotein metabolism, are first responders that undergo an adaptive shift in an attempt to address the overload and maintain homeostasis. (howwechangedourminds.com)
  • Lipid overload leads to formation of lipid droplet-accumulating microglia which resemble the foamy macrophages of atherosclerotic lesions. (howwechangedourminds.com)
  • Membrane glycosphingolipid (GSL) expression positively and sphingomyelin (SM) negatively correlated with multiploid cell formation, indicating the importance of lipid environment in the psychosine-mediated endomitosis. (sphingolipidclub.com)
  • These data indicated that membrane lipid environment could be important for the proper mitotic event(s). (sphingolipidclub.com)
  • Moreover, endomitotic cell cycles could be modulated by the lipid composition of the membrane among GSL, SM and phosphoinositides. (sphingolipidclub.com)
  • Membrane embedded proteins are functionally regulated by the lipid composition of the surrounding bilayer. (sphingolipidclub.com)
  • The transmembrane protein contains two active site aspartate residues in its extracellular protein domain and may function as a dimer. (pipelinedrugs.com)
  • Extracellular cleavage of APP by BACE1 creates a soluble extracellular fragment and a cell membrane-bound fragment referred to as C99. (pipelinedrugs.com)
  • As a consequence, drug development has focused on the least metabolically dynamic and most pathologically apparent end-stage sequelae of the disease: amyloid plaques and tau tangles. (howwechangedourminds.com)
  • Amyloid-beta plaques and tau protein tangles - hallmarks of the pathology - are most likely a non-specific result of the disease process, rather than a cause (Lee et al. (maxwellmagneticmeds.co.za)
  • 3 beta ( GSK-3β), N-methyl-D-aspartate (NMDA) receptor, monoamine oxidases (MAOs), metal ions in the brain, 5-hydroxytryptamine (5-HT) receptors, the third subtype of histamine receptor (H 3 receptor), to phosphodiesterases (PDEs), along with a summary of their respective relationship to the disease network. (encyclopedia.pub)
  • when these proteins bind to pattern recognition receptors in microglia and astroglia, they trigger an innate immune response characterized by the release of inflammatory mediators. (biomedcentral.com)
  • The receptors are members of the seven-transmembrane G protein-coupled receptor family. (lookformedical.com)
  • Cleavage of C99 within its transmembrane domain by γ-secretase releases the intracellular domain of APP and produces amyloid-β. (pipelinedrugs.com)
  • Suppression of experimental allergic neuritis by an antibody to the intracellular adhesion molecule ICAM-1. (2medicalcare.com)
  • ZO-1 is a protein located on a cytoplasmic membrane surface of intercellular tight junctions. (thermofisher.com)
  • In addition, we found monocyte chemoattractant protein-1(MCP-1) levels significantly increased, whereas intercellular adhesion molecule-1(ICAM-1) significantly decreased, and microglial marker (Iba1) did not change in the treatment group compared to the control. (biomedcentral.com)
  • Inhibition of experimental autoimmune encephalomyelitis by an antibody to the intercellular adhesion molecule ICAM-1. (2medicalcare.com)
  • Solanezumab -- Eli Lilly --Solanezumab, or sola, binds the amyloid-β peptides that aggregate and form plaques in the brain that are an early pathological feature of Alzheimer's disease. (pipelinedrugs.com)
  • Generation of the 40 or 42 amino acid-long amyloid-β peptides that aggregate in the brain of Alzheimer's patients requires two sequential cleavages of the amyloid precursor protein (APP). (pipelinedrugs.com)
  • C3G treatment reduced the levels of soluble and insoluble Aβ (Aβ40 and Aβ42) peptides and reduced the protein expression of the amyloid precursor protein, presenilin-1, and β-secretase in the cortical and hippocampal regions. (biomedcentral.com)
  • Apelin peptides are cognate ligands for the apelin receptor, a G-protein-coupled receptor (GPCR). (phoenixpeptide.com)
  • they provide insight into the factors that drive amyloid plaque development and are potential biomarkers or therapeutic targets for Alzheimer's disease (AD). (researchsquare.com)
  • We focused our study on early onset AD as the drivers of the more aggressive pathology development in these cases is unknown and it is unclear whether amyloid-plaque enriched proteins differ between subtypes of early onset AD. (researchsquare.com)
  • Amyloid plaques and neighbouring non-plaque tissue were microdissected from human brain sections using laser capture microdissection and label-free LC-MS was used to quantify the proteins present. (researchsquare.com)
  • Previous studies have shown that many of these plaque proteins have mechanistic role in AD. (researchsquare.com)
