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MYOC encodes the protein myocilin, which is believed to have a role in cytoskeletal function. Additionally we are shipping Myocilin Proteins (23) and Myocilin Kits (5) and many more products for this protein.
Showing 10 out of 57 products:
Mouse (Murine) Polyclonal MYOC Primary Antibody for IHC, WB - ABIN3022197
Polansky, Fauss, Chen, Chen, Lütjen-Drecoll, Johnson, Kurtz, Ma, Bloom, Nguyen: Cellular pharmacology and molecular biology of the trabecular meshwork inducible glucocorticoid response gene product. in Ophthalmologica. Journal international d'ophtalmologie. International journal of ophthalmology. Zeitschrift für Augenheilkunde 1997
Show all 5 references for ABIN3022197
Mutated myocilin and heterozygous Sod2 (show SOD2 Antibodies) deficiency act synergistically in a mouse model of open-angle glaucoma
myocilin promotes cell proliferation and resistance to apoptosis via the ERK1/2 (show MAPK1/3 Antibodies) MAPK (show MAPK1 Antibodies) signaling pathway.
Myocilin binds to ErbB2 (show ERBB2 Antibodies)/ErbB3 (show ERBB3 Antibodies), activates these receptors, and affects the downstream PI3K-AKT (show AKT1 Antibodies) signaling pathway
Myocilin also stimulated osteogenic differentiation of wild-type MSCs, which was associated with activation of the p38 (show CRK Antibodies), Erk1/2 (show MAPK1/3 Antibodies), and JNK (show MAPK8 Antibodies) MAP kinase (show MAPK1 Antibodies) signaling pathways
We suggest that intracellular myocilin plays a role as a regulator of muscle hypertrophy pathways, acting through the components of dystrophin (show DMD Antibodies) associated protein complex.
The TIGR is implicated in resistance to oxidative stress. Despite the presence of a SOD motif, which is necessary for protection in mammalian cells, the protein is not a functional SOD, but might be involved in SOD activity.
TIGR is a newly identified component of the CNS glial scar that is likely to contribute to neuronal regenerative failure characteristic of the mammalian CNS.
Results do not support a causative role for increased MYOC levels or the MYOC gene in steroid-induced glaucoma.
Results show that myocilin and gamma-synuclein (show SNCG Antibodies) interact and as a result, myocilin's properties are changed.
These data suggest that production, apparent misfolding, and nonsecretion of mutant MYOC are not, by themselves, sufficient to cause glaucoma in vivo.
Familial linkage studies for primary angle-closure glaucoma have been performed and identified MYOC causative primary angle-closure glaucoma disease
The rate of CYP1B1 (show CYP1B1 Antibodies) mutations in Lebanese patients with primary congenital glaucoma (PCG) is lower than that reported in other Arab and Middle Eastern populations and suggests other genes are responsible.
Data show that predictive genetic testing for early onset Myocilin glaucoma can facilitate early detection of disease or discharge from routine ophthalmic examinations.
This study does not confirm a role for genetic variants in the MYOC, NR3C1 (show NR3C1 Antibodies) and FKBP5 (show FKBP5 Antibodies) genes in the pathogenesis of corticosteroid-induced ocular hypertension.
Glaucomatous MYOC mutations activate the IL-1beta (show IL1B Antibodies)/NF-kappaB (show NFKB1 Antibodies) inflammatory stress response and the glaucoma marker SELE (show SELE Antibodies) in trabecular meshwork cells.
Secondary structure prediction of the Ser341Pro MYOC gene mutation suggested that the MYOC protein was misfolded.
Mutations in myoc ofactomedin domain are causative in the autosomal dominant inherited form of the prevalent ocular disorder glaucoma.
A novel heterozygous missense mutation c.761CMYOC gene was identified as being co-segregated with the primary open-angle glaucoma phenotype in this family.
All POAG samples underwent full sequencing of the MYOC gene, and we found a sensitivity of 100%, specificity of 99.91%, positive predictive value of 95.65%, and negative predictive value of 100% between imputation and sequencing.
FAs (show FAS Antibodies), expression of fibrogenic markers, and myocilin in HTM cells. These characteristics of Hic-5 (show TGFB1I1 Antibodies) in TM cells indicate its importance in regulation of AH outflow through the TM in both normal and glaucomatous eyes.
endoproteolytic processing might regulate the activity of myocilin; the inhibition of the processing by pathogenic mutations impairs the normal role of myocilin
MYOC encodes the protein myocilin, which is believed to have a role in cytoskeletal function. MYOC is expressed in many occular tissues, including the trabecular meshwork, and was revealed to be the trabecular meshwork glucocorticoid-inducible response protein (TIGR). The trabecular meshwork is a specialized eye tissue essential in regulating intraocular pressure, and mutations in MYOC have been identified as the cause of hereditary juvenile-onset open-angle glaucoma.
, trabecular meshwork-induced glucocorticoid response protein
, mutated trabecular meshwork-induced glucocorticoid response protein