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Human Polyclonal OPTN Primary Antibody pour ICC, IF - ABIN4341482
Smith, Sewell, Levine, Chew, Dunne, OShea, Smith, Harrison, Macdonald, Bloom, Segal: Disruption of macrophage pro-inflammatory cytokine release in Crohn's disease is associated with reduced optineurin expression in a subset of patients. dans Immunology 2014
ALS-Associated E478G Mutation in Human OPTN (Optineurin) Promotes Inflammation and Induces Neuronal Cell Death.
review of optineurin dysfunction in amyotrophic lateral sclerosis and glaucoma [review]
The results of this study support the notion that OPTN mutations may lead to multiple proteins aggregation and neuronal degeneration.
OPTN may be a potential antisenescence factor in diabetic nephropathy.
these findings expand our knowledge on the molecular mechanism of ubiquitin- decorated autophagic substrates recognition by OPTN as well as the mutual regulation between OPTN and TBK1 in selective autophagy.
study performed mutational analysis of optineurin (OPTN) in six patients with amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) in Guam on the Kii Peninsula to reveal whether OPTN is associated with the pathomechanisms of Kii ALS/PDC. This is the first report of OPTN-positive inclusions in patients with Kii ALS/PDC.
rs1561570 may contribute to Paget's disease of bone since its T allele results in the loss of a methylation site in patients' DNA, leading to higher levels of OPTN gene expression and a corresponding increase in protein levels in patients' osteoclasts.
Results suggest that Optn potentiates LC3-II production and maturation of the phagophore into the autophagosome, by facilitating the recruitment of the Atg12-5-16L1 complex to Wipi2-positive phagophores.
Immunohistochemical analyses of motor neurons from OPTN-associated amyotrophic lateral sclerosis patients reveal that linear ubiquitin and activated NF-kappaB are partially co-localized with cytoplasmic inclusions, and that activation of caspases is elevated.
This study describes the crystal structures of optineurin/TBK1 complex and the related NAP1/TBK1 complex, uncovering the detailed molecular mechanism governing the optineurin and TBK1 interaction, and revealing a general binding mode between TBK1 and its associated adaptor proteins.
Data suggest that OPTN mRNA and protein expression are significantly decreased in fetal membranes and myometrium during spontaneous term labor; there appears to be no effect of preterm labor on OPTN expression in fetal membranes. In cultured myometrial cells, RNA interference of OPTN up-regulates expression of inflammation mediators in response to IL1B (inteleukin-1B).
When yeast genetic interaction partners held in common between human OPTN and ANG were validated in mammalian cells and zebrafish, MAP2K5 kinase emerged as a potential drug target for amyotrophic lateral sclerosis therapy
A new variant associated with Paget's Disease of Bone in OPTN, reinforcing the relevance of this gene for the development of this bone disease.
OPTN colocalizes with LC3 (autophagic vesicle marker) and alpha-synuclein positive puncta in rotenone-treated animals, potentially indicating an important role in autophagy and PD pathogenesis
Given the critical roles of TBK1, important regulatory mechanisms are required to regulate its activity. Among these, Optineurin (Optn) was shown to negatively regulate the interferon response, in addition to its important role in membrane trafficking, protein secretion, autophagy and cell division.
E50K, M98K, Q398X and E478G mutations in OPTN affect neuronal viability under normal or oxidative stress conditions.
We report a five-generation pedigree with a complex pattern of primary open angle glaucoma(POAG) inheritance; familial clustering of POAG in this pedigree is consistent with dominant inheritance of a glaucoma-causing gene, mutations were not detected in genes previously associated with autosomal dominant glaucoma, suggesting the involvement of a novel disease-causing gene in this pedigree.
These results suggest that the IRAK1-binding protein OPTN negatively regulates IL-1beta/LPS-induced NF-kappaB activation by preventing polyubiquitination of TRAF6.
This study therefore provides novel information regarding the role of Optn during T-cell activation, suggesting the possible importance of Optn during inflammation and/or autoimmune diseases.
Frontotemporal dementia -linked mutations in gene OPTN encoding autophagy adaptor proteins , indicate that impaired autophagy might cause Frontotemporal dementia.
Reduced TBK1 activation and IFN-beta production in primary microglia frommouse model in which the Ub-binding region of optineurin was deleted (Optn(470T)) upon Toll-like receptor stimulation. Also diminished expression and activation of several transcription factors that support the amplification loop for IFN-beta production including STAT1, IRF7 and IRF9.
findings suggest that changes in their accumulation, determined via quantitative comparison of the OPTN foci and IBs in the cells, are involved in pathological features of ALS
Report establishes optineurin as a positive regulator TBK1 via a bipartite interaction between these molecules.
OPTN-deficient mice were more susceptible to infection with Salmonella, confirming in vivo the importance of OPTN in bacterial clearance.
Optineurin knockdown enhances osteoclast differentiation. Optineurin inhibits osteoclast formation by modulating NF-kappaB and IFN-beta signaling.
Mutation in Optineurin gene is associated with Glaucoma.
Disruption in optineurin and myosin VI-mediated cellular trafficking is associated with amyotrophic lateral sclerosis.
OPTN plays a role in acute inflammation and neutrophil recruitment, potentially via defective macrophage proinflammatory cytokine secretion.
Its mutation is associated with open-angle glaucoma.
that ubiquitin (Ub)-binding domain mutants compromise the maturation of autophagosomes, which in turn interfered with optineurin-mediated autophagy and clearance of inclusion bodies
results indicated that optineurin trimers may be the basic unit of these oligomers. The oligomeric state can be affected by many factors that induce covalent bonds, such as H2O2 or E50K
Loss of optineurin in vivo results in elevated cell death and alters axonal trafficking dynamics
HACE1-OPTN axis synergistically suppresses growth and tumorigenicity of lung cancer cells.
Mutants in which the entire Ub-binding C-terminal region is deleted showed that optineurin is dispensable for NF-kappaB activation but necessary for optimal IRF3 activation in immune cells.
We found that OPTN knockdown induced neuronal cell death via NF-kappaB activation
We suggest that OPTN abundance is an important cellular factor in considering the cell type-specific vulnerability of striatal neurons in Huntington's disease
OPTN binds to polyubiquitylated species formed in response to LPS and poly(I:C), enhancing the activation of TBK1 that is required for optimal phosphorylation of IRF3 and production of IFNbeta.
The optineurin gene and protein are evolutionary conserved between humans and the rhesus monkey. High similarity of ocular expression and tissue distribution between the two optineurin proteins.
This gene encodes the coiled-coil containing protein optineurin. Optineurin may play a role in normal-tension glaucoma and adult-onset primary open angle glaucoma. Optineurin interacts with adenovirus E3-14.7K protein and may utilize tumor necrosis factor-alpha or Fas-ligand pathways to mediate apoptosis, inflammation or vasoconstriction. Optineurin may also function in cellular morphogenesis and membrane trafficking, vesicle trafficking, and transcription activation through its interactions with the RAB8, huntingtin, and transcription factor IIIA proteins. Alternative splicing results in multiple transcript variants encoding the same protein.
, E3-14.7K-interacting protein
, Huntingtin interacting protein L
, huntingtin yeast partner L
, huntingtin-interacting protein 7
, huntingtin-interacting protein L
, nemo-related protein
, optic neuropathy-inducing protein
, transcription factor IIIA-interacting protein
, transcrption factor IIIA-interacting protein
, tumor necrosis factor alpha-inducible cellular protein containing leucine zipper domains
, 14.7K-interacting protein 2
, FIP-2-like protein