  • Previous studies have typically used immunohistochemistry to identify amyloid plaque proteins. (researchsquare.com)
  • Mass spectrometry-based proteomics is an alternative approach that allows efficient quantification of thousands of amyloid plaque proteins simultaneously. (researchsquare.com)
  • In my February 2010 blog entry New views of Alzheimer's disease and new approaches to treating it , I cited evidence for the hypothesis that microglial cell senescence is probably a fundamental cause for AD, a cause upstream of beta amyloid plaque production and the setting in of tau tangles. (anti-agingfirewalls.com)
  • Failure to clear amyloid beta, and prionlike proliferation of pathologic proteins, including amyloid plaque and tau tangle formation, represent the end stage of the disease. (howwechangedourminds.com)
  • Microglia are a type of glial cell that are the resident macrophages of the brain and spinal cord , and thus act as the first and main form of active immune defense in the central nervous system (CNS). (anti-agingfirewalls.com)
  • Microglia constitute 20% of the total glial cell population within the brain. (anti-agingfirewalls.com)
  • Adlkofer K, Frei R, Neuberg DH, Zielasek J, Toyka KV, Suter U. Heterozygous peripheral myelin protein 22-deficient mice are affected by a progressive demyelinating tomaculous neuropathy. (2medicalcare.com)
  • Anzini P, Neuberg DH, Schachner M, Nelles E, Willecke K, Zielasek J, Toyka KV, Suter U, Martini R. Structural abnormalities and deficient maintenance of peripheral nerve myelin in mice lacking the gap junction protein connexin 32. (2medicalcare.com)
  • This Review addresses single-molecule force spectroscopy experiments conducted on proteins with a known role in mechanosensing and mechanotransduction in eukaryotic cells. (ibecbarcelona.eu)
  • With the advent, development and refining of single-molecule nanomechanical techniques that enable the conformational dynamics of individual proteins under the effect of a calibrated force to be probed, we have begun to acquire a comprehensive knowledge of the diverse physicochemical principles that regulate the elasticity of single proteins. (ibecbarcelona.eu)
  • The treatment of Alzheimer's disease will require addressing the pillars of pathogenesis, namely, the advent and spread of neurotoxic oligomeric aggregates of beta-amyloid, the production of tau tangles, and chronic local inflammatory responses in the brain. (pipelinedrugs.com)
  • NPT088 from Neurophage binds with high affinity and specificity to aggregates of misfolded proteins, including those that form the canonical amyloid motif, which is implicated in the pathology of many serious diseases such as AD and PD. (pipelinedrugs.com)
  • Beta-secretase drugs and monoclonal antibodies are currently being tested to target beta-amyloid. (pipelinedrugs.com)
  • Additional studies have revealed a potential mechanism of action of anti-Aβ antibodies via experiments on transgenic mice overexpressing mutant human amyloid precursor protein (PDAPP) under the control of the mini-promoter of platelet-derived growth factor (PDGF) [ 9 ]. (biomedcentral.com)
  • However, protein levels of components of cell membranes, vesicles and synapses, RNA modulation, and cellular structures (including tau and tubulin filaments) are markedly altered from the age of 75. (ibecbarcelona.eu)
  • In addition, I will discuss recent studies demonstrating that SphK1 is recruited to sphingosine-enriched endocytic vesicles and that phosphorylation of sphingosine to S1P by SphK1 is involved in endocytic membrane trafficking and autophagy and in the crosstalk between endocytosis and autophagy. (sphingolipidclub.com)
  • The amino acid changes could alter the protein charge and stability, inducing distinct physiological functions. (dovepress.com)
  • They play a pivotal role in many physiological processes, including membrane remodelingand cell signaling [ 1, 2 ], and are involved in neurodegenerative disorders [ 3, 4 ]. (pharmaceuticalintelligence.com)
  • It is becoming increasingly clear that, particularly for chronic neurodegenerative disorders occurring late in life, a complex combination of risk factors can initiate disease development and modify proteins that have a physiological function into ones with pathological roles via a number of defined mechanisms (Moreno-Gonzalez and Soto, 2011). (maxwellmagneticmeds.co.za)
  • Memory tests showed mild to a strong improvement in memory function, increased expression levels of postsynaptic density protein 95 (PSD95), and low-density lipoprotein receptor-related protein 1 (LRP1), which are involved in synaptic plasticity and amyloid-beta (Aβ) elimination, respectively. (biomedcentral.com)
  • C3G administration mitigated tau phosphorylation and improved synaptic function and plasticity by upregulating the expression of synapse-associated proteins synaptophysin and postsynaptic density protein-95. (biomedcentral.com)
  • Ceramide generated in late endosomal compartments is recognized as a potent regulator of cell signaling, but its molecular interactions with late endosomal transmembrane proteins have not been studied in depth. (sphingolipidclub.com)
  • Here we uncover structural motifs required for ceramide interaction with the four membrane spanning Lysosome Associated Protein Transmembrane 4B (LAPTM4B). (sphingolipidclub.com)
  • Cell surface glycoproteins that bind to chemokines and thus mediate the migration of pro-inflammatory molecules. (lookformedical.com)
  • Extracts containing these terpene indole alkaloids (TIAs) can inhibit the formation and destabilize preformed fibrils of amyloid β protein (a pathological marker of Alzheimer's disease), and have been shown to improve the cognitive function of mice with Alzheimer-like symptoms. (biomedcentral.com)
  • in the brain this occurs in the microglia, which have the same embryonic origin as macrophages. (howwechangedourminds.com)
  • I. Muthukumarasamy, S.M. Buel, J.M. Hurley, and J.S. Dordick (2023), "NOX2 Inhibition Enables Retention of the Circadian Clock in BV2 Microglia and Primary Macrophages," Front. (rpi.edu)
  • A disintegrin and metalloproteinase domain-containing protein 10) and λ-secretase to produce soluble Aβ fragments. (biomedcentral.com)
  • See reference 8--After a string of failed trials, drugs that target protein build-up in the brain appear to slow disease progress. (pipelinedrugs.com)
  • 2 In the blood, APOE protein could interact with lipids, resulting in lipoproteins, including very-low-density lipoproteins (VLDL). (dovepress.com)
  • Previous studies showed that the NHD of PE-conjugated ATG8s mediates membrane hemifusion via a direct interaction with lipids in trans-membrane association, which would require the NHD in lipidated ATG8s to adopt a solvent-oriented, "open", conformation that unmasks a UBL domain surface needed for membrane tethering. (bvsalud.org)
  • As stated by Ikeuchi (2002) it cleaves the protein Notch1 so is thought by Koizumi (2001) to have a role in somitogenesis in the embryo. (wikipedia.org)
  • Formative event in AD, production of Amyloid beta is the result of cleavage of amyloid precursor protein (APP) which amyloid beta is high in AD [ 4 ]. (omicsonline.org)
  • Initial cleavage of APP by alpha-secretase rather than BACE1 prevents eventual generation of amyloid-β. (pipelinedrugs.com)
  • A multifunctional role of Atg8-family proteins (Atg8 from yeast and human LC3 and GABARAP subfamilies, all referred to here as ATG8s) in macroautophagy/autophagy is carried out by two protein domains, the N-terminal helical domain (NHD) and ubiquitin-like (UBL) domain. (bvsalud.org)
  • The Atg12 protein in yeast is an indispensable polypeptide in the highly conserved ubiquitin-like conjugation system operating in the macroautophagy/autophagy pathway. (bvsalud.org)
  • Based on meta-analysis and comprehensive review, high-profile studies support the theory that transplanted BMMSCs activate autophagy, as evidenced by the expression levels of signal molecules such as Beclin-1, Atg5, LC3-II, and mTOR. (biomedcentral.com)
  • Atg12 is comprised of a ubiquitin-like (UBL) domain preceded at the N terminus by an intrinsically disordered protein region (IDPR), a domain that comprises a major portion of the protein but remains elusive in its conformation and function. (bvsalud.org)
  • Mechanical force modulates the conformation and function of individual proteins, and this underpins many mechanically driven cellular processes. (ibecbarcelona.eu)
  • even 1 in 3 people die from Alzheimer's disease, and it is a growing epidemic across the globe fruits and vegetables rich in glucosinolates (GLCs), the precursors of isothiocyanates (ITCs), have long been known for their pharmacological properties and recently attracted increased interest for the possible prevention and treatment of neurodegenerative diseases. (frontiersin.org)
  • More recently, it has been demonstrated that mitochondrial dynamics likely plays a key role in AD and PD as proteins that regulate mitochondrial fission and fusion are altered in some neurodegenerative diseases [ 3 , 8 ]. (biomedcentral.com)
  • A monocyte chemoattractant protein that has activity towards a broad variety of immune cell types. (lookformedical.com)
  • Sola binds the central epitope of monomeric amyloid-β, KLVFFAD, (PDB ID 4XXD) with picomolar affinity. (pipelinedrugs.com)
  • Isolation and characterization of an oligodendrocyte precursor-derived B-cell epitope in multiple sclerosis. (2medicalcare.com)
  • Characterization of high-resolution structures and detergent micelle interactions of apelin-17 led to a two-step membrane-catalyzed binding and GPCR activation mechanism hypothesis recapitulated in longer isoforms. (phoenixpeptide.com)
  • Moreover, p66Shc (−/−) diabetic mice show significantly less cognitive dysfunction and decreased levels of OS and the numbers of microglia. (nature.com)
  • At the Alzheimer's Association International Conference® 2013 (AAIC®), researchers reported that the drug significantly lowered beta-amyloid levels in people with mild-to-moderate Alzheimer's. (pipelinedrugs.com)
  • Many of these proteins were more significantly enriched in amyloid plaques than Aβ. (researchsquare.com)
  • Morphological plasticity is a characteristic feature of microglia that is evident even in the static images of traditional microscopy, as shown here. (biomedcentral.com)
  • Recently, one important pathway for ROS regulation has been discovered, mediated by the signaling protein p66Shc. (nature.com)
  • Next, we showed that the resulting hybrids can differentiate and acquire a proto-neural electrophysiology profile when the Wnt/beta-catenin pathway is activated in the adult stem cells prior fusion. (regenerativemedicine.net)
  • Crenezumab -- Genentech and Roche --Crenezumab is a humanized monoclonal antibody against human 1-40 and 1-42 Beta amyloid, which is being investigated as a treatment of Alzheimer's disease. (pipelinedrugs.com)
  • CNP520 --Novartis' CNP520 is an oral drug designed to prevent the production of different forms of amyloid and has the potential to prevent, slow or delay the symptoms associated with Alzheimer's disease. (pipelinedrugs.com)
  • In two recent Cell Reports papers, scientists led by Scott Small, Columbia University, New York, detail new insights into the function of the retromer, an endosome protein complex linked to Alzheimer's disease. (alzforum.org)
  • Amyloid plaques are a neuropathological hallmark of Alzheimer's disease and primarily consist of the protein beta amyloid (Aβ). (researchsquare.com)
  • In the March 2011 blog entry Alzheimer's Disease Update I included a discussion on this hypothesis and on how with aging microglia lose their capability to get rid of beta amyloid via phagocytosis. (anti-agingfirewalls.com)
  • CD11, along with CD18, form a heterodimer adhesion molecule. (thermofisher.com)
  • The role of adhesion molecules in multiple sclerosis: biology, pathogenesis and therapeutic implications. (2medicalcare.com)
  • About Beta Secretase --Beta-secretase 1 (BACE1), also known as beta-site amyloid precursor protein cleaving enzyme is an enzyme that in humans is encoded by the BACE1 gene. (pipelinedrugs.com)
  • We then went on to demonstrate significant reductions in amyloid beta (Aβ) levels after AAV-based delivery of VHH-B9 into the CNS of a mouse model of cerebral amyloidosis. (biorxiv.org)
  • In addition, there is the potential for Fc receptor-mediated immunogenicity, mediated by microglia, which can cause vasogenic edema and cerebral microhemorrhage ( Panza et al , 2014 ). (biorxiv.org)
  • Several lines of evidence indicate that cerebral amyloid angiopathy (CAA) acts as a significant contributor to the AD pathology [ 13 , 14 ]. (biomedcentral.com)
  • In addition to limited and fragmented insights into the complex and interconnecting biologic pathways driving the disease, imprecision in diagnosis-specifically, grouping dementias despite dissimilarities-has contributed to slow progress. (howwechangedourminds.com)
  • The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. (oncotarget.com)
  • Thus, diabetes seems to affect cognitive function through not only AD-dependent mechanisms but also AD-independent mechanisms apart from amyloid metabolism. (nature.com)
  • The full-length PGRN can thus effectively reduce the calcification of valve interstitial cells, and the granulin precursor (GRN), among the degradation products of PGRN, can be beneficial. (biomedcentral.com)
  • It also has an action on an amyloid precursor protein, which gives its probable role in the pathogenesis of FAD. (wikipedia.org)
  • and group 4 (late-elderly, 75-85).Protein levels and deregulated protein phosphorylation linked to similar biological terms/functions, but involving different individual proteins, are found in FC with age. (ibecbarcelona.eu)
  • Noteworthy, protein levels of large clusters of hierarchically-related protein expression levels are stable until 70. (ibecbarcelona.eu)
  • Compromised c-Myc levels were encapsulated by a failure to engage translational machinery resulting in impaired metabolic protein and solute carrier production among others. (biomed.news)
  • Apfel R, Lottspeich F, Hoppe J, Behl C, Durr G, Bogdahn U. Purification and analysis of growth regulating proteins secreted by a human melanoma cell line. (2medicalcare.com)
  • B cell responses to the PNS protein P0 in experimental autoimmune neuritis. (2medicalcare.com)